March 31, 1987
820K87117
1,2-DICHLOROETHANE
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models* There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
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1,2-Dichloroethane March 31, 1987
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This Health Advisory is based on information presented in the Health
Assessment Document for 1,2-Dichloroethane (Ethylene Dichloride) (U.S. EPA,
1985a). Individuals desiring further information on the toxicological data
should use this document. Information on the Quantification of Toxicological
Effects (QTE) section is contained in the QTE Document (PB#86-118080). Both
documents are available for review at each EPA Regional Office of Drinking
Water counterpart (e.g., Water Supply Branch or Drinking Water Branch), or
for a fee from the National Technical Information Service, U.S. Department of
Commerce, 5285 Port Royal Road, Springfield, VA 22161. The toll-free number
is (800) 336-4700; in the Washington, D.C. area: (703) 487-4650.
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 107-06-2
Structural Formula
H H
I I
Cl - C - C - Cl
I I
H H
1 , 2-Dichloroethane
Synonyms
0 Ethylene dichloride, EDO, 1,2-DCE
Uses (U.S. EPA, 1985a)
0 The major use for EDC is in the production of vinyl chloride. In
addition, it is used as a starting material for the production of
other solvents, as an additive (lead scavenger) in gasolines and is
widely exported. Some of its minor uses include its use as a solvent
in metal degreasing and textile and PVC cleaning, in paints, coatings
and adhesives, as a grain fumigant, a varnish and finish remover,
in soaps and scouring compound, as a wetting and penetrating agent,
in ore flotation and as a chemical intermediate.
*
Properties (EPA, 1985a; Amoore and Hautala, 1983)
Chemical Formula
Molecular Weight 98.96
Physical State Clear, colorless, volatile, oily liquid
Boiling Point 83.7°C
Melting Point -35.3°C
Density (20°C) 1.2529 g/mL
Vapor Pressure 64 torr (20°C)
Water Solubility (208C) 8820 mg/L
Log Octanol/Watar Partition 1.48
Coefficient
Organoleptic Threshold (water) 29 mg/L
Odor Threshold (air) 3 ppm
Conversion Factor 1 ppm • 4.05 mg/rn^
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Occurrence
0 Dichloroethane is a synthetic chemical with no natural sources.
0 Production of dichloroethane was approximately 12 billion pounds in
1983 (U.S. ITC, 1984). However, the vast bulk of dichloroethane is
used as a feed stock for the production of other chlorinated compounds
and it is not readily released to the environment. Releases of
dichloroethane largely result from the approximately 3 million pounds
used as solvents and metal cleaners.
• Releases of dichloroethane are largely to air, with smaller amounts
released to surface and ground waters. Because metal working opera-
tions are performed nationwide, dichloroethane releases occur in all
industrialized areas.
* Dichloroethane released to the air slowly degrades over a few months.
Photooxidation is thought to be the predominant environmental process
determining the fate of 1,2-dichloroethane (U.S. EPA, 1979). Dichloro-
ethane released to surface waters migrates to the atmosphere in a few
days or weeks where it also degrades. Dichloroethane released to the
land does not sorb onto soil but migrates readily to ground water
where it is expected to remain for months to years.
0 Due to dichloroethane1s limited releases, it is a relatively rare
environmental contaminant. Dichloroethane has been detected in both
ground and surface waters but, unlike other volatile organic compounds,
higher levels were reported in surface waters than in ground waters.
The Agency estimates that 0.3% of all ground water supplies contain
concentrations of dichloroethane ranging from 0.5 to 5 ug/I«—-Surface
waters contain higher levels, with 3% of all wells estimated to have
from 0.5 to 20 ug/L. Dichloroethane commonly occurs in air in urban
and suburban areas at concentrations of less than 0.2 ppb. No infor-
mation on the levels of dichloroethane in food have been reported.
0 For the majority of the U.S. population, the greatest source of
dichloroethane exposure is from air. Drinking water is the greatest
source only for populations with drinking water levels greater than
6 ug/L.
III. PHARMACOKINETICS
Absorption
0 1,2-Dichloroethane is absorbed by humans and laboratory animals
through the lungs (Spencer et al., 1951; Urusova, 1953) gastro-
intestinal tract (Alumot et al., 1976) and skin (Urusova, 1953).
0 The proportions of a dose of 1,2-dichloroethane absorbed through the
skin and gastrointestinal tract are unknown. The nature of its other
chemical and physical properties would suggest that this substance
would be absorbed completely when ingested.
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Distribution
0 Forty-eight hours after the administration of a single oral dose of
150 mg/kg of 1,2-dichloroethane to rats, the liver and kidneys were
reported to have the highest concentration of the chemical. Success-
ively lower concentrations occurred in the forestomach, stomach and
spleen (Reitz et al.r 1980).
0 1,2-Dichloroethane readily passes the blood/brain barrier. Distribu-
tion is also known to occur into milk (Urosova, 1953).
Metabolism
0 Following intraperitoneal administration to mice, 1,2-dichloroethane
is metabolized to 2-chloroethanol, converted to alcohol and aldehyde
dehydrogenases, to monochloroacetic acid, and further dehalogenated by
enzyme interaction of monochloroacetate with glutathione or cysteine
to yield 5-carboxymethylcysteine and thiodiacetic acid (Yllner,
1971a,b).
0 Urinary metabolites of 1,2-dichloroethane intraperitoneally administered
to mice include chloroacetic acid, 2-chloroethanol, 5-carboxymethyl
cysteine, conjugated 5-carboxymethyl cysteine, thiodiacetic acid and
5,5-ethylene-bis-cysteine (Yllner, 1971a,b).
\
0 Following oral administration of 1,2-dichloroethane (750 mg/kg) or
2-chloroethanol (80 mg/kg) to rats, the blood level of 2-chloroethanol
at four hours was 67.8 or 15.8 ug/mL, respectively (Kokarovtseva and
Kiseleva, 1978). These levels declined in accordance with first-order
kinetics with a half-life of about nine hours. The relatively low
blood concentrations found were postulated to be due to initial
sequestration of 1,2-dichloroethane in adipose and other tissues
with gradual diffusion redistribution as liver metabolism of 1,2-
dichloroethane to chloroethanol and chloroethanol to chloroacetic
acid proceeded..
Excretion
Mice intraperitoneally injected with a dose of 0.05 to 0.17 gAg of
1,2-dichloroethane excreted 11 to 46% of the dose, unchanged, via the
lungs; 5 to 13% of the dose was metabolized to carbon dioxide and
water; 50 to 73% of the dose was excreted as urinary metabolites
(Yllner, 1971a).
Within 48 hours after dosing, 96% of the radioactivity of a single
oral dose of 150 mg/kg was eliminated from the body by rats (Reitz
et al., 1980).
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IV. HEALTH EFFECTS
Humans
0 Clinical symptoms of acute 1,2-dichloroethane poisoning by ingestion
usually appear within two hours after exposure and typically include
headache, dizziness, general weakness, nausea, vomiting of blood and
bile, dilated pupils, heart pains and constriction, pain in the
epigastric region, diarrhea and unconsciousness. Pulmonary edema
and increasing cyanosis also may occur. These symptoms may disappear
if exposure is sufficiently brief (Wirtschafter and Schwartz, 193$;
McNally and Fostvedt, 1941).
0 A 14-year-old male who drank 15 ml (340 mg/kg) of 1,2-dichloroethane
died six days later despite supportive treatment (Yodaiken and Babcock,
1973). During treatment, serum enzyme and calcium levels increased,
blood glucose decreased and blood clotting time increased. Autopsy
findings revealed extensive liver necrosis and epithelial cell damage
in the entire cortico-tubular structure of the kidneys accompanied by
degeneration in the proximal tubules.
0 While not all instances of 1,2-dichloroethane ingestion are fatal,
death has resulted in the majority of reported cases. Death is most
often attributed to circulatory and respiratory failure (Budanova,
1965; Yodaiken and Babcock, 1973; Luzhnikov et a.l., 1974, 1976; and
Zhizhonkov, 1976).
0 A number of neurological effects following ingestion of 20 to 200 ml
of 1,2-dichloroethane have been reported (Akimov et al., 1976, 1978).
The most common of these involved disturbances in consciousness,
mental disorders and cerebellar and extrapyramidal disorders.
Animals
Short-term Exposure
• Information on the acute oral toxicity of 1,2-dichloroethane indicates
the following: rat LD5n - 680 mgAg; rabbit LDso - 860 mg/kg; (NIOSH,
1977).
0 The principal acute effect of 1,2-dichloroethane in mammals is central
nervous system depression with unconsciousness and coma resulting
from exposure to high concentrations (Spencer et al., 1951; Irish,
1963). Visible signs of 1,2-dichloroethane poisoning include rest-
lessness, intolerance to handling, extreme weakness, intoxication,
dizziness, muscle incoordination, irregular respiration and loss of
consciousness. Deaths occurring within a few hours after recovery
from narcosis are usually the result of shock or cardiovascular
collapse; deaths delayed by several days most often result from
renal damage.
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Reproductive Effects
0 No reproductive effects, as measured by fertility, gestation, viability
or lactation indices, pup survival and weight gain, were indicated in
a multigeneration reproduction study using male and female ICR Swiss
mice receiving 0, 5, 15 or 50 mg/kg/day in drinking water. No effect
on the adult generations was evident after 25 weeks of dosing as
measured by body weight, fluid intake or gross paiiioiogy (Lane et al.,
1982).
Developmental Effects
0 In a study in which male and female mice were exposed to 1,2-dichloro-
ethane in drinking water at doses of 0, 5, 15 or 50 mg/kg/day, no
statistically significant dose-related developmental effects were
observed, as indicated by incidence of fetal visceral or skeletal
anomalies (Lane et al., 1982).
Mutagenicity
0 1,2-Dichloroethane has been shown to be weakly mutagenic in Salmonella
typhimurium strains TA 1530, 1535 and 1538 and in DNA polymerase-defi-
cient Escherichia coli (Brem et al., 1974).
0 1,2-Dichloroethane has been found to be highly mutagenic in Salmonella
typhimurium strains TA 1530 and 1535 with S-9 activation (Rannug and
• Beije, 1979).
0 1,2-Dichloroethane has been shown to induce sex-linked recessive
lethals in Drosophila melanogaster (Rapport, 1960; Shakarnis, 1969).
0 1,2-Dichloroethane was not mutagenic in Salmonella microsome assay
system (McCann et al., 1975).
Carcinogenicity
0 In an NCI (1978) bioassay, 1,2-dichloroethane was administered by
gavage at levels of 47 or 95 mg/kg body weight to Osborne-Mendel rats
five times per week for 78 weeks. Statistically significant increases
in the incidence of squamous cell carcinomas of the forestomach and
hemangiosarcomas of the circulatory system were observed in male
rats(p <0.04). Female rats had a statistically significant increased
incidence of adenocarcinoma of the mammary glands (p <0.002).
• In the same NCI (1978) bioassay, B6C3Fi mice received 1,2-dichloroethane
by gavage five times per week for 78 weeks; males were dosed at levels
of 97 or 195 mg/Tug body weight and females at 149 or 299 mg/kg body
weight. Statistically significant increases in the incidence of
mammary adenocarcinoma (p <0.04) and endometrial stromal polyps or
sarcomas (p <0.016) were seen in female mice. Ihe incidence of
alveolar/bronchiolar adenomas was increased in both sexes (p <0.028).
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March 31, 1987
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V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA , (NOAEL or LOAEL) X (BW)
(UF) x ( L/day)
mg/L ( ug/L)
where:
NOAEL or LOAEL » No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
BW » assumed body weight of a child (10 kg) or
an adult (70 kg).
UF = uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
. L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day and Ten-day Health Advisories
Appropriate data for the derivation of One-day and Ten-day HAs were not
located. It is recommended that the Longer-term HA of 0.74 mg/L for the
10 kg child be used as a conservative estimate for One-day and Ten-day
exposures.
Longer-term Health Advisory
A combination of three inhalational studies in which various animal
species were exposed to 1,2-dichloroethane for up to eight months are consid-
ered appropriate to use in calculating a Longer-term HA. In these studies,
exposures of rats and guinea pigs to air containing 100 ppm 1,2-dichloroethane
for 6 to 7 hours/day, 5 days/week resulted in no mortality and no adverse
effects as determined by general appearance, behavior, growth, organ function
or blood chemistry. However, similar exposures of rats, guinea pigs, rabbits,
and monkeys to air containing 400 or 500 ppm 1,2-dichloroethane resulted in
high mortality and varying pathological findings including pulmonary conges-
tion, diffused myocarditis, slight to moderate fatty degeneration of the
liver, kidney, adrenal, and heart, and increased plasma prothrombin time
(Heppel et al., 1946; Spencer et al., 1951; Hofmann et al., 1971).
The Longer-term HA is calculated as follows:
Step 1: Determination of Total Absorbed Dose (TAD)
TAD - (405 mq/m3) (1 m3/hr) (6 hr) (0.3) (S/7) „ 521 mg/day , 7 4 ma/kq/dav
70 kg 70 kg * 9 y
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1,2-Dichloroethane March 31, 1987
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where:
405 mg/m3 « NOAEL of 100 ppm (1 ppm * 4.05 mg/m3) for adverse effects
in rats and guinea pigs.
1 m3/hr * respiratory rate of adult human (pulmonary rate/body
weight ratio assumed to be the same for humans and
test animals).
6 hr - exposure duration per day.
0.3 * fraction of test substance assumed to be absorbed.
5/7 « conversion of 5-day dosing regimen to full 7-day week.
70 kg » assumed body weight of an adult.
Step 2: Determination of the Longer-term HA
For a 10-kg child:
Longer-term HA - (7.4 mg/kg/day) (10 kg) = 0>74 mg/L (740 ug/L)
(100) (1 L/day)
For a 70-kg adult:
Longer-term HA - (7.4 mgAg/dav) (70 kg) = 2.6 mg/L (2600 ug/L)
(100) (2 L/day)
where:
7.4 mg/kg/day - total absorbed dose (TAD).
10 kg - assumed body weight of a child.
1 L/day • assumed daily water consumption of a child.
70 kg - assumed body weight of an adult.
2 L/day - assumed daily water consumption of an adult.
100 « uncertainty factor, chosen in accordance with NAS/OEW
guidelines for use with a NOAEL from an animal study.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
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1,2-Dichloroethane March 31, 1987
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the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DMEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
No appropriate data are available for determining a reference dose and
drinking water equivalent level (DWEL) for 1,2-dichloroethane. A Lifetime
Health Advisory is not estimated for this chemical.
Evaluation of Carcinogenic Potential
0 1,2-Dichloroethane was shown to be carcinogenic in rats and mice
following gavage exposure in the NCI bioassay (NCI, 1978).
0 IARC has not classified 1,2-dichloroethane (IARC, 1982).
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), 1,2-dichloroethane may be
classified in Group B2: Probable Human Carcinogen. This category is
for agents for which there is inadequate evidence from human studies
and sufficient evidence from animal studies.
• The most recent calculations by EPA's Carcinogen Assessment Group
(CAG) indicates the cancer risk estimate for 1,2-dichloroethane
corresponding to a 10-5 risk level is 3.8 ug/L, using the multistage
model (95% confidence limit) (U.S. EPA, 1985d).
0 The linear multistage model is only one method of estimating carcino-
genic risk. Using the 95% upper-bound estimate of risk at 1 mg/kg/day
for hemangiosarcomas in male rats, the following comparisons can be
made: Multistage, 6.0 x 10-2; Probit, 2.81 x 10-1; Weibull, 2.7 x 10~1
(U.S. EPA, 1985a). Each model is based on differing assumptions. No
current understanding of the biological mechanisms of carcinogenesis
is able to predict which of these models is more accurate than another.
0 While recognized as statistically alternative approaches, the range of
risks described by using any of these modelling approaches has little
biological significance unless data can be used to support the selection
of one model over another. In the interest of consistency of approach
and in providing an upper bound on the potential cancer risk, the Agency
has recommended use of the linearized multistage approach.
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1,2-Dichloroethane March 31, 1987
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VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 U.S. EPA (19S5d) has promulgated a final Recommended Maximum Contami-
nant Level (RMCL) of zero for 1,2-dichloroethane in drinking water
based upon its carcinogenic potential and has proposed a Maximum
Contaminant Level (MCL) of 0.005 mg/L.
0 Due to the lack of appropriate data, the National Academy of Sciences
did not calculate a chronic Suggested-No-Adverse-Response-Level
(SNARL) for 1,2-dichloroethane (NAS, 1980).
0 ACGIH (1984) has recommended a threshold limit value (TLV) of 10 ppm
( ^ 40 mg/m3) and a short-term exposure level (STEL) of 15 ppm (•«•• 60
mg/m3) due to its hepatotoxic effects.
VII. ANALYTICAL METHODS
0 Analysis of 1,2-dichloroethane is by a purge-and-trap gas chromato-
graphic procedure used for the determination of volatile organohalides
in drinking water (U.S. EPA, 1985b). This method calls for the
bubbling of an inert gas through the sample and trapping 1,2-dichloro-
ethane on the adsorbant material. The adsorbant material is heated
to drive off the 1,2-dichloroethane onto a gas chromatographic column.
The gas chromatograph is temperature programmed to separate the
method analytes which are then detected by a halogen specific detector.
This method is applicable to the measurement of 1,2-dichloroethane
over a concentration range of 0.2 to 1,500 ug/L. Confirmatory analysis
for 1,2-dichloroethane is by mass spectrometry (U.S. EPA, 1985c). The
detection limit for confirmation by mass spectrometry is 0.3 ug/L.
VIII. TREATMENT TECHNOLOGIES
0 Treatment technologies which will remove 1,2-dichloroethane from
water include granular activated carbon (GAC) adsorption, aeration
and boiling.
• Dobbs and Cohen (1980) developed adsorption isotherms for several
organic chemicals including 1,2-dichloroethane. It was reported
that Fibrasorb® 300 carbon exhibited adsorptive capacities of 3.5 mg
and 0.5 mg 1,2-dichloroethane/gm carbon at equilibrium concentrations
of 1,000 and 100 mg/L, respectively. Also, Love (1983) reported
that Witcarb® 950 carbon exhibited adsorptive capacities of 1.9 mg
and 0.6 mg 1,2-dichloroethane/gm carbon at equilibrium concentrations
of 100 and 10 mg/L, respectively. USEPA-DWRD installed pilot-scale
adsorption columns in New Jersey to treat contaminated groundwater
(Love and Eilers, 1982). A Witcarfc® 950 carbon column removed 1,2-
dichloroethane from a concentration as high as 8 mg/L to 0.1 mg/L.
Breakthrough occurred at 1,700 bed volumes (BV) with an empty bed
contact time (EBCT) of 18 minutes. Similar studies in Louisiana
showed removal of 1,2-dichloroethane from a concentration of 8 mg/L
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1,2-Dichloroethane March 31, 1987
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to less than 0.1 mg/L after 39 days of continuous operation by a
full-scale GAC column containing Nuchar* WP-G activated carbon (Love,
1983).
1,2-Dichloroethane is amenable to aeration on the basis of its Henry's
Law Constant of 61 atm (Kavanaugh and Trussell, 1980). In a pilot-
scale diffused air aeration column, removal efficiency of 42% of
1,2-dichloroethane was achieved at an air-to-water ratio of 4:1
(Love and Eilers, 1982). In a pilot-scale packed tower aeration
study removal efficiencies of 85 to 98.5% for 1,2-dichloroethane were
achieved on air-to-water ratios of 5-45, respectively (ESE, 1985).
Boiling also is. effective in eliminating 1,2-dichloroethane from water
on a short-term, emergency basis. Studies have shown that 5 to 10
minutes of vigorous boiling will remove 88 to 98% of 1,2-dichloroethane
originally present (Love, 1983).
Air stripping is an effective, simple and relatively inexpensive
process for removing 1,2-dichloroethane and other volatile organics
from water. However, use of this process then transfers the contaminant
directly to the air stream. When considering use of air stripping as
a. treatment process, it is suggested that careful consideration be
given to the overall environmental occurrence, fate, route of exposure
and various other hazards associated with the chemical.
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1,2-Dichloroethane March 31, 1987
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IX. REFERENCES
ACGIH. 1984. American Conference of Governmental Industrial Hygienists.
Documentation of threshold limit values. 4th ed. 1980-1984 supplement.
pp. 181-182.
Akimov, G.A. et al., 1976. Changes in the nervous system in acute dichloro-
ethane poisoning. Voenno-meditisinskiy Zhurnal. 5:35-37.
Akimov, G.A. et al., 1978. Neurological disorders in acute dichloroethane
poisoning. Zh. Nevropatol. Psikhiatr. 78(5):687-692.
Araoore, J.E., and E. Kautala. 1983. Odor as an aid to chemical safety:
Odor thresholds compared with threshold limit values and volatilities
for 214 industrial chemicals in air and water dilution. J. T. Appl. Tox.
3:272-290.
Brem, H., A. Stein and H. Rosenkrantz. 1974. The mutagenicity and DNA-
modifying effect of haloalkanes. Cancer Res. 34:2576-2579.
Budanova, L.F. 1965. On the clinical picture specific to acute peroral
dichloroethane poisoning. Ter Arkh. 37(3):11 0-112.
Dobbs, R.A., and J.M. Cohen. 1980. Carbon adsorption isotherms for toxic
organics. Office of Research and Development, MERL, Wastewater Treatment
Division, Cincinnati, Ohio. EPA 600/8-80-023.
ESE. 1985. Environmental Science and Engineering. Draft technologies and
costs for the removal of volatile organic chemicals from potable water
supplies. No. 84-912-0300. Prepared for U.S. EPA, Science and
Technology Branch, CSD, ODW, Washington, D.C.
Heppel, L.A., P.A. Neal, T.L. Perrin, K.M. Endicott and V.T. Porterfield.
1946. The toxicology of 1,2-dichloroethane (ethylene dichloride).
J. Ind. Hyg. Tox. 28s 4, 113-120.
Hofmann, H. Th., H. Birnsteil and P. Jobst. 1971. Zur inhalationtoxicitat
von 1,1- and 1,2-dichloroathan. Arch. Toxikol. 27:248-265.
IARC. 1982. International Agency For Research on Cancer. IARC monographs
on the evaluation of the carcinogenic risk of chemicals to humans.
IARC Monographs Supplement 4.
Irish, D.D. 1963. Aliphatic halogenated hydrocarbons. In: Industrial
Hygiene and Toxicology, 2nd Ed., Vol. II. Interscience Publishers, New
York, pp. 1280-1284.
Kavanaugh, M.C., and R.R. Trussell. 1980. Design of aeration towers_to
strip volatile contaminants from drinking water. JAWWA.
Kokarovtseva, M.G., and N.I. Kiseleva. 1978. Chloroethanol (ethylene chloro-
hydrin) - a toxic metabolite of 1,2-dichloroethane.' Farmakologiya i
Toksikologiya, 1978, No. 1. 118-121.
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1,2-Dichloroethane March 31, 1987
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Lane, R.W., B.L. Riddle and J.F. Borzelleca. 1982. Effects of 1,2-dichloro-
ethane and 1,1,1-trichloroethane in drinking water on reproduction and
development in mice. Toxicol. Appl. Pharmacol. 63:409-421.
Love, O.T., Jr., and R.G. Eilers. 1982. Treatment of drinking water containing
trichloroethylene and related industrial solvents. JAWWA.
Love, O.T., Jr. 1983. Treatment of volatile organic compounds in drinking
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