TOXICOLOGICAL PROFILE FOR 

1,1-DICHLOROETHANE 

Agency for Toxic Substances and Disease Registry 

U.S. Public Health Service 

December 1990 
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 

1. PUBLIC HEALTH STATEMENT 

This Statement was prepared to give you information about l,l-dichloroethane and to emphasize 

the human health effects that may result from exposure to it. The Environmental Protection Agency 

(EPA) has identified 1,177 sites on its National Priorities List (NPL). l,l-Dichloroethane has been found at 

189 of these sites. However, we do not know how many of the 1,177 NPL sites have been evaluated for 

l,l-dichloroethane. As EPA evaluates more sites, the number of sites at which l,l-dichloroethane is found 

may change. The information is important for you because l,l-dichloroethane may cause harmful health 

effects and because these sites are potential or actual sources of human exposure to l,l-dichloroethane. 

When a chemical is released from a large area, such as an industrial plant, or from a container, 

such as a drum or bottle, it enters the environment as a chemical emission. This emission, which is also 

called a release, does not always lead to exposure. You can be exposed to a chemical only when you 

come into contact with the chemical. You may be exposed to it in the environment by breathing, eating, 

or drinking substances containing the 

chemical or from skin contact with it. 

If you are exposed to a hazardous substance such as l,l-dichloroethane several factors will 

determine whether harmful health effects will occur and what the type and severity of those health effects 

will be. These factors include the dose (how much), the duration (how long), the route or pathway by 

which you are exposed (breathing, eating, drinking, or skin contact), the other chemicals to which you are 

exposed, and your individual characteristics such as age, sex, nutritional status, family traits, life style, 

and state of health. 

1.1 WHAT IS l,l-DICHLOROETHANE? 

l,l-Dichloroethane is a colorless, oily, man-made liquid. It evaporates quickly at room temperature and 

has an odor like ether. l,l-Dichloroethane burns easily. When l,l-dichloroethane is released to the 

environment, it usually exists as a vapor rather than a liquid. It is used primarily to make l,l,ltrichloroethane and a number of other chemicals. It is also used to dissolve other substances such as paint, 

varnish and finish removers, and to remove grease. l,l-Dichloroethane was used as a surgical anesthetic, 

but is no longer. 

Almost all of the l,l-dichloroethane from industrial sources that is released goes into the air. l,lDichloroethane can also be found in the environment as a breakdown product of l,l,l-trichloroethane in 

landfills where no air comes in contact with the l,l,l-trichloroethane. l,l-Dichloroethane does not dissolve 

easily in water. The small amounts released to water can 
2 

1. PUBLIC HEALTH STATEMENT 

evaporate easily into the air. l,l-Dichloroethane remains as a vapor in the air for about 2 months and 

dissolved in water for about 5 days. The vapor in air can be washed out by rain or broken down by 

sunlight. l,l-Dichloroethane in water will evaporate. Small amounts of l,l-dichloroethane released to soil 

can also evaporate into the air or move through the soil to enter groundwater. It is not known how long l,ldichloroethane remains in the soil. Although it does not dissolve easily in water, low levels can be found 

in water. 

More information on the chemical and physical properties of l,l-dichloroethane can be found in 

Chapter 3, on its production and uses in Chapter 4, and on its occurrence and fate in the environment in 

Chapter 5. 

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

You can be exposed to l,l-dichloroethane by breathing air containing its vapors in the outdoor air or in 

your workplace, or by drinking water contaminated with it. Releases from industrial processes are the 

main source of this chemical in the air. Some members of the general population may be exposed to 

low levels of l,l-dichloroethane from this source (0.08-0.14 parts per billion [l part l,l-dichloroethane per 1 

billion parts of air, or ppb]). Levels in . this range have been measured around industrial plants in Magna, 

Utah (0.082 ppb); Iberville, Louisiana (0.12 ppb); Deer Park, Texas (0.14 ppb); and Baton Rouge (0.058 

ppb) and Geismary, Louisiana (0.14 ppb). You may be part of a much smaller population of workers who 

could be exposed to higher levels of l,l-dichloroethane in your workplace, if you are employed in the 

chemical, rubber and plastic, electrical, or oil and gas industries. However, since current levels of 

production and use are not known, it is difficult to predict how often exposure might occur from these 

sources of l,l-dichloroethane. Exposure can also occur near sites where the chemical was improperly 

disposed of or spilled on the ground. 

The average concentration of l,l-dichloroethane in the air across the United States is reported to be 55 

parts of l,l-dichloroethane per one trillion parts of air (ppt). These ambient levels may be from chlorinated 

water or building materials. The air levels of l,l-dichloroethane are usually lower in rural areas and higher 

in industrialized areas. Higher levels have been found in the air around some small sources of release, 

such as hazardous waste sites. l,l-Dichloroethane has been found in drinking water (that is, 

water that has usually been treated and that comes out of your tap) in the United States at levels that range 

from trace amounts to 4.8 parts of l,l-dichloroethane per one billion parts of water (ppb). l,lDichloroethane has not been detected in any surface water samples from rivers, lakes, or ponds. No 

information is available on background levels of l,l-dichloroethane in soil or food. 

Additional information on the levels of l,l-dichloroethane in the environment and human exposure to l,ldichloroethane can be found in Chapter 5. 
3 

1. PUBLIC HEALTH STATEMENT 

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

l,l-Dichloroethane can enter your body if you breathe contaminated air or drink contaminated 

water. l,l-Dichloroethane is believed to rapidly enter your body when it is breathed or swallowed. It is not 

known what factors affect how quickly l,l-dichloroethane enters your body. Studies in animals show that 

it is likely that l,l-dichloroethane can also enter your body through your skin. 

The most common way you could be exposed to l,l-dichloroethane released from hazardous waste 

sites would be by breathing contaminated air around the site. Soil and water in and around hazardous 

waste sites are not likely to contain high concentrations of l,l-dichloroethane because it escapes quickly 

into the air. Therefore, though this route of exposure cannot be ruled out completely, exposure of the skin 

from soil or water contaminated with l,l-dichloroethane is much less likely. 

Experiments in animals indicate that the l,l-dichloroethane that is inhaled or swallowed may go to 

many organs of the body, depending on the amount taken in. However, most of the l,l-dichloroethane 

taken in is usually removed unchanged from the body in the breath within 2 days. A small part of 

the l,l-dichloroethane taken in is broken down, and these breakdown products are quickly removed in the 

breath or urine. 

Additional information on how l,l-dichloroethane can enter and leave the body is presented in 

Chapter 2. 

1.4 HOW CAN l,l-DICHLOROETHANE AFFECT MY HEALTH? 

Reliable information on how l,l-dichloroethane affects the health of humans is not available. 

Because brief exposures to l,l-dichloroethane in the air at very high levels have caused death in animals 

(16,000 ppm), it is likely that exposure to such high levels of l,l-dichloroethane in the air can also cause 

death in humans. Some studies in animals have shown that l,l-dichloroethane can cause kidney disease 

after long-term, high-level exposure in the air. l,l-Dichloroethane caused cancer in animals given very 

high doses (over 3,000 mg/kg/day) by mouth for a lifetime. Delayed growth was observed in the offspring 

of animals who breathed high concentrations of l,l-dichloroethane during pregnancy. The severity of these 

effects may increase when people or animals are exposed to increased levels of l,l-dichloroethane. Since 

these effects were seen in animals at high doses, it is also possible that they could occur in humans 

exposed to high levels of l,l-dichloroethane. However, we have no information to indicate that these 

effects do occur in humans. More information on health effects associated with exposure to l,ldichloroethane can be found in Chapter 2. 
4 

1. PUBLIC HEALTH STATEMENT 

1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN HARMFUL HEALTH EFFECTS? 

There is no reliable information on what levels of exposure to l,l-dichloroethane have resulted in 

harmful health effects in humans. l,l-Dichloroethane is deadly to animals if large enough quantities are 

breathed or swallowed. Tables l-1 through l-4 show the relationship between exposure to l,ldichloroethane and known health effects in humans and animals. l,l-Dichloroethane can be smelled when 

it is present in the air at levels of 120 to 200 parts of l,l-dichloroethane per one million parts of air (ppm). 

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

l,l-DICHLOROETHANE? 

Tests are available that measure l,l-dichloroethane in urine, blood, breath and body tissues. 

Because urine, blood, and breath samples are easily obtained, these samples are examined to determine if 

a person has been exposed to l,l-dichloroethane. These tests are not routinely available at a doctor's 

office and would require special equipment for sampling and detection of the compound. Since most of 

the l,l-dichloroethane that is taken into the body leaves within two days, these tests must be done soon 

after exposure occurs. Although these tests can confirm that a person has been exposed to 

l,l-dichloroethane, it is not yet possible to use the test results to predict the type or severity of any health 

effects that might occur or the level of exposure that may have occurred. Because exposure to l,ldichloroethane at hazardous waste sites is likely to include exposure to other similar chemicals 

at the same time, levels of l,l-dichloroethane measured through these types of medical tests may not 

reflect exposure to l,l-dichloroethane alone. Information regarding tests for the detection of 1,1-dichloroethane 

in the body is presented in Chapters 2 and 6. 

1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

There are no regulatory standards or advisories for l,l-dichloroethane in drinking water and food. 

The Environmental Protection Agency (EPA) has determined that any release to the environment in 

excess of 1,000 pounds should be reported. 

Rules and regulations have been developed to protect individuals from the potential health effects 

of l,l-dichloroethane in air. The American Conference of Governmental Industrial Hygienists (ACGIH) 

has set a threshold limit value (TLV) of 810 mg/m3

 (200 ppm) l,l-dichloroethane in workroom air to 

protect workers during an S-hour shift over a 40-hour work week. The Occupational Safety and Health 

Administration (OSHA) has issued a permissible exposure limit (PEL) of 400 mg/m3

 (98.9 ppm). 

For more information on criteria and standards for l,l-dichloroethane exposure, see Chapter 7. 




9 

1. PUBLIC HEALTH STATEMENT 

1.8 WHERE CAN I GET MORE INFORMATION? 

If you have any more questions or concerns not covered here, please contact your State Health or 

Environmental Department or: 

Agency for Toxic Substances and Disease Registry.
 

Division of Toxicology
 

1600 Clifton Road, E-29
 

Atlanta, Georgia 30333
 

This agency can also give you information on the location of the nearest occupational and 

environmental health clinics. Such clinics specialize in the recognizing, evaluating, and treating illnesses 

that result from exposure to hazardous substances. 

11 

2. HEALTH EFFECTS 

2.1 INTRODUCTION
 

This chapter contains descriptions and evaluations of studies and interpretation of data on the 

health effects associated with exposure to l,l-dichloroethane. Its purpose is to present levels of significant 

exposure for l,l-dichloroethane based on toxicological studies, epidemiological investigations, and 

environmental exposure data. This information is presented to provide public health officials, physicians, 

toxicologists, and other interested individuals and groups with (1) an overall perspective of the 

toxicology of l,l-dichloroethane and (2) a depiction of significant exposure levels associated with various 

adverse health effects. 

2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

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

waste sites, the data in this section are organized first by route of exposure -- inhalation, oral, and dermal ­

- and then by health effect -- death, systemic, immunological, neurological, developmental, 

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

periods -- acute, intermediate, and chronic. 

Levels of significant exposure for each exposure route and duration (for which data exist) are 

presented in tables and illustrated in figures. The points in the figures showing no-observed-adverse-effect 

levels (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. These distinctions are intended to help the users of the document identify the levels of exposure at 

which adverse health effects start to appear, determine whether or not the intensity of the 

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

effects to human health. 

The significance of the exposure levels shown on the tables and graphs may differ depending on 

the user's perspective. For example, physicians concerned with the interpretation of clinical findings in 

exposed persons or with the identification of persons with the potential to develop such disease 

may be interested in levels of exposure associated with "serious" effects. Public health officials and 

project managers concerned with response actions at Superfund sites may want information on levels of 

exposure associated with more subtle effects (LOAEL) in humans or animals or exposure levels below 

which no adverse effects (NOAEL) have been observed. Estimates of levels posing minimal risk to 

humans (Minimal Risk Levels, MRLs) are of interest to health professionals and citizens alike. 
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2. HEALTH EFFECTS 

Estimates of exposure posing minimal risk to humans (MRLs) have been made, where data were 

believed reliable, for the most sensitive noncancer end point for each exposure duration. MRLs include 

adjustments to reflect human variability and, where appropriate, the uncertainty of extrapolating from 

laboratory animal data to humans. Although methods have been established to derive these levels (Barnes 

et al. 1987; EPA 1986a; EPA 1989), uncertainties are associated with the techniques. 

2.2.1 Inhalation Exposure 

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

inhalation exposure in humans or animals. l,l-Dichloroethane was used in the past as an anesthetic at a 

pressure of 0.026 atm, which is approximately equivalent to a concentration of 105,000 mg/m3

 (26,000 

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

cardiac arrhythmias at anesthetic doses (Browning 1965). 

ATSDR, in consultation with EPA, is evaluating the inhalation exposure database for 

development of inhalation MRLs. The evaluation process will be completed following the public 

comment period for this document. 

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

inhalation exposure levels at varying time and exposure durations. 

2.2.1.1 Death 

No studies were located regarding death in humans following inhalation exposure to l,ldichloroethane. No deaths were observed in rats exposed to 4,000 ppm for 8 hours, but an 8-hour 

exposure to 16,000 ppm was lethal (Smyth 1956). It has been reported in the early literature that the lethal 

exposure level of l,l-dichloroethane in mice was 17,500 ppm (Browning 1965). These values were 

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

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

dichloroethane for an additional 13 weeks was not lethal to rats, rabbits, guinea pigs, or cats (Hofmann et 

al. 1971). Based on these limited data in laboratory animals, it would appear that l,l-dichloroethane causes 

death in animals at high concentrations (16,000 ppm). 

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

2-l and plotted in Figure 2-l. 

2.2.1.2 Systemic Effects 

One study of the subchronic effects of inhaled l,l-dichloroethane in animals was located. No 

adverse clinical effects were noted in rats, rabbits, 



16 

2. HEALTH EFFECTS 

or guinea pigs exposed to 1000 ppm l,l-dichloroethane for 13 weeks, which followed a prior 13 week 

exposure to 500 ppm of l,l-dichloroethane (Hofmann et al. 1971). Histological examination of the liver 

and kidneys after 26 weeks revealed no treatment-related lesions. These NOAELs are recorded in Table 

2-l and plotted in Figure 2-l. However, this study is limited in that an inadequate number of animals was 

tested. Also, it is not clear how the lack of effects observed in these experiments relates to continuous 

exposure to 1000 ppm l,l-dichloroethane over a 26-week period. This is particularly relevant for humans 

living in the vicinity of hazardous waste sites since exposure to l,l-dichloroethane in this situation is 

expected to be continuous. No studies were located regarding respiratory, gastrointestinal, hematological, 

musculoskeletal, or dermal/ocular effects in humans or animals following inhalation exposure to l,ldichloroethane. 

Cardiovascular Effects. A cardiostimulatory effect resulting in arrhythmias prompted the 

discontinuance of the use of l,l-dichloroethane as an anesthetic in humans (Browning 1965). This effect 

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

equivalent to 105,000 mg/m3

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

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

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

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

serum glutamic oxaloacetic transaminase (SGOT) or serum glutamic pyruvic transaminase (SGPT) 

activity after intermittent 6-hour inhalation exposure to 500 ppm l,l-dichloroethane for 13 weeks followed 

by 13 weeks of exposure 6 hours per day to 1,000 ppm l,l-dichloroethane (Hofmann et al. 1971). 

Furthermore, no treatment-related histopathological lesions were noted in the livers of these animals after 

this 26 week exposure regimen. Six days after the tenth and last daily 7-hour exposure to 6,000 ppm l,ldichloroethane, female rats exhibited a slight but statistically significant increase in relative liver weight 

(Schwetz et al. 1974). However, there was no increase in SGPT activity over control values and no 

changes in the gross appearance of the liver were noted at necropsy in these animals. These results 

indicate that under the conditions of these studies, l,l-dichloroethane is not hepatotoxic. 

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

to l,l-dichloroethane. Renal injury was apparent in cats intermittently exposed 6 hours daily to 1,000 ppm 

l,l-dichloroethane for 13 weeks following 13 weeks of intermittent exposure to 500 ppm l,ldichloroethane (Hofmann et al. 1971). Serum urea and creatinine were increased in these animals. One cat 

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

tubules (including crystalline precipitates and dilation) were noted at necropsy. The ill health of these 

animals was also manifest by a progressive decrease in 
17 

2. HEALTH EFFECTS 

body weight. Rats, rabbits, and guinea pigs similarly exposed to l,l-dichloroethane exhibited no adverse 

effects. Thus, based on the results of this study, cats appear to be uniquely sensitive to the nephrotoxic 

effects of l,l-dichloroethane. This study is limited in that only four cats were used and it is not clear how 

the effects observed in this experiment relate to continuous exposure to 1000 ppm l,l-dichloroethane over 

a 26-week period. A NOAEL of 500 ppm was identified for cats. However, the observation that all 

cats exhibited a high degree of renal toxicity suggests that these findings were toxicologically significant. 

2.2.1.3 Immunological Effects 

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

exposure to l,l-dichloroethane. 

2.2.1.4 Neurological Effects 

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

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

neurologic effects of inhaled l,l-dichloroethane in humans. 

No studies were located regarding neurologic effects in animals after inhalation exposure to l,ldichloroethane. 

2.2.1.5 Developmental Effects 

No studies were located regarding developmental effects in humans following inhalation 

exposure to l,l-dichloroethane. 

In the only animal study located, retarded fetal development without any significant toxic effects was 

observed following inhalation exposure 7 hours daily to l,l-dichloroethane in pregnant rats during days 6 

through 15 of gestation (Schwetz et al. 1974). Except for a significant increase in the incidence gf fetuses 

with delayed ossification of sternebrae at an exposure level of 6,000 ppm, no other malformations were 

observed. The use of only two exposure levels precluded the assessment of a dose-dependent response. 

Maternal food consumption and body weight were significantly reduced in the treated animals during the 

exposure period but returned to normal by day 21 of gestation. No other adverse effects were noted in the 

dams. This study showed that l,l-dichloroethane is only slightly fetotoxic, though not teratogenic, in rats 

following inhalation exposure to high levels of the chemical, and it is not likely that humans would 

experience adverse developmental effects as a result of low-level exposure to l,l-dichloroethane. 

Based on the observed effects, the LOAEL value for the developmental toxicity of l,l-dichloroethane in 

rats was 6,000 ppm; the NOAEL was 3,800 ppm. These values are listed in Table 2-1 and plotted in 

Figure 2-1. 
18 

2. HEALTH EFFECTS 

2.2.1.6 Reproductive Effects 

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

exposure to l,l-dichloroethane. 

2.2.1.7 Genotoxic Effects 

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

exposure to l,l-dichloroethane. 

2.2.1.8 Cancer 

No studies were located regarding cancer in humans or animals after inhalation exposure to l,ldichloroethane. 

2.2.2 Oral Exposure 

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

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

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

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

with oral exposure levels at varying time and exposure durations. No MRLs to humans for adverse effects 

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

2.2.2.1 Death 

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

Secondary sources report the following oral LD50 in rats: 725 mg/kg (RTECS 1988) and 14.1 

g/kg (Grayson 1978). Since these values were obtained from secondary sources, no details were available 

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

the chronic bioassay conducted by NCI (1977), but a significant dose-related trend for mortality was 

noted in the male rats and mice. The deaths could not be attributed to cancer or any other non-neoplastic 

lesions, though pneumonia was observed in a large percentage of the rats, and this was thought to be 

related to the increased mortality (NCI 1977). 

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

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




23 

2. HEALTH EFFECTS 

2.2.2.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, 

musculoskeletal, hepatic, renal, or dermal/ocular effects in humans or animals following oral exposure to 

l,l-dichloroethane. There were no treatment-related histopathological changes in the liver, kidneys, or 

other tissues of the rats examined in the NCI (1977) study. Similarly, no histopathological alterations 

were noted in the liver, kidneys, or lungs of male mice that ingested relatively high levels of 

l,l-dichloroethane in drinking water (up to 2500 mg/L) for 52 weeks (Klaunig et al. 1986). 

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

oral exposure to l,l-dichloroethane. 

2.2.2.3 Immunological Effects 

2.2.2.4 Neurological Effects 

2.2.2.5 Developmental Effects 

2.2.2.6 Reproductive Effects 

2.2.2.7 Genotoxic Effects 

2.2.2.8 Cancer 

No studies were located regarding carcinogenic effects in humans following oral exposure to l,ldichloroethane. The results of the bioassay conducted by NCI (1977) suggest carcinogenic effects induced 

by l,l-dichloroethane in rats and mice. A significant positive dose-related trend was observed for the 

incidence of hemangiosarcomas and mammary adenocarcinomas in female rats, hepatocellular carcinoma 

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

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

animals. There are several limitations to this study. Survival was poor in both treated and control animals, 

thereby limiting the validity of these results. Although it appears that the maximum tolerated 

dose (MTD) had been reached (475 mg/kg/day for rats; 3,331 mg/kg/day for mice), it is not clear that the 

increase in mortality was treatment-related. Furthermore, there were no other treatment-related effects on 

body weight, clinical signs, or the incidence of non-neoplastic lesions. Because of the high mortality in 

both the treated and control animals, the authors concluded that not enough animals survived to be at risk 

for late-developing tumors. Thus, though the results of this bioassay suggest that l,l-dichloroethane is 

carcinogenic to rats and mice, the evidence is not conclusive. 
24 

2. HEALTH EFFECTS 

The carcinogenicity of l,l-dichloroethane was studied in mice chronically 

exposed to 475 mg/kg/day of the compound in the drinking water (Klaunig et 

al. 1986). A two-stage carcinogenesis protocol was also employed in this 

study to assess the ability of l,l-dichloroethane to act as a tumor promoter. 

Neither l,l-dichloroethane-treated animals initiated with diethylnitrosamine 

(DENA) or animals treated with l,l-dichloroethane without initiation showed a 

significant increase in the incidence of lung or liver tumors over their 

corresponding controls. The authors concluded that l,l-dichloroethane was not 

carcinogenic to mice and that it did not act as a tumor promoter following 

initiation with DENA under the conditions of this study. This was generally a 

well-conducted study: the MTD was used (as demonstrated in preliminary rangefinding 

studies), an adequate number of animals was used, and the appropriate 

clinical, gross, and microscopic observations were made. However, the 

conclusion that l,l-dichloroethane is not a tumor promoter may not be entirely 

justified since a maximal response was observed in terms of tumor incidence in 

the DENA-alone-treated mice (100% tumor incidence at 52 weeks). Therefore, an 

increase in the incidence of liver tumors due to l,l-dichloroethane following 

DENA initiation, if it existed, could not have been detected. Furthermore, 

since measurement of water consumption and replenishment were only done once a 

week, there was no way to determine the extent, if any, evaporation 

contributed to loss of the test chemical and affected the reported level of 

exposure. However, precautions were taken to minimize the loss of test 

chemical during the l-week period; amber bottles with Teflon stoppers and 

double sipper tubes were used. Since l,l-dichloroethane is a volatile 

chemical, this may present a limitation to the interpretation of results 

obtained from drinking water administration. 

The difference in results (e.g., induction of liver tumors) between the 

NC1 (1977) and Klaunig et al. (1986) studies may be due to the method of 

administration, vehicle, and/or doses used. The pharmacokinetics of 

l,l-dichloroethane may vary considerably when administered in drinking water 

ad libitum over a week as compared to bolus doses given in corn oil. 

Evidence obtained with carbon tetrachloride indicates that corn oil likely 

acts as a reservoir in the gut to delay and diminish the systemic absorption 

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

when ingested in water (Kim et al. 1990a,b). Furthermore, the doses given to 

mice by gavage were approximately six times higher than the drinking water 

concentrations. Species differences in susceptibility may also have played a 

role, as rats used in the NC1 study showed adverse effects at a dose that was 

without effect in the Klaunig et al. (1986) study. Sufficient information is 

not available to assess the contributions of these factors to the apparently 

disparate responses; i.e., the finding of 475 mg/kg/day as a LOAEL in the NC1 

study and the same dose as a NOAEL in the Klaunig study. 

2.2.3 Dermal Exposure 

No studies were located regarding the following health effects in humans 

or animals after dermal exposure to l,l-dichloroethane. 
25 

2. HEALTH EFFECTS 

2.2.3.1 Death 

2.2.3.2 Systemic Effects 

2.2.3.3 Immunological Effects 

2.2.3.4 Neurological Effects 

2.2.3.5 Developmental Effects 

2.2.3.6 Reproductive Effects 

2.2.3.7 Genotoxic Effects 

2.2.3.8 Cancer 

2.3 TOXICOKINETICS 

2.3.1 Absorption 

2.3.1.1 Inhalation Exposure 

No studies were located in humans or animals regarding the absorption of inhaled l,ldichloroethane. However, its use as a gaseous anesthetic agent in humans provides evidence of its 

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

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

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

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

coefficient of l,l-dichloroethane, its solubility in tissues, and the individual's ventilation rate and cardiac 

output. One of the most important factors controlling pulmonary absorption is the blood/air partition 

coefficient of the chemical. The concentration of the chemical and the duration of exposure are 

also important determinants of the extent of systemic absorption. 

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

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

four times that of l,l-dichloroethane. This suggests that l,l-dichloroethane would not be absorbed into the 

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

Nakajima 1987). However, the excretion of metabolites in the urine indicated that l,l-dichloroethane was 

absorbed following inhalation exposure, though the rate or extent of dichloroethane absorption is not 

known, since this represents theoretical estimates rather than actual data (Sato and Nakajima 1987). 
26 

2. HEALTH EFFECTS 

2.3.1.2 Oral Exposure 

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

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

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

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

(Mitoma et al. 1985). 

2.3.1.3 Dermal Exposure 

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

following dermal exposure. However, Browning (1965) reported evidence that l,l-dichloroethane 

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

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

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

color observed after 1 hour indicated that the halogen ion was absorbed into the bloodstream, though no 

quantitative assessment of the extent or rate of absorption was possible. 

2.3.1.4 Other Routes of Exposure 

Binding of radiolabeled l,l-dichloroethane or its metabolites to macromolecules (e.g. DNA, RNA, 

and proteins) in the liver, stomach, lung, and kidney of rats and mice following intraperitoneal injection is 

evidence that absorption of l,l-dichloroethane occurs (Colacci et al. 1985). 

2.3.2 Distribution 

2.3.2.1 Inhalation Exposure 

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

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

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

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

lipophilic chemical (i.e. the higher the lipid content of a tissue, the greater its uptake of l,l-dichloroethane) 

(Sato and Nakajima 1987) 

2.3.2.2 Oral Exposure 

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

humans or animals. 
27 

2. HEALTH EFFECTS 

2.3.2.3 Dermal Exposure 

No studies were located regarding the distribution of l,l-dichloroethane following dermal 

exposure in humans or animals. 

2.3.2.4 Other Routes of Exposure 

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

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

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

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

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

stomach were the only tissues analyzed in this study. 

2.3.3 Metabolism 

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

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

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

biotransformation of l,l-dichloroethane is mediated by hepatic microsomal cytochrome P-450 system. 

Large portions of orally administered l,l-dichloroethane are excreted unchanged by rats and mice 

in the expired air (Table 2-3). Forty-eight hours after oral administration of quite high doses of [14C]-1,1­

dichloroethane, 7.4% and 29.3% of the dose was metabolized by rats and mice, respectively. The 

predominant metabolite in both species was [14C]-CO2 (Mitoma et al. 1985). It is likely that the ingested 

radiolabeled l,l-dichloroethane underwent first-pass extraction by the liver. It has been suggested that high 

doses such as those used in this study exceed the capacity of the animals to metabolize l,l-dichloroethane 

(Bruckner 1989). The radiolabeled compound that was not excreted unchanged in the expired air was 

probably largely metabolized in the liver, followed by subsequent redistribution of labeled metabolites to 

other organs prior to their excretion. 

l,l-Dichloroethane was added to phenobarbital-induced and uninduced hepatic microsomes from 

rats, and P-450 enzyme activity was monitored by measuring the production of metabolite 

spectrophotometrically. Induction with phenobarbital significantly stimulated the binding, as well as 

hepatic microsomal NADPH oxidation, demonstrating the involvement of the P-450 system. 

Increased P-450 levels resulted in an increased affinity of enzyme for l,l-dichloroethane, thus increasing 

the rate of metabolism. ,6-naphthaflavone, an agent that specifically induces P-448, had no effect on the 

extent of l,l-dichloroethane binding, suggesting that P-448 is not involved in 

29 

2. HEALTH EFFECTS 

l,l-dichloroethane metabolism (McCall et al. 1983). The rate and extent of l,l-dichloroethane metabolism
 

was increased 6.3 times in the hepatic microsomes of rats that were induced by chronic ethanol
 

consumption (Sato et al. 1980). Chronic ethanol consumption increased the levels of P-450,
 

supporting the role of cytochrome P-450 in the metabolism of l,l-dichloroethane.
 

Colacci et al. (1985) reported that l,l-dichloroethane binds to nucleic acids and proteins in vivo 

and in vitro. This binding is also mediated by the liver cytochrome-P-450 system. Phenobarbital enhances 

the extent of covalent macromolecular binding. Hence, metabolites of l,l-dichloroethane bind to the 

DNA, RNA, and tissue proteins. The involvement of P-450 was confirmed by a reduction in binding 

when rats were pretreated with SKF-525-A, a P-450 inhibitor. Liver microsomes are the only tissue 

microsomes that are efficient in bioactivating l,l-dichloroethane. Therefore, binding to macromolecules of 

various organs in vivo could be due to an hepatic metabolite that is sufficiently stable to reach 

extrahepatic organs. Addition of GSH to the microsomal system suppresses the extent of binding and 

minimizes the potential for toxic effects. 

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

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

(Table 2-4) (McCall et al. 1983). On the basis of these results, pathways for the metabolism of 

l,l-dichloroethane were proposed (Figure 2-3). The initial steps in the metabolism of l,l-dichloroethane 

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

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

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

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

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

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

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

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

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

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

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

only one hydrogen. In a microsomal incubation, 13.5% of the 36C1 of l,l-dichloroethane was 

enzymatically removed after 30 minutes, while less than 0.5% of the 36C1 of 1,2-dichloroethane was 

removed (Van Dyke and Wineman 1971). 

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

free radicals is much less when compared to 
30 

2. HEALTH EFFECTS 

TABLE 2-4. Production of Metabolites from l,l-Dichloroethane with
 

Hepatic Microsomes from Phenobarbital-Induced Rats
 

Metabolites Metabolite Productiona 

(nmoles/mg microsomal proteion/20 min) 

Acetic acid 179 (15) 

2,2-Dichloroethane 0.12 (0.02) 

Chloroacetic acid 0.22 (0.08) 

Dichloroacetic acid 0.048 (0.005) 

Chloroacetaldehyde <0.07 (0.03) 

a

Values represent means (SD) for determinations in triplicate on three to five 

separate preparations of hepatic microsomes. 

Source: McCall et al. 1983. 

32 

2. HEALTH EFFECTS 

other chlorinated hydrocarbons like trichloroethane and carbon tetrachloride. It has been suggested that 

these free radicals possess the potential to induce toxic and carcinogenic effects. There is no correlation 

between the ease of free radical activation, covalent binding formation, or carcinogenic potency 

(Tomasi et al. 1984). 

2.3.4 Excretion 

One study was located regarding the extent or rate of l,l-dichloroethane excretion in humans (Sato 

and Nakajima 1987). They reported that 59% of the l,l-dichloroethane inhaled was metabolized and 

excreted in the urine and 41% was excreted in expired air. This amount of inhaled l,l-dichloroethane that 

was metabolized and excreted in the urine was considerably less than the 88% of inhaled 1,2­

dichloroethane that was metabolized and excreted in the urine. However, these values are theoretical and 

not actual. 

A study conducted by Mitoma et al. (1985) indicated that more than 90% of an oral dose in rats 

(700 mg/kg) and mice (1,800 mg/kg) was excreted unchanged or as carbon dioxide within 48 hours after 

administration. However, no blood, urine, or tissue concentrations were monitored over time to determine 

the elimination kinetic parameters. No studies were located in humans or animals regarding excretion of 

l,l-dichloroethane following dermal exposure. 

2.4 RELEVANCE TO PUBLIC HEALTH 

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

animals. However, the limited data available in animals indicate that it is less toxic than its isomer, 1,2­

dichloroethane, and most other chlorinated aliphatics (Bruckner 1989). Chlorinated aliphatics as a class 

are known to cause central nervous system depression, and respiratory tract and dermal irritation when 

humans are exposed by inhalation to sufficiently high levels (Parker et al. 1979). 

The available data in animals suggest that inhaled l,l-dichloroethane may be nephrotoxic. 

However, this finding is limited to one species (cat) and was not observed in three other species tested 

under the same conditions. Another effect observed in animals but not humans following inhalation 

exposure to l,l-dichloroethane exposure is fetotoxicity. Suggestive, but inconclusive, evidence of 

carcinogenicity was obtained in an oral chronic bioassay of l,l-dichloroethane in rats and mice. 

Death. No reports of death in humans following exposure to l,l-dichloroethane were found. Death has 

been observed in laboratory animals following inhalation and oral exposure to l,l-dichloroethane. No 

reliable LC50 or LD50 data were found, but lethal doses of l,l-dichloroethane are perhaps 5 to 10 times 

higher than those required to produce death following exposure to 1,2-dichloroethane or 

tetrachlorocarbons (EPA 1985; Hofmann et 
33 

2. HEALTH EFFECTS 

al. 1971; Smyth 1956). Thus, it is likely that l,l-dichloroethane can be fatal to humans, if exposure to high 

enough levels occurs. 

The cause of death in animals following exposure to l,l-dichloroethane has not been well-defined, 

but Plaa and Larson (1965) reported that deaths observed following intraperitoneal injection of this 

compound appeared to be due to fatal central nervous system depression. 

Systemic Effects. The use of l,l-dichloroethane as an anesthetic was discontinued when it was 

discovered that this compound induced cardiac arrhythmias in humans at anesthetic doses (approximately 

105,000 mg/m3

, or 26,000 ppm). The mechanism of action for the induction of cardiac arrhythmias 

by l,l-dichloroethane is not known. However, when the cardiac muscle is markedly depressed, it is more 

susceptible to the effects of catecholamines. Secretion of catecholamines is increased in this situation by 

compensatory and other mechanisms, resulting in excessive spontaneous contractions of the heart. This is 

an effect common to exposure to other chlorinated aliphatics at high concentrations (Reinhardt et al. 

1971). Cardiovascular toxicity has not been reported in animals following exposure to l,l-dichloroethane. 

No reports of adverse renal effects in humans following exposure to l,l-dichloroethane were 

found. Nephrotoxicity has been observed in cats following subchronic inhalation exposure to l,ldichloroethane. However, rats, rabbits, and guinea pigs exposed under the same conditions failed to 

exhibit any toxic effects on the kidney (Hofmann et al. 1971). Plaa and Larson (1965) tested renal 

function in mice following intraperitoneal injection of l,l-dichloroethane, and found that adverse effects 

on the kidney were only observed at lethal doses. These effects included increased glucose and protein in 

the urine and tubular swelling. Though data obtained following intraperitoneal injection provides 

information on potential health effects, data from oral, inhalation and dermal experiments are more 

relevant to possible exposures in humans. No histopathological changes in the kidney were noted after 

chronic ingestion of l,l-dichloroethane by rats and mice (Klaunig et al. 1986; NCI 1977). The 

toxicological significance of the nephrotoxicity observed in cats and the mice with regard to human health 

is not known given the small number of animals tested (cats), the lack of a nephrotoxic effect in other 

species and in other studies where l,l-dichloroethane was administered orally, and the fact that 

nephrotoxicity is not an effect commonly attributed to the halogenated hydrocarbons. 

Immunological Effects. No studies were located regarding immunologic effects in humans or 

animals following exposure to l,l-dichloroethane, and it is not known if l,l-dichloroethane is immunotoxic 

in humans. 

Neurological Effects. Chlorinated aliphatics as a class are known to cause central nervous system 

depression following high-level exposure in humans and animals. No reliable dose-response data were 

found on the central 
34 

2. HEALTH EFFECTS 

nervous system depression induced by l,l-dichloroethane, though l,l-dichloroethane was once used as an 

anesthetic agent in humans. However, Plaa and Larson (1965) attributed deaths observed in mice 

following intraperitoneal injection to fatal central nervous system depression. Neurologic effects 

associated with long-term exposure to l,l-dichloroethane in humans or animals have not been reported. 

Developmental Effects. Adverse developmental effects in humans associated with exposure to 

l,l-dichloroethane have not been reported. One study in rats indicated that inhalation exposure to l,ldichloroethane resulted in retarded fetal development (delayed ossification of vertebrae) in the absence of 

significant maternal toxicity (Schwetz et al. 1974). The absence of maternal toxicity implies a direct 

effect on the fetus, rather than effects due to illness in the dam. The implications of the findings from one 

study with regard to potential developmental effects in humans are not known. 

Reproductive Effects. No studies were located regarding reproductive effects in humans or 

animals following exposure to l,l-dichloroethane, and it is not known if l,l-dichloroethane has the 

potential to cause adverse reproductive effects in humans. 

Genotoxic Effects. No studies were located regarding in vivo genotoxic effects in humans. The 

genotoxic potential of l,l-dichloroethane has been investigated in vitro in Salmonella tvphimurium (Riccio 

et al. 1983; Simmon et al. 1977), Saccharomyces cerevisiae (Bronzetti et al. 1987; Simmon et al. 1977), 

and Syrian hamster embryo cells (Hatch et al. 1983). In addition in vitro and in vivo assays have been 

conducted using rat and mouse organs (Colacci et al. 1985). Results of these studies are summarized in 

Table 2-5. Results from three studies conducted in S. typhimurium tester strains were conflicting. l,lDichloroethane was nonmutagenic in yeast cells even in the presence of metabolic activation system. 

However, because of insufficient reporting of data by Bronzetti et al. (1987) and Simmon et al. (1977), no 

assessment of the genotoxic potential of l,l-dichloroethane in S. cerevisiae can be made. The available 

data from the remaining studies indicate that, although l,l-dichloroethane did not induce cell 

transformation in BALB/c-3T3 cells (Tu et al. 1985), it increased the frequency of transformations 

induced by Simian adenovirus (SA7) in hamster embryo cells (Hatch et al. 1983). 

In the Ames assay, l,l-dichloroethane was nonmutagenic in Salmonella strains TA97, TA98, 

Ta100, and TA102 (Nohmi et al. 1985). The compound was tested with and without metabolic activation. 

The highest dose was toxic to all strains of bacteria. In contrast, l,l-dichloroethane was mutagenic to 

strains TA1537, TA98, TA100, and TA1535 exposed to its vapor in a desiccator 

in the presence and absence of S9 mix (Riccio et al. 1983). Although the tests were conducted using three 

dose levels, the authors did not report the actual doses tested, and therefore the presence of a dosedependent response could not be assessed. Simmon et al. (1977) on the other hand obtained 

36 

2. HEALTH EFFECTS 

negative results using the same strains of Salmonella and a similar protocol. The concentrations of l,ldichloroethane tested were not reported. Because the reporting of data was insufficient in studies by 

Riccio et al. (1983) and Simmon et al. (1977), the discrepancies in their reported results cannot be 

explained at this time. 

l,l-Dichloroethane was nonmutagenic in yeast strains D3 and D7, even in the presence of S9 mix 

(Bronzetti et al. 1987; Simmon et al. 1977). Bronzetti et al. (1987) conducted an assay using strain D7 of 

Saccharomvces cerevisiae from the stationary and logarithmic growth phase. The cells harvested from 

the log phase cultures contained cytochrome P-450 and were capable of metabolizing promutagens to 

genetically active products. Both studies lacked details regarding doses of l,l-dichloroethane tested, 

though conflicting results may also be due to impurities in the chemicals used. 

Tu et al. (1985) exposed BALB/c-3T3 cells to l,l-dichloroethane in a sealed chamber for 24 

hours. No cell transformation was detected. This lack of effect may be due to the short period of 

exposure. However, l,l-dichloroethane increased the frequency of transformation induced by SA-7 virus 

in Syrian hamster embryo cells (Hatch et al. 1983). Embryo cell cultures were exposed in a sealed 

treatment chamber to volatilized l,l-dichloroethane for 20 hours and then treated with SA7 virus for 3 

hours. l,l-Dichloroethane treatment significantly increased the viral transformation frequency in cells 

in a dose-dependent manner. The highest concentration (1,000 μg/mL) was cytotoxic. These results 

reflect the capacity of l,l-dichloroethane to interact with cellular DNA in hamster embryo cells. 

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

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

following a single intraperitoneal injection of approximately 1.2 mg/kg. In vitro binding of l,ldichloroethane to nucleic acids and proteins was mediated by liver P-450 dependent microsomal mixed 

function oxidase system. Glutathione-s-transferase shifted the equilibrium of the enzymatic reaction and 

thereby decreased binding, presumably by reducing the amount of toxic metabolite available for 

binding to macromolecules. On the other hand, phenobarbital increased binding by increasing cytochrome 

P-450 activity, thus generating more toxic metabolites available for binding to macromolecules. 

Presumably the metabolites generated from P-450 enzymatic action on l,l-dichloroethane bind 

to cellular macromolecules. Lung microsomes were weakly effective whereas kidney and stomach 

microsomal fractions were ineffective. Therefore, the binding to macromolecules of various organs 

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

extrahepatic organs. Pretreatment with phenobarbital enhanced the binding to DNA, microsomal RNA 

and proteins while addition of glutathione-s-transferase (GSH) to the microsomal systems caused 

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

μmole bound represents l,l-dichloroethane or its metabolite(s). However, the fact 
37 

2. HEALTH EFFECTS 

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

appears to play a detoxification role in the metabolism of l,l-dichloroethane. The fact that l,ldichloroethane binds to nucleic acid suggests that it may have a potential to produce mutation in a 

mammalian system. 

Cancer. There is inconclusive evidence that l,l-dichloroethane may be carcinogenic in humans. A 

significant positive dose-related trend was observed for the incidence of hemangiosarcomas and 

mammary adenocarcinomas in female rats, hepatocellular carcinoma in male mice, and endometrial 

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

mice was significantly increased over the corresponding control animals. Limitations in this study (e.g., 

poor survival in both treated and control animals) preclude the consideration of these results as 

conclusive evidence of carcinogenicity (NCI 1977). 

Results of a recently reported drinking water bioassay in mice indicated that l,l-dichloroethane is 

not carcinogenic (Klaunig et al. 1986). Possible differences in the pharmacokinetics of l,l-dichloroethane 

between the NCI (1977) and Klaunig et al. (1986) studies because of the different methods of 

administration and different vehicle and/or differences in dose levels employed may account for the 

disparate results. An in vitro assay of carcinogenicity initiation also yielded negative results for l,ldichloroethane (Herren-Freund and Pereira 1986). 

The induction of γ-glutamyltranspeptidase (GTP) foci, which are putative preneoplastic lesions, 

in isolated rat liver hepatocytes correlates well with carcinogenicity. l,l-Dichloroethane failed to induce 

GTP foci in liver hepatocytes obtained from rats and mice treated with l,l-dichloroethane for 7 days 

followed by promotion with phenobarbital (Herren-Freund and Pereira 1986). This suggests that l,ldichloroethane is not carcinogenic, though these results are not conclusive. 

There is limited evidence that neither confirms or dispels the carcinogenic potential of l,ldichloroethane. Thus, these results are inconclusive as to whether it poses a cancer threat for humans. The 

EPA has classified l,l-dichloroethane as a Class C chemical which is defined as a possible human 

carcinogen (IRIS 1990). 

2.5 BIOMARKERS OF EXPOSURE AND EFFECT 

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

They have been classified as markers of exposure, markers of effect, and markers of susceptibility 

(NAS/NRC 1989). 

A biomarker of exposure is a xenobiotic substance or its metabolite(s) or the product of an 

interaction between a xenobiotic agent and some target 
38 

2. HEALTH EFFECTS 

molecule or cell that is measured within a compartment of an organism (NAS/NRC 1989). The preferred 

biomarkers of exposure are generally the substance itself or substance-specific metabolites in readily 

obtainable body fluid or excreta. However, several factors can confound the use and interpretation of 

biomarkers of exposure. The body burden of a substance may be the result of exposures from more than 

one source. The substance being measured may be a metabolite of another xenobiotic (e.g., high urinary 

levels of phenol can result from exposure to several different aromatic compounds), Depending on 

the properties of the substance (e.g., biologic half-life) and environmental conditions (e.g., duration and 

route of exposure), the substance and all of its metabolites may have left the body by the time biologic 

samples can be taken. It may be difficult to identify individuals exposed to hazardous substances that are 

commonly found in body tissues and fluids (e.g., essential mineral nutrients such as copper, zinc and 

selenium). Biomarkers of exposure to l,l-dichloroethane are discussed in Section 2.5.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration 

within an organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

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

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

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

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

by l,l-dichloroethane are discussed in Section 2.5.2. 

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

ability to respond to the challenge of exposure to a specific xenobiotic. It can be an intrinsic genetic or 

other characteristic or a preexisting disease that results in an increase in absorbed dose, biologically 

effective dose, or target tissue response. If biomarkers of susceptibility exist, they are discussed in Section 

2.7, "POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE." 

2.5.1 Biomarkers Used to Identify or Quantify Exposure to l,l-Dichloroethane 

Although analytical methods are available to determine levels of l,l-dichloroethane in blood, 

urine, and expired breath, no information was located on levels of l,l-dichloroethane found in human 

tissues following exposure to measured quantities of this chemical. 

2.5.2 Biomarkers Used to Characterize Effects Caused by l,l-Dichloroethane 

l,l-Dichloroethane was used as an anesthetic in the early part of this century (Browning 1965; 

Konietzko 1984). However, no information was 
39 

2. HEALTH EFFECTS 

available on blood levels associated with anesthesia or the occurrence of anesthesia-induced cardiac 

arrhythmias. 

2.6 INTERACTIONS WITH OTHER CHEMICALS 

No information was located regarding toxic interactions of l,l-dichloroethane with other 

xenobiotics. Evidence exists to indicate that l,l-dichloroethane is detoxified by glutathione (Colacci et al. 

1985). Thus, it is likely that other substances that deplete glutathione stores such as other chlorinated 

hydrocarbons (e.g. l,l-dichloroethene and 1,2-dichloroethane), acetaminophen, and bromobenzene may 

enhance the toxicity of l,l-dichloroethane. Substances that alter the activity of the microsomal 

enzymes that are responsible for the metabolism of l,l-dichloroethane may also affect the toxicity of this 

chemical. For example, it has been shown that ethanol increases the metabolism of l,l-dichloroethane in 

vitro (Sato et al. 1980). 

2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

No populations unusually susceptible to l,l-dichloroethane or chlorinated ethanes in general have 

been identified. NIOSH (1978) has identified the following individuals as possibly being at increased risk 

from exposure to l,l-dichloroethane: (1) Individuals with skin disease because of the purported dermal 

irritant effects induced by l,l-dichloroethane. (2) Individuals with liver disease because of the role of this 

organ in the biotransformation and detoxification of xenobiotics such as l,l-dichloroethane. (3) Individuals 

with impaired renal function because of the limited evidence that l,l-dichloroethane is nephrotoxic in 

animals. (4) Individuals with chronic respiratory disease because of the purported respiratory irritant 

effects induced by l,l-dichloroethane. Although there are no data to substantiate this, additional 

populations that may be unusually susceptible to l,l-dichloroethane include children and the elderly 

because of immature or compromised metabolic capabilities, and phenobarbital or alcohol consumers 

because of the ability of these substances to alter the activity of the cytochrome P-450 system. 

It should be noted that no reliable data were found regarding dermal or respiratory irritant effects 

of l,l-dichloroethane. 

2.8 ADEQUACY OF THE DATABASE 

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

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

adequate information on the health effects of l,l-dichloroethane is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects 
40 

2. HEALTH EFFECTS 

(and techniques for developing methods to determine such health effects) of l,l-dichloroethane. 

The following categories of possible data needs have been identified by a joint team of scientists 

from ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met 

would reduce or eliminate the uncertainties of human health assessment. In the future, the identified 

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

2.8.1 Existing Information on the Health Effects of l,l-Dichloroethane 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and 

animals to l,l-dichloroethane are summarized in Figure 2-4. The purpose of this figure is to illustrate the 

existing information concerning the health effects of l,l-dichloroethane. Each dot in the figure indicates 

that one or more studies provide information associated with that particular effect. The dot does not imply 

anything about the quality of the study or studies. Gaps in this figure should not be interpreted as "data 

needs" information. 

Figure 2-4 graphically depicts the information that currently exists on the health effects of l,ldichloroethane. The literature reviewed concerning the health effects of l,l-dichloroethane in humans 

consisted solely of an anecdotal report describing the occurrence of cardiac arrhythmias when this 

compound was used as a gaseous anesthetic. Chlorinated aliphatics as a class are known to cause central 

nervous system depression. Respiratory tract and dermal irritation also result when humans are exposed 

by inhalation to sufficiently high levels. It has been inferred that l,l-dichloroethane causes these latter 

effects, but no reliable data were found that verified this activity. 

The database for the health effects of l,l-dichloroethane in experimental animals is lacking, and 

the studies reviewed consisted primarily of one subchronic inhalation study, one inhalation developmental 

toxicity study, and two oral chronic bioassays. No information is available on the effects of l,ldichloroethane following dermal exposure. The limited information available in animals suggests that l,ldichloroethane may be nephrotoxic, fetotoxic, and possibly carcinogenic. The data also indicate that 

l,l-dichloroethane is considerably less toxic than 1,2-dichloroethane and the tetrachlorinated aliphatics. 

2.8.2 Identification of Data Needs 

Acute-Duration Exposure. No reliable information is available on the effects of single-dose 

exposures in humans and animals. LD50 values are available in secondary sources, but no details are 

available to assess the 


43 

2. HEALTH EFFECTS 

study provided suggestive evidence of carcinogenicity, but because there was poor survival in this study 

and the statistical significance of the cancer incidence is uncertain, the results could not be considered 

conclusive. The other bioassay yielded negative results for l,l-dichloroethane. No chronic toxic effects 

other than lethality were noted in either bioassay. The possibility that significant differences between the 

two studies could be due to administering l,l-dichloroethane in drinking water as compared to bolus 

doses in corn oil needs to be evaluated. Given the limitations present in the one study, the fact that 1,2­

dichloroethane and certain other chlorinated aliphatics are carcinogenic and hepatotoxic, and the 

observations that l,l-dichloroethane possibly forms DNA adducts and metabolizes to free radicals, more 

information obtained from well-conducted carcinogenicity studies would be useful to assess more fully 

the carcinogenic potential of l,l-dichloroethane in humans and animals. Studies conducted by the 

inhalation route would be useful. 

Genotoxicity. With one exception, the genotoxic potential of l,l-dichloroethane has been 

investigated almost exclusively using in vitro assays. Though the available data are conflicting, l,ldichloroethane is generally considered to be nongenotoxic. l,l-Dichloroethane has been observed 

to enhance cell transformation in Syrian hamster embryo cells and results suggest that l,l-dichloroethane 

or a metabolite can bind to cellular macromolecules such as DNA. More information on the genotoxic 

effects of l,l-dichloroethane in animals both in vitro and in vivo would be useful to resolve the 

discrepancies in the present data and to assess the genotoxic hazard of this chemical in humans. 

Reproductive Toxicity. No information on the reproductive effects of l,l-dichloroethane in 

humans or animals is available. Reproductive toxicity studies in animals would be useful particularly by 

the inhalation route since this is the most likely route of human exposure. 

Developmental Toxicity. No information on the developmental effects of l,l-dichloroethane in 

humans Is available. One study was located that investigated the developmental effects of inhaled l,ldichloroethane in animals. The results from this study indicated that l,l-dichloroethane is fetotoxic in rats, 

causing retarded fetal development (i.e., delayed ossification of the vertebrae) in the absence of 

significant maternal toxicity. Additionally, well-conducted developmental toxicity studies on 

l,l-dichloroethane, particularly by the inhalation route since this is the most likely route of human 

exposure, would be useful to verify the data from the single study that suggest this compound may cause 

adverse developmental effects. Data that compared the effects caused from different routes of 

exposure in mammalian species would also be useful to determine the likeliness of effects in humans. 
44 

2. HEALTH EFFECTS 

Immunotoxicity. No information is available on the immunotoxic effects of l,l-dichloroethane in 

humans or animals. Immunotoxicity studies in animals, particularly by the inhalation route since this is 

the most likely route of human exposure, would be useful to assess the potential risk for l,ldichloroethane-induced adverse immunologic effects in humans. 

Neurotoxicity. Chlorinated aliphatics as a class are known to cause central nervous system 

depression in humans exposed by inhalation to sufficiently high levels. l,l-Dichloroethane can also cause 

this effect, evidenced by its former use as an anesthetic. However, no reliable data were 

found that indicated a threshold level for this effect. No data (behavioral, histopathological, 

neurochemical, or neurophysiological) are available on possible neurotoxic effects of long-term low level 

exposures to l,l-dichloroethane. More information on potential short- and long-term neurotoxic effects of 

inhaled l,l-dichloroethane would be useful to determine whether this compound can produce neurotoxic 

effects following low level, long-term exposures, and to determine the threshold exposure level for 

l,l-dichloroethane-induced central nervous system depression. 

Epidemiological and Human Dosimetry Studies. No epidemiological studies were located on 

l,l-dichloroethane. Well-controlled epidemiological studies of people living in close proximity to areas 

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

occurred, people living near hazardous waste sites, and of occupationally exposed people could add to the 

limited database and clarify health effects in humans induced by l,l-dichloroethane. However, while this 

information would be useful, it is unlikely that it could be easily obtained from occupational studies. 

Other short-chain halogenated hydrocarbons are usually encountered in the same facilities where l,ldichloroethane is manufactured or used, thus confounding the results obtained in such a study. 

Biomarkers of Exposure and Effect. For high exposure to l,l-dichloroethane, the levels of this 

compound in the blood, urine, and breath may be used for biomarkers of exposure. However, these 

methods should be more sensitive and quantitative. The development of methods for detecting 

metabolites in the fluids and tissue of humans is needed to indicate l,l-dichloroethane exposure. 

Biomarkers of effect would be useful for identifying l,l-dichloroethanespecific injury (e.g., 

hepatotoxicity, renal toxicity, neurotoxicity) for short-, intermediate- and long-term exposure. Presently, 

no biomarkers of effect are available; however, DNA adducts may be useful for indicating 

carcinogenicity in animals or humans following chronic exposure to l,l-dichloroethane. 

Absorption, Distribution, Metabolism, and Excretion. Studies of the pharmacokinetics of l,ldichloroethane are very limited. Much of the 
45 

2. HEALTH EFFECTS 

information regarding the disposition of l,l-dichloroethane is based on indirect evidence. Pharmacokinetic 

data are useful for providing information on mechanisms of toxicity and can often support findings of 

toxicity studies. 

Absorption of l,l-dichloroethane occurs following exposure via all routes. The presence of a l,ldichloroethane metabolite in urine and expired air and its binding to tissue macromolecules provide 

evidence of its absorption. Studies regarding the direct analysis of the extent and rate of l,l-dichloroethane 

absorption are lacking and would provide useful information on the potential health hazards associated 

with exposure to l,l-dichloroethane via inhalation of contaminated air or ingestion of contaminated water. 

Studies in humans and animals regarding tissue distribution of l,l-dichloroethane are not 

available. Its lipophilicity suggests that the compound would be well absorbed and distributed to tissues 

according to their lipid content. Binding studies conducted in rats following intraperitoneal injection 

indicate that l,l-dichloroethane localizes in the liver, kidney, lung, and stomach. However, analysis has 

been limited to these tissues. Distribution studies using routes of administration relevant to human 

exposure (inhalation, oral) would provide useful information on potential target organs of l,ldichloroethane-induced toxicity in humans. 

Characterization of l,l-dichloroethane's metabolism relies heavily on in vitro data. These studies 

reveal that the biotransformation process is mediated by cytochrome P-450 with hepatic microsomes 

being the most effective. Identification of products in these microsomal studies allows for the 

prediction of metabolic pathways. However, exposure to l,l-dichloroethane under in vivo conditions may 

alter substrate availability and consequently alter the metabolic scheme. In vivo studies would provide a 

better understanding of the rate and extent of l,l-dichloroethane metabolism and a more realistic 

perspective of its metabolic fate. This information would allow more accurate prediction of the potential 

of l,l-dichloroethane to induce toxic effects, and aid in devising methods to detoxify exposed persons. 

Studies regarding the excretion of l,l-dichloroethane by humans were not available. One study 

was located in animals regarding the extent or rate of l,l-dichloroethane excretion. Studies monitoring 

levels in blood and excretion would be useful to estimate pharmacokinetic parameters. 

Comparative Toxicokinetics. The absorption, distribution, metabolism, and excretion data for 

l,l-dichloroethane are all derived from animal studies. It is likely that human disposition would follow a 

scheme similar to that found in animals, but this conclusion is highly speculative. However, similar 

results obtained in vivo across several animal species would provide supportive evidence for the 

assumption that l,l-dichloroethane is handled in a similar manner in humans. 
46 

2. HEALTH EFFECTS 

2.8.3 On-going Studies 

No on-going studies were identified that explored the health effects or toxicokinetics of l,ldichloroethane or attempted to associate l,l-dichloroethane levels in human tissues with effects. 
47 

3. CHEMICAL AND PHYSICAL INFORMATION 

3.1 CHEMICAL IDENTITY 

The synonyms, and identification numbers for l,l-dichloroethane are listed in Table 3-l. 

3.2 PHYSICAL AND CHEMICAL PROPERTIES 

Important physical and chemical properties of l,l-dichloroethane are listed in Table 3-2. 



51 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL 

4.1 PRODUCTION
 

l,l-Dichloroethane is produced commercially through the reaction of hydrogen chloride and vinyl 

chloride at 20o

-55°C in the presence of an aluminum, ferric, or zinc chloride catalyst (Grayson 1978). 

Other production methods include the direct chlorination of ethane, the reaction of PCl, with 

acetaldehyde as a by-product during the manufacture of chloral (Browning 1965)) and as an intermediate 

in the production of vinyl chloride and l,l,l-trichloroethane by photochlorination (Windholz 1983). 

Information regarding the volume of l,l-dichloroethane production is limited. At least 4.55x1010 

grams were produced in 1977 (HSDB 1988). No information was found regarding U.S. production 

volumes after this date. 

Major companies producing l,l-dichloroethane within the United States include PPG Industries, 

Inc., Continental Oil Company, and Vulcan Materials, all based in Louisiana, and Dow Chemical located 

in Texas. Each of these companies manufactures l,l-dichloroethane primarily to be used as an 

intermediate in the manufacture of l,l,l-trichloroethane. 

4.2 IMPORT 

No information was found concerning U.S. imports and exports of l,l-dichloroethane. 

4.3 USE 

The largest individual use of l,l-dichloroethane is as an intermediate in the manufacture of other 

products such as vinyl chloride, l,l,l-trichloroethane, and to a lesser extent high vacuum rubber. It also has 

limited use as a solvent for plastics, oils, and fats, and thus is employed as both a cleaning agent and a 

degreaser. In the past, l,l-dichloroethane was used as an anesthetic, but that use has been discontinued. 

Other uses of l,l-dichloroethane include fabric spreading, varnish and finish removers, organic synthesis, 

ore flotation, and as a fumigant and insecticide spray (EPA 1985; Grayson 1978; HSDB 1988). No 

information is available regarding the use proportions among these categories. 

4.4 DISPOSAL 

l,l-Dichloroethane may be disposed of by atomization within a combustion chamber equipped 

with an appropriate effluent gas cleaning device, by hightemperature incineration with a hydrochloric acid 

scrubber, or by placing product residues and sorbent media into 17H epoxy-lined drums and disposing of 
52 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL 

them at an EPA-approved site. However, the criteria for treatment or sanitary landfill disposal practices 

are currently undergoing revision. Consultation with environmental regulatory agencies is advised (HSDB 

1988; NIOSH 1978; OHMTADS 1988). 
53 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.1 OVERVIEW
 

The primary disposition of l,l-dichloroethane in the environment is related to the production, 

storage, consumption, transport, and disposal of l,l-dichloroethane used as a chemical intermediate, 

solvent, finish remover, and degreaser. Releases from industrial processes are almost exclusively to 

the atmosphere. Releases of the compound to surface waters and soils are expected to partition rapidly to 

the atmosphere through volatilization. Hydrolysis, photolysis, and biodegradation do not appear to be 

important processes in determining the environmental fate of l,l-dichloroethane. It has been detected at 

generally low levels in ambient air, surface water, groundwater, drinking water, and human breath. 

Concentrations in environmental media are greatest near source areas (e.g., industrial point 

sources, hazardous waste sites). 

Inhalation of l,l-dichloroethane in ambient or workpiace air is generally the main route of human 

exposure to the compound. Estimates of populations potentially exposed to l,l-dichloroethane in 

workplace environments range from 715 to 1,957 workers (NIOSH 1976, 1984). Inhalation of ambient air 

and ingestion of contaminated drinking water may also be important routes of exposure for populations 

living near industrial facilities and hazardous waste sites. 

5.2 RELEASES TO THE ENVIRONMENT 

There are no known natural sources of l,l-dichloroethane, but McCarty et al. (1986) reported that 

l,l,l-trichloroethane is biodegraded in anaerobic methanogenic environments, such as those found in 

landfills, to form l,l-dichloroethane. Laboratory studies designed to elucidate the degradation 

reactions of chloroethenes and chloroethanes have been described by Hallen et al. (1986) and Vogel and 

McCarty (1987). Hallen et al. (1986) observed that dechlorination reactions appear to be reversible, 

and'chlorinated ethanes can be converted to chlorinated ethenes. Releases of the compound to the 

environment result from industrial manufacturing and use processes. Additional sources of environmental 

release are fugitive emissions from storage, distribution, and disposal; use as an extraction solvent and 

fumigant; and as a constituent of medicines and stone, clay, and glass products (Infante and Tsongas 

1982). 

EPA has identified 1,177 NPL sites. We do not know how many of the 1,177 NPL sites have 

been evaluated for 1,1-dichloroethane. l,l-Dichloroethane has been found at 248 of the total number of 

sites evaluated for that compound. As more sites are evaluated by EPA, this number may change (VIEW 

1989). The frequency of these sites within the United States can be seen in Figure 5-l. 

55 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.2.1 Air 

Emissions to the atmosphere comprise more than 99% of all releases of l,l-dichloroethane to the 

environment (Perwak et al. 1982). l,l-Dichloroethane released in the production of l,l,l-trichloroethane 

accounts for about 52% of the atmospheric releases, with the production of 1,2-dichloroethane 

accounting for about 35%. Pellizzari (1982) reported the presence of low levels of l,l-dichloroethane in 

ambient air of the Baton Rouge industrial area and at the Kin-Buc waste disposal site outside Edison, New 

Jersey. Approximately 52,000 kg of l,l-dichloroethane are released to the atmosphere by privately owned 

treatment work facilities (POTWs) each year (EPA 1980). 

5.2.2 Water 

Industrial releases of l,l-dichloroethane, to surface waters are minor in comparison to releases to 

the atmosphere. Releases from solvent use and POTWs account for only 2,000 kg annually (Perwak et al. 

1982). Industrial processes involving the use of l,l-dichloroethane as a chemical intermediate or cleaning 

solvent are believed to be the largest sources of surface water releases, Young et al. (1983) reported l,ldichloroethane in the primary, secondary, and final effluents from municipal wastewater treatment plants. 

Approximately 1,000 kg of l,l-dichloroethane are discharged in effluent from POTWs each year 

(EPA 1980). 

l,l-Dichloroethane has been detected in groundwater samples taken at an estimated 9% of the 

NPL hazardous water sites participating in the Contract Laboratories Program (CLP) at a geometric mean 

concentration of 23.1 ppb for the positive samples (CLP 1989). The compound was also detected in 

surface water samples taken at an estimated 2% of the NPL hazardous waste sites participating in the CLP 

at a geometric mean concentration of 24 ppb for the positive samples. Note that these data from the CLP 

Statistical Database represent frequency of occurrence and concentration information of NPL sites 

only. 

5.2.3 Soil 

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

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

1978 (Perwak et al. 1982). Approximately 4,000 kg of l,l-dichloroethane from POTWs are dispersed on 

land each year as sludge (EPA 1980). 

l,l-Dichloroethane has been detected in soil samples taken at an estimated 0.7% of the NPL 

hazardous waste sites participating in the Contract Laboratory Program (CLP) at a geometric mean 

concentration of 40.8 ppb for the positive samples (CLPSD 1989). Note that these data from the CLP 

Statistical 
56 

5. POTENTIAL FOR HUMAN EXPOSURE 

Database represent frequency of occurrence and concentration information for NPL sites only. 

5.3 ENVIRONMENTAL FATE 

5.3.1 Transport and Partitioning 

Releases of l,l-dichloroethane to the environment as a result of industrial activity are expected to 

be primarily to the atmosphere (see Section 5.2). l,l-Dichloroethane released to the atmosphere may be 

transported long distances before being washed out in precipitation. For example, Pearson and McConnell 

(1975) attributed the presence of chlorinated organic compounds, including l,l-dichloroethane, in upland 

waters to longrange aerial transport and deposition in precipitation. Perwak et al. (1982) discussed the 

atmospheric fate of l,l-dichloroethane in the Gulf Coast area, where there is a high percentage of cloudy 

days. Increased atmospheric losses due to washout in frequent, heavy rains could occur, although much of 

the l,l-dichloroethane could be revolatilized. Dichloroethanes released in this area could be transported 

north by the prevailing winds to populated areas before significant photochemical degradation could 

occur. 

Cupitt (1980), however, considered the loss of 1,2-dichloroethane from the atmosphere by 

dissolution into rain drops or adsorption onto aerosols insignificant compared with loss from chemical 

degradation based on mathematical calculations. Since l,l-dichloroethane has higher volatility and 

lower aqueous solubility than the 1,2-isomer, physical removal of l,l-dichloroethane from the atmosphere 

would be even less likely to be important (EPA 1985). Pellizzari et al. (1979) measured actual 

concentrations of airborne contaminants in the vicinity of known emission sources of l,l-dichloroethane, 

making aerial transport the logical source of downwind concentrations. 

Henry's law constant value for l,l-dichloroethane (4.2x10-2 atm-m3

/mol) suggests that it should 

partition rapidly to the atmosphere. Evaporation half-life depends on a number of factors: wind speed and 

mixing conditions of the receiving waters are particularly important. Dilling et al. (1975) and Dilling 

(1977) estimated a volatilization half-life of 22 minutes for l,l-dichloroethane present at 1 ppm 

concentration in an open water column held at 25°C and stirred at 200 rpm. Under these conditions 90% 

of the compound was removed within 109 minutes. Volatilization half-lives determined in the laboratory 

are related to actual environmental situations by a correction factor that takes into account the oxygen 

reaeration rate ratio. The reaeration rate ratio has been determined to be 0.55 for l,l-dichloroethane 

(Cadena et al. 1984). Using the values of Mabey et al. (1981) for oxygen reaeration rates in ponds and 

rivers (0.19 and 0.96 day-l, respectively), the evaporation half-life of l,l-dichloroethane is estimated to be 

approximately five times longer for ponds than for rivers (more than 1 day for river water and more than 

6 days for pond water). Therefore, evaporation may be the most 
57 

5. POTENTIAL FOR HUMAN EXPOSURE 

significant means of removal of l,l-dichloroethane from aquatic media (EPA 1985). 

No information was found regarding partitioning of l,l-dichloroethane from the water column 

onto sediments. However, analogs of the compound (i.e., dichloromethane, trichloromethane, and l,l,ltrichloroethane) have not been found to concentrate selectively onto sediments (Dilling et al. 1975; 

Pearson and McConnell 1975). The KOC values for these compounds are similar to the KOC for l,ldichloroethane; therefore, adsorption onto sediments would not be considered significant for l,ldichloroethane (EPA 1985). 

l,l-Dichloroethane released to land surfaces in spills would rapidly volatilize to the atmosphere, 

but l,l-dichloroethane remaining on soil surfaces would be available for transport into groundwater, since 

the compound does not sorb to soil particulates unless the organic content of the soil is high. 

Experimentally derived KOC values for a silt loam soil also indicate that little sorption of l,ldichloroethane to low organic content soil is expected. Wilson et al. (1981) found that although 50% of 

the applied l,l-dichloroethane volatilized to the atmosphere, the remainder percolated rapidly through a 

sandy soil, suggesting ready availability to groundwater transport processes. Environmental surveys 

conducted by EPA have detected l,lcdichloroethane in groundwater sources in the vicinity of 

contaminated sites (EPA 1985). 

Gossett et al. (1983) analyzed the tissues of several species of aquatic organisms for l,ldichloroethane near the discharge of the Los Angeles County wastewater treatment plant. The 

concentration of l,l-dichloroethane in the effluent was 3.5 ppb, however none was found in the animal 

tissues (detection limit of 0.3-0.5 ppb). These results may be evidence that the potential for l,ldichloroethane to bioconcentrate is low in aquatic organisms. EPA (1984) estimated the bioconcentration 

factor from the KOW as 6.6, indicating that bioconcentration would not be expected. 

5.3.2 Transformation and Degradation 

5.3.2.1 Air 

In the atmosphere, l,l-dichloroethane is oxidized by reaction with hydroxyl radicals. The 

residence time of the compound in the atmosphere has been estimated by several investigators to be 44 

days (Singh et al. 1981; Howard and Evenson 1976). 

5.3.2.2 Water 

l,l-Dichloroethane in surface water is expected to be lost to the atmosphere through volatilization before 

undergoing any significant chemical or biological degradation. The hydrolytic half-life of l,ldichloroethane at pH 7 and 25°C has been estimated to be 60 years (Jeffers et al. 1989). 
58
 

5. POTENTIAL FOR HUMAN EXPOSURE 

According to McCarty et al. (1986), l,l-dichloroethane appears to be produced by biodegradation 

of l,l,l-trichloroethane in groundwater. Further degradation could also occur. In the absence of oxygen and 

in the presence of anaerobic, methane-producing bacteria, halocarbons are transformed by reductive 

dehydrohalogenation in a step-wise manner: l,l,l-trichloroethane -> l,l-dichloroethane → chloroethane →

ethanol → carbon dioxide. Under aerobic conditions, Tabak et al. (1981) reported about 50% degradation 

of l,l-dichloroethane by unadapted microorganisms isolated from municipal waste water inoculum after 7 

days, which was increased to 78% degradation by adapted organisms in the same time period. l,lDichloroethane has been reported to be resistant to biological degradation by bacteria isolated from 

shallow aquifer aerobic groundwater after 8-16 weeks incubation (Wilson et al. 1983). 

Data from landfill sites with a documented contamination history were examined by Cline and 

Viste (1984). They observed that l,l-dichloroethane was detected in groundwater at sites where the 

compound had not been handled or disposed of and concluded that l,l-dichloroethane had been produced 

by anaerobic degradation of other compounds present, particularly l,l,l-trichloroethane. 

5.3.2.3 Soil 

l,l-Dichloroethane in soils is expected to volatilize to the atmosphere or be transported to 

groundwater before undergoing significant abiotic transformation; the compound is not expected to sorb 

to soils of low organic content. As in surface waters, direct photolysis of l,l-dichloroethane on soil 

surfaces is not expected. The rate of biodegradation of l,l-dichloroethane in soils is unknown. In 

subsurface soil, the loss of l,l-dichloroethane through biodegradation is expected to be insignificant 

(Wilson et al. 1983). The biodegradation half-life of l,l,l-trichloroethane under anaerobic conditions has 

been reported to be about 16 days, whereas the half-life of l,l-dichloroethane has been reported to be 

greater than 30-60 days (Wood et al. 1985). 

5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

l,l-Dichloroethane has been detected in ambient urban and rural air, in waste gas generated from 

garbage dumps, and in surface water, groundwater, and drinking water. Quantitative concentration 

information is presented in the following sections by environmental medium. 

5.4.1 Air 

l,l-Dichloroethane was not seen at a detection limit of 5 ppt in ambient rural air samples taken in 

southeastern Washington state (Grimsrud and Rasmussen 1975). It has been found at higher 

concentrations in ambient air samples from urban areas of the United States. Brodzinsky and Singh 

(1983) tabulated atmospheric levels at urban, rural, and industrial sites across the 
59 

5. POTENTIAL FOR HUMAN EXPOSURE 

United States and reported a median concentration of 55 ppt. Pellizzari (1982) reported the detection of 

low levels (unspecified concentrations) of the compound in the vicinity of the Baton Rouge industrial 

area. Singh et al. (1983) reported that the average concentration of the compound in the air of 

seven urban locations in 1980-1981 ranged from 0.1 to 1.5 ppb. It has also been detected in samples of 

ambient air collected in the vicinity of hazardous waste disposal sites, such as the Kin-Buc site near 

Edison, New Jersey, at a level of 23 μg/m3

 (5.68 ppm) (Pellizzari 1982). Hoefler et al. (1982) found a 

level of 1.1 mg/kg of the compound in waste gas generated at a garbage dump. Pellizzari (1978) tabulated 

analytical results for l,l-dichloroethane in the ambient air of various locations generally in close proximity 

to industrial plants, including Magna, Utah (0.082 ppb); Iberville, Louisiana (0.12 ppb); Deer Park, Texas 

(0.14 ppb); and Baton Rouge (0.058 ppb) and Geismar, Louisiana (0.14 ppb). 

Barkley et al. (1980) found no l,l-dichloroethane in the ambient air surrounding nine houses 

bordering the old Love Canal. Gupta et al. (1984) found l,l-dichloroethane at higher levels indoors (mean 

concentration of 3.2 ppb) than outdoors (not detected) in residences in suburban Knoxville, 

Tennessee, and concluded that there must be a source of the compound inside the home. Possible sources 

were not identified except to suggest building materials or chlorinated water. 

5.4.2 Water 

Perwak et al. (1982) summarized data from EPA's STORET database, where reported 

concentrations of l,l-dichloroethane range from undetected (<l0 ppb) to 1,900 ppb, with the highest 

reading in the Upper Mississippi River basin at Alton, Illinois. However, they observed that monitoring 

results reported for l,l-dichloroethane in surface waters are almost always below the detection 

limit (generally 10 ppb). The compound has also been found in samples of urban runoff from Long 

Island, New York, and Eugene, Oregon, at concentrations of 1.5 and 3 ppb, respectively (Cole et al. 

1984). Coniglio et al. (1980) summarized groundwater monitoring data obtained by numerous state 

agencies and reported that l,l-dichloroethane was found in 18% of the wells tested, with a maximum 

concentration of 11,330 ppb. They cautioned that the state data may have been biased since the 

monitoring was generally conducted by the states in areas where contamination was suspected. However, 

l,l- dichloroethane has been detected in groundwater sampled during random testing of water supplies 

(see further discussion). 

Finished water supplies obtained from groundwater sources were tested by EPA for 

contaminants. It was reported that up to 10.8% of 158 nonrandom sample sites from across the United 

States contained detectable levels of l,l-dichloroethane. The maximum concentration was 4.2 ppb 

(Westrick et al. 1984). l,l-Dichloroethane was detected at a maximum concentration of 220 ppb 

in samples from 193 private wells in Rhode Island analyzed over a period of nine years (RIDH 1989). A 

maximum concentration of 40 ppb l,l-dichloroethane 
60 

5. POTENTIAL FOR HUMAN EXPOSURE 

was detected in 6 public drinking water systems in Rhode Island between April 1982, and April 1989 

(RIDH 1989). 

Drinking water samples from a number of urban and rural locations in the United States have 

been reported to be contaminated with l,l-dichloroethane. Unspecified levels of the compound have been 

detected in drinking water samples taken from Philadelphia (Suffet et al. 1980). Private drinking water 

wells in Wisconsin were found to contain unspecified levels of l,l-dichloroethane in 11 of 617 wells 

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

supplies in Iowa (Kelley 1985). 

Groundwater samples taken from 178 hazardous waste disposal sites were found to contain l,ldichloroethane at 18% frequency (Plumb 1987), with an average concentration of 0.31 ppm and a 

maximum of 56.1 ppm (Yang and Rauckman 1987). Using the STORET database, Staples et al. (1985) 

reported median concentrations of less than 0.1 ppb in 8,716 samples of ambient water (3% detectable 

values), less than 1.0 ppb in 1,375 effluent samples (5% detectable values), less than 5.0 ppb in 354 

sediment samples (0.6% detectable values), and less than 0.05 ppb in 94 biota samples (no detectable 

values). Also using the STORET database, Perwak et al. (1982) reported that l,l-dichloroethane was 

not found in the sediment of the lower Mississippi or the western Gulf of Mexico; however, a maximum 

concentration of 5 ppb was detected in sediment samples from the Pacific Northwest. 

5.4.3 Soil 

No information was found on the ambient concentrations of l,l-dichloroethane in soil, or on the 

current disposal of waste products containing the compound in landfills. The compound has more 

commonly been detected in ambient air and groundwater samples taken at hazardous waste sites, and it is 

expected that the lack of available soil monitoring data is at least in part due to rapid partitioning of l,ldichloroethane released to soils to these other media. 

5.4.4 Other Media 

Little information was found on the levels of l,l-dichloroethane in other media. Ferrario et al. 

(1985) measured 33 ppb wet weight of l,l-dichloroethane in oysters from Lake Pontchartrain near New 

Orleans, Louisiana, however, l,l-dichloroethane was not detected in 2 types of clams. Kallonen et al. 

(1985) detected l,l-dichloroethane in the effluent gases of burning polyester fiber fill. Data on 

concentrations in human breath are presented in Section 5.5. 
61 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
 

The greatest source of exposure to l,l-dichloroethane for most of the U.S. population is inhalation 

of the compound in contaminated air. Another potential route of human exposure is ingestion of the 

compound in contaminated drinking water. There have been no reports of adverse effects associated with 

occupational inhalation of l,l-dichloroethane in humans, and amounts dermally absorbed are reported to 

be insufficient to cause systemic injury (ACGIH 1971). Industrial exposures can result from the use of l,ldichloroethane as a chemical intermediate, solvent, and a component of fumigant formulations 

(ACGIH 1971). 

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

estimated that 715 workers in 143 plants were potentially exposed to l,l-dichloroethane in the workplace 

in 1970 (NIOSH 1976). These estimates were derived from observations of the actual use of l,ldichloroethane (90% of total estimate) and the use of trade name products known to contain l,ldichloroethane (10%). The exposed workers were in the rubber and plastic, chemical and allied products, 

electrical equipment and supply, medical and other health services, miscellaneous business services, and 

oil and gas extraction industries. The occupational groups with exposed workers we're assemblers, 

agricultural and biological technicians, chemists, electrical and electronic engineering technicians, 

therapists, geologists, and machine operators. 

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

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

were potentially exposed to l,l-dichloroethane in the workplace in 1980 (NIOSH 1984). The exposed 

workers were employed in the chemical and allied products and business service industries, as chemical 

technicians; plumbers, pipefitters, and steamfitters; supervisors in production occupations; electricians; 

machinists; chemical engineers; and welders and cutters. The estimates were based on direct observation 

by the surveyor of the actual use of the compound (100%). 

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

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

workers potentially exposed to the chemicals. 

NIOSH (1978) noted that there was a large potential for exposure to l,l-dichloroethane in the 

workplace during its use as a dewaxer of mineral oils, extractant for heat-sensitive substances, or 

fumigant, and in the manufacture of vinyl chloride and high-vacuum rubber and silicon grease. 

Zweidinger et al. (1982) and Wallace et al. (1982) conducted a study of the levels of l,ldichloroethane in the inhaled and exhaled air and drinking water of college students in Texas and North 

Carolina. Low levels (<0.49 ppb) 
62 

5. POTENTIAL FOR HUMAN EXPOSURE 

of l,l-dichloroethane were found in the personal air quality monitors of the Texas students, whose campus 

bounded a petrochemical manufacturing area, but none was detected in the exhaled breath samples. l,lDichloroethane was not detected in the breathing zone air of the North Carolina students. 

Barkley et al. (1980) found a trace of l,l-dichloroethane in the expired breath of one resident 

whose home bordered the old Love Canal, but none was detected in ambient air. Wallace et al. (1984) 

found a trace of l,l-dichloroethane in the expired breath and drinking water of one resident of New 

Jersey). 

Assuming a median ambient air level of 55 ppt reported by Brodzinsky and Singh (1983) and a 

theoretical average inhalation of 20 m3

 of air per day, the average inhalation exposure to l,ldichloroethane for an individual in the United States is estimated at 4 μg/day (EPA 1985). 

5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Human exposure to l,l-dichloroethane is expected to be highest among certain occupational 

groups (e.g., chemical and allied products industry workers) and members of the general population living 

in the vicinity of industrial point emission sources (EPA 1985) and hazardous waste sites. The 

compound has been detected in both ambient air and water in low concentrations, with substantially 

higher concentrations in localized areas around industrial and disposal sites. No information was found 

regarding the number of people potentially exposed around hazardous waste sites. 

5.7 ADEQUACY OF THE DATABASE 

Section 104(i) of CERCLA directs the Administrator of ATSDR (in consultation with the 

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

adequate information on the health effects of l,l-dichloroethane is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to-determine 

such health effects) of l,l-dichloroethane. 

The following categories of data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substancespecific informational needs that, if known, would 

reduce or eliminate the uncertainties of human health assessment. Each data need discussion 

highlights the availability, or absence, of the relevant exposure information. A statement that reflects the 

importance of identified data needs is also included. In the future, these data needs will be evaluated and 

prioritized, and a substance-specific research agenda will be proposed. 
63 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.7.1 Identification of Data Needs 

Physical and Chemical Properties. The physical/chemical properties of l,l-dichloroethane are 

sufficiently well characterized to enable assessment of the environmental fate of this compound. 

Production, Use, Release, and Disposal. Based on its industrial use, l,l-dichloroethane is 

primarily released to the atmosphere, and humans are potentially exposed to this chemical through the 

inhalation or ingestion of contaminated air or water. However, because the data available on production, 

import, export, use, and disposal are limited, it is difficult to estimate whether or not the potential for 

human exposure to l,l-dichloroethane may be substantial. Data concerning the production and use of l,ldichloroethane both within the United States and worldwide are extremely limited. Information regarding 

possible disposal methods, criteria, and regulations are available; however, the present criteria may 

undergo revision in the near future. Information on current production levels, quantities imported and 

exported, proportions allocated to various uses, and proportions and efficiencies associated with differing 

modes of disposal is not available. This information would be useful in identifying potential sources and 

levels of exposure, thus enabling identification of exposed populations. 

Environmental Fate. Releases from industrial processes are almost exclusively to the 

atmosphere, and releases of the compound to surface waters and soils are expected to partition rapidly to 

the atmosphere through volatilization. l,l-Dichloroethane released to the atmosphere may be transported 

long distances before being washed out in precipitation. Although l,l-dichloroethane released to land 

surfaces in spills would rapidly volatilize to the atmosphere, the l,l-dichloroethane remaining on soil 

surfaces would be available for transport into groundwater. The atmospheric residence time of l,ldichloroethane is about 44 days. The dominant removal mechanism is reaction with hydroxyl free 

radicals. Hydrolysis and biodegradation do not appear to be important processes in the environmental 

fate of this compound. Data are lacking on the partitioning of l,l-dichloroethane from the water column 

onto sediments. Additional information on the atmospheric transformation and on the rate of 

biodegradation of l,l-dichloroethane in soils would be useful in the determination of its 

environmental fate. 

Bioavailability from Environmental Media. Data are incomplete on the bioavailability of l,ldichloroethane from environmental media. Animal data on l,l-dichloroethane exposure via inhalation and 

oral administration in drinking water suggest that the compound is bioavailable following inhalation 

of ambient air and ingestion of drinking water. Additional information on the bioavailability of l,ldichloroethane from air, water, soil, and sediment would be useful in determining actual risks associated 

with exposure to environmental levels of l,l-dichloroethane. 
64 

5. POTENTIAL FOR HUMAN EXPOSURE 

Food Chain Bioaccumulation. The information located on the potential for bioconcentration of l,ldichloroethane in plants, aquatic organisms, or animals is limited. An analysis of animal tissues from 

several species of aquatic organisms near the discharge of a wastewater treatment plant did not 

detect l,l-dichloroethane in the animal tissues, although the compound was found in the effluent. 

However, l,l-dichloroethane has been detected in oysters (33 ppb wet weight). An estimated 

bioconcentration potential of less than 1 from the KOW suggests that bioconcentration would not be 

expected. Very little information was found regarding the biomagnification of l,l-dichloroethane among 

food chain trophic levels. Additional information on bioconcentration and biomagnification would be 

useful in determining if food chain bioaccumulation is an important source of,human exposure. 

Exposure Levels in Environmental Media. Limited information is available regarding ambient 

concentrations of l,l-dichloroethane in soils. Based on a median ambient air level reported in 1982, the 

average inhalation exposure to l,l-dichloroethane for an individual in the United States has been estimated 

to be 4 μg/day. The information on foodstuffs is limited to the detection of l,l-dichloroethane in oysters 

(33 ppb wet weight). Additional site-specific concentration data for ambient air, drinking water, soil, and 

biota would be helpful in estimating potential exposure of the general population as well as 

populations in the vicinity of hazardous waste sites. 

Exposure Levels in Humans. Although relatively recent estimates of the size of the population 

occupationally exposed to l,l-dichloroethane are available from NIOSH, monitoring data on workplace 

exposures are generally limited, with a few observations about l,l-dichloroethane included in detailed 

studies of 1,2-dichloroethane. A study of the levels of l,l-dichloroethane in the inhaled and exhaled air 

and drinking water of college students in Texas and North Carolina found low levels (<0.49 ppb) of l,ldichloroethane in the personal air quality monitors of the Texas students, whose campus bounded a 

petrochemical manufacturing area, but none in samples of their exhaled breath. Additional information on 

the availability of biomarkers that could be used to indicate human exposure to l,l-dichloroethane would 

be helpful. 

Exposure Registries. No exposure registries for l,l-dichloroethane were located. This 

compound is not currently one of the compounds for which a subregistry has been established in the 

National Exposure Registry. The compound will be considered in the future when chemical 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 the exposure to this compound. 
65 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.7.2 On-going Studies 

Long-term research studies on the environmental fate of l,l-dichloroethane have not been 

identified. The data generated as a result of the remedial investigation/feasibility studies of the 189 sites 

on the National Priority List (NPL) known to be contaminated with l,l-dichloroethane should add to the 

current knowledge regarding the environmental transport and fate of the compound. 

As part of the Third National Health and Nutrition Evaluation Survey (NHANES III), the 

Environmental Health Laboratory Sciences Division of the Center for Environmental Health and Injury 

Control, Centers for Disease Control, will be analyzing human blood samples for l,l-dichloroethane 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. 

67 

6. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting 

and/or measuring and monitoring l,l-dichloroethane in environmental media and in biological samples. 

The intent is not to provide an exhaustive list of analytical methods that could be used to detect 

and quantify l,l-dichloroethane. Rather, the intention is to identify wellestablished methods that are used 

as the standard methods of analysis by various Federal agencies. Many of the analytical methods used to 

detect l,l-dichloroethane in environmental samples are methods approved by federal agencies such as 

EPA and NIOSH. Other methods presented in this chapter are those that are approved by trade 

associations such as the Association of Official Analytical Chemists (AOAC) and the American Public 

Health Association (APHA). A third category of analytical methods emphasizes research and 

development activities, where efforts are underway to refine previously used methods, to obtain lower 

detection limits, and to increase accuracy and precision. 

The analytical methods used to quantify l,l-dichloroethane in biological and environmental 

samples are summarized below. Table 6-l lists the applicable analytical methods used for determining l,ldichloroethane in biological fluids and tissues, and Table 6-2 lists the methods used for determining l,ldichloroethane in environmental samples. 

6.1 BIOLOGICAL MATERIALS 

The determination of trace levels of l,l-dichloroethane in biological tissues and fluids has been 

restricted to gas chromatography (GC) equipped with mass spectrometry (MS) or flame ionization 

detection (FID). 

Recent work conducted by Cramer and co-workers (1988) showed that l,l-dichloroethane can be 

detected at nanogram per liter (ppt) levels in whole human blood using a dynamic headspace analyzer and 

GC/MS technique. A disadvantage of the GC/MS technique is that only limited mass scanning can be 

employed to obtain better sensitivity of target volatile organic compounds at ppt levels. This is because of 

the inherent differences in sensitivity between the full-scan MS and the limited mass scanning MS 

techniques (Cramer et al. 1988). 

Hara et al. (1980) employed GC/MS for the analysis of trace amounts of mixed halogenated 

compounds in the blood and tissue of humans. Identification and quantitative analysis of various 

compounds was achieved by monitoring the mass fragments for selectively molecular, abundant or 

characteristic ions for each compound. Thus, the monitoring ion (m/z) for quantification of 

l,l-dichloroethane was set at 83 [(M)+-CH3]. A lower detection limit of 20 to 20 pg per sample was 

achieved. 




72 

6. ANALYTICAL METHODS 

Uehori and co-workers (1987) developed a retention index in GC to screen and quantify volatile 

organic compounds in blood. A dynamic headspace analyzer and GC/FID with retention indices were 

employed for the detection of l,l-dichloroethane at nanogram levels. Uehori and co-workers noted that 

this method is simple, reliable and requires little or no sample preparation. 

Gas purging-and-trapping on a Tenax GC adsorbent and GC/MS technique has been employed by 

Barkley et al. (1980) for the determination of trace levels of volatile halogenated compounds (including 

l,l-dichloroethane) in water, human blood, and urine. 

6.2 ENVIRONMENTAL SAMPLES 

A GC equipped with an appropriate detector is the most frequently used analytical technique for 

determining the concentrations of l,l-dichloroethane in air, water, soil, fish, diary products, and various 

foods. Volatile organic compounds in environmental samples may exist as complex mixtures or at 

very low concentrations (ppt to ppb range). Subsequently, the GC technique must be supplemented by 

some method of sample preconcentration. 

Gas purging-and-trapping is the generally accepted method for the isolation, concentration, and 

determination of volatile organic compounds in water and various environmental samples (Bellar et al. 

1977; EPA 198613, 1987; Krasner et al. 1981; Lopez-Avila et al. 1987a, 1987b; Reding 1987; Wylie 

1987, 1988). This method appears to be most adaptable for use with almost any GC detector -- MS, FID, 

electron capture detector (ECD), and electrolytic conductivity detector (EICD). In addition, the method 

offers an important preliminary separation of highly volatile compounds from often highly complex 

samples prior to GC analysis. Detection limits at less than 1 μg of l,l-dichloroethane per liter of sample 

have been achieved by this method (Dreisch and Munson 1983; Kingsley et al. 1983; Krasner et al. 1981; 

Lopez- Avila et al. 1987a, 1987b; Otson and Williams 1982). Bruner et al. (1978) employed purge-andtrap technique on charcoal adsorbent and GC/ECD for determination at ppt levels of volatile halo organic 

compounds in air. A major problem is that some of the halocarbons in the atmosphere are present as 

ultra-trace impurities in highly pure commercial inert gases. Subsequently, these impurities may interfere 

with the quantitative and qualitative analysis of l,l-dichloroethane in environmental samples. 

Recently, Badings et al. (1985) and Pankow and Rosen (1988) employed the purge-and-trap 

technique with cryogenic trapping (cryofocusing) of volatile organic compounds in water samples as an 

effective concentration method prior to capillary GC analysis. The purge-and-trap technique offers 

advantages over other techniques in that it allows easy isolation and concentration of target 

compounds, which reduces interference, thereby improving overall limits of detection and recovery of 

sample (Otson and Chan 1987). Among the other advantages of the purge-and-trap technique with 

cryofocusing are its 
73 

6. ANALYTICAL METHODS 

simplicity and therefore its reliability; the low background contamination since no sorbent traps are 

needed; and the relatively short time of sample analysis (Pankow and Rosen 1988). 

Dynamic headspace analyzer GC has been used for the analysis and identification of l,ldichloroethane in water and fish tissue (Comba and Kaiser 1983; Mehran et al. 1985, 1986; Otson and 

Williams 1982; Reinert et al. 1983; Trussell et al. 1983). The analytic sample is placed in a sealed flask 

connected to the headspace analyzer, which is directly interfaced with the injection port of the GC system. 

This arrangement allows for a greater proportion of compound contained in a sample to be analyzed. This 

method is simple and does not require any sample preparation (Mehran et al. 1985). Detection limits of 

less than 1 μg l,l-dichloroethane/L water and less than 1 μg l,l-dichloroethane/g fish tissue were achieved 

(Mehran et al. 1986; Otson and Williams 1982; Reinert et al. 1983; Trussel et al. 1983). A disadvantage 

of this technique is that the inherent volatility of the halo organic compounds gives rise to an excessive 

foaming in the headspace system, thereby forming low yields and causing interference with the GC 

quantification. The typical yield of l,l-dichloroethane was approximately 32% (Reinart et al. 

1983). The authors indicated that use of an antifoaming agent such as silicone surfaces greatly reduced 

the foam, but extraneous chromatographic comp.Fnents and peak masking problems were encountered. 

Pellizzari (1982) initiated the development and evaluation of trace levels of volatile organic 

compounds in industrial and chemical waste disposal sites. Ambient air samples were collected by a 

sampler equipped with Tenax GC adsorbent cartridges. Compounds were thermally removed from the 

adsorbent and analyzed by capillary GC/MS. The detection limit was at the μg/m3 level (Pellizzari 1982). 

Blanchard and Hardy (1985, 1986) developed a method that allows for continuous monitoring or 

intermittent analysis of volatile organic priority pollutants in environmental media. The method is based 

on permeation of volatile organic compounds through a silicone polycarbonate membrane from 

wastewater sample matrix, into an inert gas stream and directed into a capillary GC/FID via a sampling 

loop (Blanchard and Hardy 1986). Advantages of this procedure are that it is simple, it does not require 

time-consuming preconcentration steps, and it can be used either in the field or in the laboratory. 

The liquid-liquid extraction procedure provides a simple, rapid, screening method for 

semiquantitative determination of l,l-dichloroethane in aqueous samples containing limited number of 

volatile organic compounds. It is less effective for aqueous samples containing large numbers of volatile 

organic compounds, Furthermore, interference from the organic (hexane) extraction solvent makes it 

more difficult to identify completely all compounds (Otson and Williams 1981). GC/EICD was employed 

by Otson and 
74 

6. ANALYTICAL METHODS 

Williams (1981) for the detection of trace amounts (less than 1 μg/L of sample) of l,l-dichloroethane in 

drinking water. 

Daft (1988) employed a photoionization detector and an electrolytic conductivity detector 

connected in series to a capillary GC to detect l,l-dichloroethane at rig/g levels in fumigants and industrial 

chemical residues of various foods (e.g., diary products, meat, vegetables, and soda). Typically, foods 

were extracted with isooctane and injected in GC column for analysis. However, foods containing lipid 

and fat were subjected to further clean-up on micro-florisil column prior to GC analysis. 

A procedure was developed by Hiatt (1983) and Dreisch and Munson (1983) to identify and 

quantify 1,1-dichloroethane in fish tissue samples by GC/MS, employing a fused-silica capillary column 

(FSCC) and vacuum distillation (extraction). An advantage of the vacuum extraction is that the system 

does not require elevated temperatures or the addition of reagents, which could produce unwanted 

degradation products (Hiatt 1981). The FSCC provides a more attractive approach than packed column 

for chromatographic analysis of volatile organic compounds, because FSCC can be heated to a highertemperature (350o

C) than that recommended for packed column thereby improving the resolution (at the 

ng/g level) of compounds at a lesser retention time. A physical limitation for compounds that can be 

detected, however, is that the vapor pressure of the compounds must be greater than 0.78 torr 

(approximately 50o

C) in the sample chamber (Hiatt 1983). 

6.3 ADEQUACY OF THE DATABASE 

Section 104(i) of CERCLA directs the Administrator of ATSDR (in consultation with the 

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

adequate information on the health effects of l,l-dichloroethane is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of l,l-dichloroethane. 

The following categories of possible data needs have been identified by a joint team of scientists 

from ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met, 

would reduce or eliminate the uncertainties of human health assessment. In the future, the identified 

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

6.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. Reliable methods are 

available for detecting and quantifying l,l-dichloroethane in the 
75 

6. ANALYTICAL METHODS 

tissues and body fluids of humans. GC/MS or GC/FID has been employed to detect l,l-dichloroethane at 

nanogram to picogram levels in blood and tissue samples of humans. No additional analytical methods for 

determining trace levels of l,l-dichloroethane in the blood of humans are needed. However, the 

report by Hara et al. (1980) did not identify what tissues were analyzed to detect l,l-dichloroethane by 

GC/MS. Also, no detection limits for detecting l,l-dichloroethane in urine samples by GC/MS were 

indicated by Barkley et al. (1980). Therefore, additional research and development of sensitive and 

selective methods for detecting and quantifying the levels of l,l-dichloroethane and its metabolites in the 

tissues and urine of humans would be useful. If methods were available, it would assist investigators in 

determining whether specific levels of l,l-dichloroethane found in the tissues/fluids of exposed persons 

correlate with any adverse health effects. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods are available to detect l,l-dichloroethane in environmental samples. GC/ECD 

and GC/MS have been used to detect and quantify l,l-dichloroethane in air and water samples at ppt and 

ppb levels [EPA methods 5030, 8240 (1986); method 601, 624, 1624 (1987)]. GC equipped with FID, 

PID, or EICD has also been used to detect and quantify l,l-dichloroethane in air, water, milk, vegetables, 

and fish at parts-per-billion levels NIOSH [method 1003 (1987)]. No additional analytical methods for 

determining track levels of l,l-dichloroethane in environmental media are needed. 

6.3.2 On-going Studies 

No on-going studies concerning methods for measuring and determining l,l-dichloroethane in 

biological and environmental samples were reported. 

The Environmental Health Laboratory Sciences Division of the Center for Environmental Health 

and Injury Control, Centers for Disease Control, is developing methods for the analysis of l,ldichloroethane and other volatile organic compounds in blood. These methods use purge and trap 

methodology and magnetic mass spectrometry which gives detection limits in the low parts per 

trillion range. 

77 

7. REGULATIONS AND ADVISORIES 

The international, national, and state regulations and advisories pertaining to l,l-dichloroethane in 

air, water, and food are summarized in Table 7-1. 

 

 

_____________________ 

79 

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99 

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 (GEL) -- 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. 
100 

9. GLOSSARY 

Immediately Dangerous to Life or Health (IDLH) -- The maximum environmental concentration of a 

contaminant from which one could escape within 30 min without any escape-impairing symptoms or 

irreversible health effects. 

Intermediate Exposure -- Exposure to a chemical for a duration of 15-364 days as specified in the 

Toxicological Profiles. 

Immunologic Toxicity -- The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals. 

In Vitro -- Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo -- Occurring within the living organism. 

Lethal Concentration(LO)(LCLO) -- The lowest concentration of a chemical in air which has been 

reported to have caused death in humans or animals. 

Lethal Concentration(50) (LC50) -- A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population. 

Lethal Dose(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)(LD50) -- 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 chemical that is likely to be without an 

appreciable risk of deleterious effects (noncancerous) 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. 
101 

9. GLOSSARY 

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. 

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, m&/kg/day for food, and 

pg/m3

 for air). 

Reference Dose (RfD) -- An estimate (with uncertainty spanning perhaps an ordkr of magnitude) of the 

daily exposure of the human population to a potential hazard that is likely to be without risk of deleterious 

effects during a lifetime. The RFD is operationally derived from the NOAEL (from animal and human 

studies) by a consistent application of uncertainty factors that reflect various types of data used to 

estimate RfDs and an additional modifying factor, which is based on a professional judgment of the entire 

database on the chemical. The RfDs are not applicable to nonthreshold effects such as cancer. 

Reportable Quantity (RQ) -- The quantity of a hazardous substance that is considered reportable under 

CERCLA. Reportable quantities are (1) 1 lb or greater or (2) for selected substances, an amount 

established by regulation either under CERCLA or under Sect. 311 of the Clean Water Act. Quantities are 

measured over a 24-hour period. 

Reproductive Toxicity -- The occurrence of adverse effects on the reproductive system that may result 

from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related 

endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior, 

fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of 

this system. 

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. 
102 

9. GLOSSARY 

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 8-hour 

workday or 40-hour workweek. 

Toxic Dose (TD50) -- A calculated dose of a chemical, introduced by a route other than inhalation, which 

is expected to cause a specific toxic effect 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. 
103 

APPENDIX 

PEER REVIEW 

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

members: Dr. Benjamin Van Duuren, Institute of Environmental Medicine, New York University 

Medical Center; Dr. James Bruckner, Department of Toxicology and Pharmacology, University of 

Georgia; Dr. Theodore Mill, Director, Physical Organic Chemistry Department, SRI International; Dr. 

Nancy Tooney, Associate Professor, Department of Chemistry, Polytechnic University, Brooklyn, New 

York; and Ms. Linda Massey, Private Toxicology Consultant, Santa Clara, California. These experts 

collectively have knowledge of l,l-dichloroethane's physical and chemical properties, toxicokinetics, key 

health end points, mechanisms of action, human and animal exposure, and quantification of risk to 

humans. All reviewers were selected in conformity with the conditions for peer review specified in 

Section 104(i)(13) of the Comprehensive Environmental Response, Compensation, and Liability Act, as 

amended. 

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

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

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

their exclusion, exists as part of the administrative record for this compound. A list of databases reviewed 

and a list of unpublished documents cited are also included in the administrative record. 

The citation of the peer review panel should not be understood to imply its approval of the 

profile's final content. The responsibility for the content of this profile lies with the Agency for Toxic 

Substances and Disease Registry.