Advisory Opinion for lf2-Dichloroethane
                     Office of Drinking Water
               U.S. Environmental Protection Agency
                     Washington, O.C.  20460


The Office of Drinking Water provides advice xon health  effects
upon requestr concerning unregulated contaminants  found in
drinking water supplies.  This information suggests the level of
a contaminant in drinking water at which adverse health effects
would not be anticipated.  A margin of safety is factored in so
as to protect the most sensitive members of the general popula-
tion.  The advisories are called Suggested No Adverse Response
Levels (SNARLs).  SNARLs have been calculated by EPA and by the
National Academy of Sciences (NAS) for selected contaminants in
drinking water.  An EPA-SNARL and a NAS-SNARL may  well  differ due
to the possible selection of different experimental studies for
use as the basis for the calculations.  Furthermore/ NAS-SNARLs
are calculated for adults while the EPA-SNARLs are established
for a 10 leg"body weight child.  Normally EPA-SNARLs are provided
for one-day, ten-day and longer-term exposure periods where
available data exist.  A SNARL does not condone the presence of a
contaminant in drinking water, but rather provides useful infor-
mation to assist in the settling of control priorities in cases
where contamination occurs.  EPA-SNARLs are provided on a case-
by-case basis in emergency situations such as spills and acci-

In the absence of a formal drinking water standard for  an identi-
fied drinking water contaminant, the Office of Drinking Water
develops EPA-SNARLs following the state-of-the-art concepts in
toxicology for non-carcinogenic risk for short and longer term
exposures.  In cases where a substance has Been identified as
having carcinogenic potential, a range of estimates for carcino-
genic risk based upon lifetime exposure as developed by the NAS
(1977 or 1980) and/or EPA Carcinogen Assessment^Group (EPA,
1980a).is presented-.^ .However,--the. EPA-SNARL calculations for all
exposures ignore the possible carcinogenic risk that may result
from these exposures.   In addition, EPA-SNARLs usually-do not
consider the health risk resulting from possible synergistic
effects of other chemicals in drinking water, food, and air.

EPA-SNARLs are not legally enforceable standards;  they  are not
issued as an official regulation,-and they may or  may not^lead
ultimately to the issuance of national standards or Maximum
Contaminant Levels (MCLs).  The latter must take into accoun.t
occurrence, relative source contribution-factors,  treatment-
technology, monitoring capability, and costs, in addition to
health effects. .--It-is quite conceivable that the  concentration

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  :TITLE:    Advisory opinion for 1,2-dichloroethane.
  :IMPRINT: Washington, D. C. :  U. S. Environmental Protection Agency, Office
of Drinking Water, 1981.
  :SERIES:  Suggested no adverse response levels.
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            . ^Chicago, i          """

set for EPA-SNARL purposes might differ from an eventual MCL.
The EPA-SNARLs may also change as additional information becomes
available.  In short, EPA-SNARLs are offered as advice to assist
those such as Regional and State environmental and health offi-
cials, local public officials, and water treatment facility
personnel who are responsible for the protection of public health
when dealing with specific contamination situations.

General Information and Properties

Dichloroethane (1,2-) (1,2-DCE; ethylene dichloride) is a
colorless liquid with a sweet taste and chloroform-like odor.
Its solubility in water is 9 g/liter at 20°C, and it is com-
pletely miscible with ethanol, chloroform, ethyl ether, and
octanol (Irish, 19'63).  1,2-Dichloroethane has a molecular weight
of 98.97, a specific gravity of 1.24 g/ml at 20°C, and a boiling
point of 83.5°C.  It is a moderately volatile compound with a
vapor pressure of 87 torr at 25°C.  A concentration of 1 part per
million in air is equivalent to 4.05 mg/m3.  One milligram per
liter of air is equivalent to 247 parts per million.

The present occupational standard for 1,2-dichloroethane is 50
ppm (200 mg/m3) for an 8-hours/day exposure (U.S. DOL, 1972;
ACGIH, 1977).

Sources of Exposure        .._  ,

Municipal water supplies were tested for 1,2-DCE as well as other
organic compounds in two EPA surveys, the National Organics
Reconnaissance Survey (NORS) in 1975 and the National Organic
Monitoring Survey (NOMS) in 1976-77.  NORS analyzed both raw and
finished water samples by gas chromatography in 80 U.S. cities.
At a detection limit pf 0.1 ug/liter, 1,2-DCE was detected in 14%
of the raw samples and 32.5% of the finished samples.  The
highest concentration reported in finished water was 6 ug/liter.
However, of the 26 finished water samples in which 1,2-DCE was
detected, 24 had concentrations of less than 1 ug/liter. .(Symons,
et al. 1975).

The NOMS examined 113 community water supplies in three sampling
and analysis phases (Meilo, 1978).  Dichloroethane was detected
at concentrations of 0.9-4.3 ug/1 in 10 o^ the 435- total- samples
gathered in all three phases of the survey.

1,2-DCE has been reported in 53 of 204 samples taken from surface
waters near industrialized areas (Swing, et al., 1977).  The
concentrations of^l=,2-DCEiranged vfromod-tS -ppb-f-~except ^for
sample from the Delaware River which was reported at 90 ppb.

The presence of  1,2-DCE  in  the  environment appears to be caused
by anthropogenic activities; no natural  source of this chemical
has been reported.  Environmental  releases of 1,2-DCE result
primarily from the direct production  and use of this chemical/
and its presence in gasoline.   Releases  have also been suggested
to occur from processes  such as chlorination of organics in raw
water during treatment,  incineration  of  chlorinated products, or
production of 1,2-DCE as a  by-product of other chemical process-
es.  Although these processes may  release 1,2-DCE to land, water,
and air, much of the land and water releases will vaporize into
the atmosphere.

The concentration of 1,2-DCE in air distant from point sources
has generally been below the detection limit of currently used
analytical methods, about 0.1 ppb  (0.5 ug/m3).  However, am-
bient levels near production and user-facilities ranged "as high
as 200-500 ug/m3 in a 10-day study at Lake Charles, Louisiana
(PEDCo, 1979).

The potential exists for small  quantities of 1,2-DCE to remain in
agricultural products after fumigation.   Lindgren et al. (1968)
reported that wheat flour retained about 1,000 ppnfT,"2HXE one
hour after termination of fumigation.  Seven days after treat-
ment, the levels had dropped to 22 ppm for surface samples and 46
ppm for center samples-.— No-dichloroethane-was fotind in bread ~-	
baked from flour treated with 1,2-DCE seven days before use.  In
another study (Munsey et.-al- ,.J.957),-Lr2-DCE-was added to flour
at a concentration of -JH ppnu—.- Bgead  prepared—from- the-t-rea^bed-^-^
flour contained less than 2 ppm residual 1,2-DCE.  However,
quick-cooling rolled oats treated  with 61 ppm 1,2-DCE retained
32-33 ppm of the substance  through the cooking process (Munsey et
al., 1957).  In a third  study  (Storey et al.,  1972),  soybeans,
"Fumigated for three days with a mixture  of~~75% 1,2-DCE and 25%
carbon tetrachloride, aerated and  stored overnight,  were reported
to contain 51 ppm 1,2-DCE residual.   The dosage equivalent was 6
gal/1000 bushels of soybeans.

Human milk was  contain-1>2^DCE when-nursing-mothers	
were exposed to the chemical by inhalation (Urusova,  1953).
Women, number .no.t^stated^E—weee-ex-posed ^to—6-3 mg/w^* o^f "5r,'2~DCE•••-•--*
for 1 hour.  Milk samples taken 0.5-2.5  hours  after exposure
showed concentrations of 1,2-DCE of 5.4-6.4 mg/liter.  In some
cases, 1,2-DCE.was detected .at -levels.-of-2=6-mg/-l-itec 18 -hours	
after exposure.
1,2 -Di chlor oe thane.>?^2absarbed^4^:4HmaTK-^
through the lungs  (Spencer, et al.,  1951,  Urusova,  1953)  gastro-
intestinal tract (Alumot, et al., 1976)  and  skin  (Urusova,  1953).
                                                                n n ;v2.-.r vtrv"

The proportion of  a  dose  of  1,2-DCE absorbed through the skin is
unknown.  The nature of its  chemical and physical properties
would suggest that significant amounts of this substance would be
absorbed when ingested; in fact,  Reitz, et al. (1980) accounted
for 96% of the radioactivity of a single oral dose of labeled
1,2-DCE in the excreta or exhaled air.  Therefore, in the devel-
opment of a SNARL  for 1,2-dichloroethane, it will be assumed that
100% of any dose ingested will be absorbed by the exposed

Action on halogenated ethanes by the cytochrome P-450 dependent
mixed function oxidases (MFOs) would be expected to yield 2-halo-
acetaldehyde initially (Hill, et al., 1978).  Thus, 2-chloroace-
taldehyde could result from  the metabolism of 1,2-dichloroethane.
Dehydration to 2-chloroacetic acid may occur (Yllner, 1971) or
further reaction with glutathione may form  s-carboxymethylglu-
tathione, which may  be -further -metabolized 'to s-carboxymethyl-
cysteine and thiodiacetic acid .( Yllner ,.-19-71; Anders —and- Livesey-,--
1980).  It is suggested that at least two reactive metabolites
are formed during  the metabolism of 1,2-DCE.

The distribution of  the chemical  in various tissues was measured
after a single oral  dose  of  150 mg/kg of 1,2-DCE in corn oil
given to rats (Reitz, et~al., 1980).  The liver and kidneys were
reported to have the highest concentration 48 hours after dosing,
followed by the •fores'tomaxrfcr, — stomach"? — and~*spre~en.~" Organ distri- ' "
bution o-f'-lrS-'DCE  foiloweTr th*e— sante—patt:errr-whien~ra'ts inhaled a  '
dose of 150 ppm (608 mg/m3)  for six hours.  It would seem,
then, that the target organs for dichloroe thane do not vary with
different routes of  exposure.  However, it can be shown that the
amount of 1,2-DCE  reaching any one target organ may differ as a
function of dose and route of exposure;  Maximum blood levels of
8-9 ug/ml were measured during the six-hour inhalation exposure
at 150 ppm, the steady-state peak being reached in 2-3 hours
( Reitz et al ; ,--1980 )•;-• -Xfcv the*- ether-trarrd-r Spreaf i-eo "e± "atv ^(-1930 )
showed that .blood - levels -

4 5 minutes after- inge-st ion-af ~l*50-*ing-/kg' BCE— by~rats~; — Marx-imum --------
blood levels were reached more  quickly at lower doses of 25 or 50
mg/kg, as could  be "expected r^Al so, ~ the* 'peak -reached was -riotr as -:.
high as after ingesting  150 mg/kg  (13 ug/ml after 25 mg/kg; 32
ug/ml after 50 mg/kg).   Similar proportional increases occur in
tissue levels as -measured—in -adipase~t±ssue 7 ~i'rver"and~±ung -after
each of the three doses.

1, 2-Dichloroethane .has. beea^shown_,to--be metabolized -rapidly -and- -
excreted. Mice injected  intraperitoneally with 0.05-0.17 g/kg
1,2-DCE were repx>rte^-to^TEfxhal-ev"l;0'-42% of--the initial- dose ' -••••i---: •-•-••'
unchanged within 24 hours  (Yllner,  1971).  By 24 hours after
dosing, 93-96% of labeled  1,2-DCE  was excreted either unchanged

or as metabolites.   Reitz,  et al.  (1980)  reported that 96% of the
radioactivity  from a single 150 mg/kg oral or a 150 ppra six hour
inhalation  exposure  of  rats to labeled 1,2-DCE was eliminated
from the body  within 48 hours.   The  results of these studies
indicate that  it  is  unlikely that  substantial bioaccumulation of
1,2-DCE occurs after a  single exposure.


The toxic effects of 1,2-DCE from  both acute and chronic exposure
include liver  and kidney dysfunction accompanied by circulatory
damage.  These effects  have been documented in humans and animals
(Plaa and Larson, 1965; Yodaiken and Babcock, 1973).  The com-
pound is also  reported  to cause conjunctival irritation in humans
exposed by  inhalation (Irish, 1963)  and corneal clouding in dogs
exposed by  subcutaneous injection  (Kuwabara, et al., 1968).
Exposure,to 1,2-DCE,is-also~reported—to-cause headache r'dlzzl-ness"
and nausea  and vomiting in  humans  (Irish,  1963).   If exposure is
continued,  death may result from respiratory or circulatory
failure (Yodaiken and Babcock,  1973).


Human ingestion of 1,2-DCE  has  been  documented in various case
reports (Yodaiken and Babcock,  1973;  Hueper and Smith, 1935;
Lockhead and Close,  1951).   The chemical has-been-ingested-under ~
different circumstances (e.g.,  recreational use,  suicide
attempts) by persons of diverse occupations and ajges-.- -Adverse	
effects also have been resjalt  from occupational	
exposure by inhalation  or dermal absorption.

Yodaiken and Babcock  (1973)  reported  on the lethal  exposure to
1,2-DCE of  a 14-year old male who  drank 15 ml (340  mg/kg) of the ,.
liquid to "get high".   Despite  supportive  treatment,  the patient
died on the sixth day after ingestion of the chemical.  During
treatment, serum enzyme-levels  -increased7-blood glucose de- '  ~"
creased, serum calcium  levels increased, and blood  clotting time
increased.  Autopsy findings  included  extensive necrosis of the
1 iver and epi thelial-"eelludamage*-.«r*-the-^entd're^ortics^ttrlsaiar - -* -* ^
structure of the kidneys accompanied  by degeneration in the
proximal tubules.

Non-fatal cases of poisoning  by ingestion  have been reported in
the literature, but all as  described  in NIOSH,  1976,  are in
foreign language journals and are  unavailable for evaluation at
this time (lenistea and Mezincesco,  1943;  Bloch,  1946; Stuhlert,
1947; plus others).
The effects ..o£^2-DCSyi
reported by Johnson (1965).  Four female rats, strain unspeci-
fied, were dosed by gavage with 1,2-DCE (400 mg/kg) dissolved in

arachis oil, glycerol formal or normal saline and killed  2 hours
after dosing.  The concentration of glutathione in liver
decreased to 53, 81, 40, and 34% of control levels in  the four
animals.  The dose of 400 mg/kg was roughly one-half the  I^Q.


Alumot, et al. (1976) reported the effects of subchronic  and
chronic exposure of rats to feed fumigated with 1,2-DCE.  In the
subchronic experiment, groups of six rats were fed a diet con-
taining 300 or 600 mg of 1,2-DCE/kg of feed for 5 weeks or 1,600
rag of 1,2-DCE/kg of feed for 7 weeks.  The fumigated feed was
stored in airtight containers; 1,2-DCE loss during the storage
period of 7-10 days was determined to be 5%.  The animals were
allowed access to the feed only at set time intervals  so  that
loss of 1,2-DCE by volatilization would be minimal.  However, the
authors did not calculate a conversion of dosages from mg/kg of
feed to mg/kg of body weight using average body weight, amount of
food consumed, and the volatilization of the substance from the
feed.  Therefore, one can not establish the actual dosage of
1,2-DCE administered.  At the end of the experiment the animals
were killed.  The animals fed the highest dosage, 1600 mg/kg of
feed, showed a 15% increase in liver fat.  No effects were seen
at the two lower doses.
In the chronic exposure (Alumot, et al., 1976), groups of 36 rats
(18 male and 18 female littermates) were fed mash containing
1,2-DCE at 0, 250, and 500 mg/kg of feed.  After 2 years, the
surviving animals were killed.  Serum values for glucose, pro-
tein, albumin, urea, uric acid, cholesterol, glutamic-oxaloacetic
transaminase, and glutamic-pyruvic transaminase in the treated
animals did not differ from those in controls.  No fatty  livers
were detected in the treated animals.  Thus, in the tests used,
the authors found no biochemical or histopathological abnormali-
ties attributable to 1,2-DCE exposure.  However, interpretation
of the results was complicated by the widespread incidence of
chronic respiratory disease in the animals and low survival rates
(12 and 17%, respectively, for dosed males, 56 and 67%, respec-
tively, for dosed females).  Although the authors report  no
adverse effects at either dose, this conclusion can be questioned
because of the poor survival and chronic infection of the
experimental animals.

Additionally, lack of detailed data (as discussed previously)
prevented conversion to mg/kg of body weight dosage units.  Thus
a dose-reponse relationship is difficult to establish.  The
authors propose an acceptable daily intake for 1,2-DCE of 25
mg/kg, but offer no detailed rationale for this amount.


1,2-DCE has been shown to be carcinogenic in rats and mice when
administered orally (NCI, 1978) but non-carcinogenic when ad-
ministered by inhalation (Maltoni, et al., 1980).

1,2-DCE at. doses of 47 or 95 mg/kg/day was administered in corn
oil by gavage five times weekly to 50 Osborne-Mendel rats of each
sex for 78 weeks followed by an observation period of 23 weeks
for males and 15 weeks for females.  A statistically significant
increase in the incidence of sguamous cell carcinoma of the
forestomach and hemangiosarcoraa of the circulatory system was
observed in male but not female rats (P < 0.04).  The female rats
had a significantly increased incidence of adenocarcinoma of the
mammary glands (P < 0.002) (NCI, 1978).

In a complementary gavage study, 50 hybrid B6C3F1 mice of each
sex were dosed five times weekly for 78 weeks with 195 or 97
mg/kg/day in corn oil for male mice and 299 or 149 mg/kg/day in
corn oil for female mice.  The mice were observed for 12-13 weeks
following cessation of the treatment.  A statistically signifi-
cant increase in the incidence of mammary adenocarcinoma (P <
.04) and endometrial stromal polyps or sarcomas  (P < .016) was
seen in the female mice; the incidence of alveolar/bronchiolar
adenomas was increased in both sexes (P < 0.028) (NCI, 1978).

In an inhalation study, Swiss mice or Sprague-Dawley rats of each
sex were exposed to 607.5, 202.5, 40.5, or 20.3 mg/m3 of
1,2-DCE for 7 hours daily, 5 days per week for 78 weeks.  At the
end of the exposure period, the animals were allowed to live out
their natural lives.  In no case did the incidence of a particu-
lar type of tumor appear to be dose-related (Maltoni, et al.,
1980).  The authors concluded that 1,2-DCE was not carcinogenic
under the conditions of their experiment.


Brem et al. (1974) found 1,2-DCE to be weakly mutagenic in
Salmonella' fcypfeimurium (Strain TA 1530, TA 1535 and TA 1538) and
in DMA polymerase deficient Escherichia coll.  A more recent
study (Rannug and Beije, 1979) extends these results.  1,2-DCE
was added to the perfusion fluid for isolated, perfused rat
liver.  Bile samples taken 15-30 minutes after addition of the
chemical to the perfusion system were highly mutagenic when
incubated with £. fcyphimurium strains TA1530 and TA1535.  Samples
of the perfusion fluid containing 1,2-DCE were only weakly
mutagenic.  The authors concluded that the highly mutagenic
substance excreted in the bile was a glutathione conjugate of


As a result of the glutathione dependent metabolic process,  the
episulfonium ion would be formed which would be highly  reactive
and could play a role in the compound's mutagenic activity
(Rannug, et al., 1978; Rannug and Beije, 1979;' Rannug,  1980).  In
addition, 2-chloroacetaldehyde, when formed during oxidative
metabolism by the P-450 MFOs, would also be reactive.   It has
been suggested that this substance is involved in the covalent
binding to tissue macroraolecules (Hill, et al., 1978).   Further-
more, this compound has been shown to be mutagenic (NcCann,  et
al. , 1975).                                                  —

In addition, 1, 2-DCE has been shown to induce  sex-linked
recessive lethals in Drosophila melahogaster larve and  adults
(Rapoport, 1960; Shakarnis, 1969; 1970).


Alumot et al. (1976) found no teratogenic or reproductive
effects, as measured by the percentage of female bearing litters,
litter size, mortality of young, or body weight of young, in rats
fed diets containing 250 or 500 ppro 1, 2-DCE for two years.   As
mentioned earlier, incomplete documentation of the study prevents
one from stating with certainty exactly how much chemical the
animals actually ingested.

SNARL' Develdpmenfc ........

The toxicity 'of 1, 2-DCE appears to be manifested principally as
liver and kidney dysfunction, and, especially  after acute expo-
sure, organ hemorrhaging apparently due to interference  with the
blood clotting mechanism.  Carcinogenicity bioassay results  are
equivocal, the oral studies suggesting that the substance is an
animal carcinogen, the inhalation studies having negative

No satisfactory dose response, no-effect level data are  available
from which a SNARL cao~be written- for any duration of exposure.
None of the accounts of occupational exposure  include adequate
information concerning dose or- duration ~af expo-sure'.'  Mo'st of "the
non-occupational ingestion case reports describe fatal  consequen-
ces or are in foreign language journals that are inaccessible at
this time.  The Subcommittee on Toxicology of the Safe  Drinking ~
Water Committee (NAS, 1980) declined to recommend a 24-hour,
7-day SNARL, concluding that there is insufficient information
available to do so.
As mentioned above:,
of Alumot et al. (1976) in rats are seriously flawed.  The
authors dicT~ not monitor volatilization of the compound from  the
feed as it was being presented to the experimental animals,  only

during the storage period; nor,  is  the  amount of feed consumed by
the animals documented.  Therefore/  no  accurate determination of
the amount of compound  ingested  per unit  of body weight of the
animals can be made.  For these  reasons/  the Alumot study cannot
be used as the basis for the setting of a longer-term SNARL.   The
National Academy of Sciences (1980)  reached much the same
conclusion/ stating that "since  the number of recent reports
suggest that DCE may be a mutagen and/or  a carcinogen/" further
studies must be carried out before  a longer-term SNARL can be

The National Academy of Sciences  (NAS)  and EPA's Carcinogen
Assessment Group (GAG) have calculated  projected incremental
excess cancer risks associated with the consumption of a specific
chemical via drinking water alone by mathematical extrapolation
from high dose animal studies.   Using the risk estimates genera-
ted by the NAS (1980) where the  multi-stage model was utilized, a
range of 1,2-DCE concentrations-can be  computed that would nor-
mally increase the risk of one excess cancer per million (106),
per hundred thousand (105) or per ten thousand (104) people
over a 70-year lifetime/ assuming daily consumption at the stated
exposure level.  The range of concentrations estimated to
represent the range of risks is  shown in  the table below.

    Drink ing'Wa£er"G6ncent^t46hs^and^Assc^-ia-feed'-CaheeT"•R'isfes ^="-—=•

Excess--Life time	—l-ir ' Range 6-f- -Concen tr a t ions •-( ug/1*) •*•'•
Cancer Risk                                          NAS (point
	 "-'CAG'{95%-CL**) ".
" "NAS" (95%"CL
) " estimate)
*  Assumes the consumption of two liters  of  water per day.
** Confidence Limit 	

A .series.of short-term-and-longer^term-experiments-with-Ir2-DCE —
on several end-points of toxicity have been  carried by a group of
inve s t iga tor s • o ver^ fche^pas t? severai^;yeaT?s i-"~Res>ults'-f rom "these- — "-
experiments should be available  in July 1981.

Experiments will- soon~be.~underway--to- investiga-te- the-ef fects of- ; -
1,2-DCE on clotting mechanisms.  This study  should provide no-
effect levels for this particular end-point  of toxicity.  Aspects
of cardiovascular toxicity may be. addressed,  in the .future.through
a request for initiation of EPA-sponsored research.

No SNARLs will be developed at this  time. The Health Effects
Branch concludes that there are  no satisfactory data available at


this time for the derivation  and subsequent scientific support of
a 1-day, 10-day or longer-term SNARL.   This decision will be
reconsidered when, and  if,  the long-awaited experimental data
become available, as promised,  in July 1981.


1,2-Dichloroe thane can  be analyzed by  the purge and trap method
used for the determination  of volatile organohalides in drinking
waters (Bellar and Lichtenberg,  1979;  U.S. EPA, 1980b).  The
volatile components are extracted by an inert gas which is bub-
bled through the aqueous sample.   The  compounds are swept from
the purging device into a short sorbent trap.  After a predeter-
mined period of time, the trapped components are .thermally- de?--- . ...
sorbed and backflushed  onto the head of a gas chromatographic
column and separated .under  programmed  conditions.    -
The reconunended-.pr4jnar^-coiumns--foc---^>rga«ohal-ide--a-nalysi-s-
adequately resolve 1,2-DCE  and  chloroform when the concentration
difference between these compounds  is  larger than a factor of
ten.  The column recommended  for  confirmatory analysis provides
unique separation of  1,2-DCE  from other organohalides, including
chloroform, under these conditions.  Therefore, it is suggested
that this column be used for  the  analysis of 1,2-DCE in finished
drinking waters.  The recommended parameters for the analysis of
this compouna~are-- detailed' tre'lowi   ^

Column: Six feet long x 0.1 inch  ID stainless steel or glass.
Packing: n-octane on  Porisil  -  C  (100/120 mesh).

Temperature: 50°C isothermal  for  3  minutes, then program at
6°/minute to 170°C.

Carrier gas: Helium at 40 ml/minute.

De-tec tor: -Hall 4nod«lel«xrtraly tic -conductivity -or- other halogen- -
specif ic -detectorv

Sample volume: 5 ml

The retention time for 1,2-DCE  under the conditions specified
above is 921 seconds.

The purge and trap procedure  is applicable to the measurement of
most organohalides over thetroncentration -range erf "Ovl to~ 1500 -
ug/1 when the Hall model^ elec.tro.lyt ic  conduct 1 vi.ty- defpctor. J-s
used .  Other halogen  spec if icr de tectors-"^are~ -genre-rally 'limited' to
measurements of 1.0 ug/1 or above.   Confirmatory analysis by
GC-MS or by a different analytical  column is highly recommended.



The information available on the removal of 1,2-DCE from drinking
water is limited (U.S. EPA, 1980c).  1,2-DCE is not easily
removed from water by aeration: for example, an air-to-water
ratio of 4:1 removed only 40 percent of the 1,2-DCE from contami-
nated well water.  Absorption of 1,2-DCE on filters containing
granular activated carbon and resins has been shown to be a more
effective means of its removal from drinking water.  Filtration
through Witcarb  R  -950 granular activated carbon resulted in an
effluent concentration of 1,2-DCE below 0.10 ug/liter for 31
weeks as compared to an average influent concentration of 1.4
ug/liter.  Conventional coagulation and filtration were not
effective in removing 1,2-DCE at average concentrations of 8
ug/liter from drinking water, but the use of a full scale
adsorber containing 76 cm of Westvaco WV-G granular activated
carbon was successful in reducing the 1,2-DCE concentration to
less than 0.1 ug/liter.

Conclusions" and'Rec5mnieri3at ions

As stated above in the SNARL Development section, no satisfac-
tory no-effect level data are available from which to derive
SNARLs for 1,2-DCE at any duration of exposure.  Therefore, the
Health Effects Branch has concluded that, at this time, no^-SNARL
for any duration will be developed.

Research is needed to identify no-effect levels for the most
sensitive end-points of toxicity, so that SNARLs can be devel-
oped.  A series of short-term and longer-term experiments with
1,2-DCE on several end-points of toxicity have been carried out
by a group of investigators over the past several years.  Results
from these experiments should be available in July 1981. Once the
data from this study become available, they will be evaluated for
possible use in the development of SNARLs for this compound.  If
these data prove inadequatey further studies' will have to be done
in order to identify no-effect levels.

Experiments will soon be underway to investigate the effects of
1,2-DCE on clotting mechanisms.  This study should provide no-
effect levels for this particular end-point of toxicity.  Aspects
of cardiovascular toxicity may be addressed in the future through
a request for initiation of EPA-sponsored research.



Alumot, E., Nachtomi,  E.,  Mandel,  E., Holstein, P., Bondi, A.
  and M. Herzberg.   1976.   Tolerance  and Acceptable Daily Intake
  of Chlorinated  Fumigants in the  Rat Diet.  Fd. Cosmet. Toxi-
  col. 14:105-110.

American Conference  of Governmental Industrial Hygienists, 1977.
  Threshold limit values  for chemical substances and physical
  agents in the workroom atmosphere.   Washington, D.C.

Anders, Wm. and J.C. Livesey.   1980.   Metabolism of 1,2-Dihalo-
  ethanes.  In: Ethylene  Dichloride:  A Potential Health Risk?
  Banbury Report  5.  Ames,  E.,  Infante/ P., Reitz, R., eds.
  Cold Spring Harbor,  NY:  Cold  Spring Harbor Laboratory.  Pp.

Bellar, T.A. and  J.J.  Lichtenberg.   1979.  Semi-Automated Head-
  space Analyses  of  Drinking Water and Industrial Waters for
  Purgeable Organic  CompoundSi—Irr: Measurements'of"Organic
  Pollutants in Water  and  Wastewater.  ASTM STP 686.   C.E. Van
  Hall, ed. American Society for Testing and Materials, pp. 108-

Brem, H., A.B. Stein and H.S.  Rosenkranz, 1974.  The Mutagenicity
  and DNA-Mod if ying -Ef-f eet-o-f "fla-laaltemesv ~€sncer - Re-s-.~ ~3 4r25~7 6-' -
  2579.                                             -i

Ewing, B.B., Chian,  E.S.K.,  Cook,  J.C., Evans, C.A.,  Hopke, P.K.
  and E.G. Perkins.  1977.   Monitoring to Detect Previously
  Unrecognized Pollutants  in Surface  Waters.  Prepared by
  Institute of Environmental Studies, University of Illinois at
  Urbana.  Washington,  D.C:  Office of Toxic Substances, U.S.
  Environmental Protection Agency.   Contract No. 68-01-3234.

GCA, 1980.  1,2-Dichloroethane  Technical_-Control-Options_Analy- _-
  sis.  Final Draft  Report*—Prepared—for—t-he-Of-f-ice- of -Ghent re a±~-
  Control, U.S. Environmental  Protection Agency.  Contract No.
  68-01-5960.  Bedford-, MAr-GCA Corp.

Hill, D.L., T.W. -Shih,  T.P.  Johnston  and R.F. Struck.  1978.
  -Macromolecular-Binding '-and -Metabolism- -of-' the—Carcinogen	~
  1,2-Dibromoethane.   Cancer Res.  38:2438.
Hooper, K., Gold, L.S»-and-B.&.,Ames. . J.980. -The,Carcinogenic- -
  Potency of Ethylene Dichloride  in' Two  Animal Bioassays: A
  Comparison'^t-^nha3^t^on.-arid-'G3'v^gre"'rSt^ada"e'sV'-r-^n^:::-'Eth:y'l'ene "• •• • —
  Dichloride: A Potential Health  Risk?  Banbury Report 5.  Ames,
  B., Infante, P., Reitz, R.,  eds.   Cold Spring Harbor, NY: Cold
  Spring Harbor Laboratory.


Hueper, W.C. and C.  Smith.   1935.   Fatal Ethylene Dichloride
  Poisoning.  Amer.  J. Med.  Sci.  189:778-784.

lenistea, C. and M.D. Mezincesco.   1943.  Fatal Poisoning by
  Ingestion of Ethylene  Dichloride.   Bull and  Med. Roum. 8:614-
  617  (Fr.).

Johns, R.  1976.  Air Pollution  Assessment of  Ethylene Dichlor-.
  ide.  Prepared by  Mitre Corp.  for U.S. Environmental Protection
  Agency.  Contract  No.  68-02-1495.   McLean, VA: Mitre Corp,
  Report No. MTR-7164.

Johnson, M.K.  1965.  The Influence of Some Aliphatic Compounds
  jon Rat. Liver -Glutathoone-.LeueJ.s-*—£dochera^-Eharmacoi,^-14-:1383--r--.

Kuwabara, T., Quevedo, A.R.  and  D.C. Cogan.  1968.  An Experi-
  mental Study of-'-BichlOTO^than^itoi^oning^-~Arch. •--©ph-thalmoi'i^ T-

Lindgren, D.L., et al.,  1968.  Residues of Raw and Processed Food
  Resulting from Post-Harvest  Insecticidal Treatment.  Residue
  Rev. 21:1-122.

Lockhead, H.B. and H.P.  Close, 1951.  Ethylene Dichloride Plastic
  Cement - A Case of Fatal Poisoning.   JAMA 146:1323.

McCann, J., V. Simmon, D. Streitwieser and B.N. Ames, 1975.
  Mutagenicity of Chloroacetaldehyde,  a Possible Metabolic
  Product of 1,2-Dichloroethane  (Ethylene Dichloride), Chloro-
  ethanol (Ethylene  Chlorohydrin), Vinyl Chloride and Cyclo-
  phosphamide.  Proc. Nat'l. Acad. Sci.  U.S.A. 72:3190.

Maltoni, C., Valgimigli, L.  and  C. Scarnato, C.  1980.  Long-
  Term Carcinogenic  Assays on  Ethylene Dichloride Administered
  by Inhalation- to~i?atg---and-Mice~«-•••-*• In;--Ethyl'ene^"Dichloride:-A^-^--  ~
  Potential Health Risk?  Banbury  Report 5. Ames, B.P., Infante,
  P., Reitz, R., Eds..  Cold  Spring-Harbor,—NY-: Cold. Spring-Harbor—

Mello, W., 1978.  National Organics Monitoring Survey, March
  1976 through January 1977.   U.S. Environmental Protection
  Agency, Washington, D.C.,  126  pp.

Munsey, V.E., "Mills, PVA-. and'A.K.' Klein.^ 1957. ' Ef^ect^of —  -

  40:201-202.   "

National Academy of  Sciences.  1977.  Drinking Water and Health.
  Volume 1, Safe Drinking Water  Committee, Washington, D.C.


National  Academy of Sciences.  1980.  Drinking Water  and  Health.
  Vol.  3,  Safe  Drinking Water Committee, National Academy of
  Sciences,  Washington, D.C., pp. 104-111.

NCI.  1978.   National Cancer Institute.  Bioassay of
  1,2-Dichloroe thane for Possible Carcinogenicity.
  Carcinogenesis Technical Report Series No. 55.  Bethesda, MD:
  Public  Health Service, U.S. Department of Health, Education,
  and Welfare.   HEW Publication No. (NIH) 78-1361.

NIOSH.  1976.   National Institute for Occupational Safety and
  Health.  Criteria for a Recommended Standard. . .Occupational
  Exposure to Ethylene Dichloride (1,2-Dichloroe thane); — Wash-
  ington,  D.C:  U.S. Department of Health, Educatioar~aad~-Wel£are
 "HEW Publication -No .""(NIOSH) 76-139."
PEDCo.   1979.   Monitoring 'of^AwbteTir*Cg^els'of~EDC-Nerf
 _ tion and  User-Facilities~~J&te^ace4>^OB**bh^
  and Development,  U.S.  Environmental Protection Agency.
  Contract  No.  68-02-2722.   Research Triangle Park, NC:
  Environmental Monitoring  and Support Laboratory, U.S.
  Environmental Protection  Agency.  Report No. 600/4-79-029.

Plaa, G.L.  and  R.Er -Larson.' — "2:965.  Relative ~Nephrotoxic  Proper-
  ties of Chlorinated Methane, Ethane, and Ethylene Derivatives
  In Mice--.^^oxicoK '"Appl^ '^Ph'atlaa'cSOTT" 7t37-44".   """"' ' • *"
Radding, S.B.,  Liu,  D.H.,  Johnson, H.L. and T. Mill.  1977.
  Review of  the Environmental Fate of Selected Chemicals.
  Prepared by Stanford  Research Institute for Office of Toxic
  Substances, U.S.  Environmental Protection Agency.  Contract  No.
  EPA 68-01-2681.   Springfield, VA: National Technical Informa-
  tion Service.  Report No.  EPA- 560/5-77-003.
Rannug r-U;  -1980.- - =The Use'^of 7D*ree^e~tte*Mef:afro^
. .  ...the El uc idat-iojr -of-^he-^lu t
 -:in Salmonella-?— In r ^Etrhylene— Dlch-rOflde"r^AJPbtentral Health
  Risk"?  Banbury  Report  5.   Ames,  B., P. Infante and R. Reitz,
  eds. Cold Spring Harbor, -New -York.- -Cold Spring Harbor Labora-
  tory.  pp.  83-92.

Rannug, -U.- and- B. -Beij"eT^1979-.: The Mutlgeri'icr-Ef feet ~of~ 1,2-Di-
  chloroethane on Salmonella Typhimurium.  II. Activation by the
  Isolated Perfused Rat  Liver.  Chem. Biol. interact. 24:265-285.

Rannug, U., A. Sundvall  and  C. -Ramel. — 1978. — The— Mutag.en4*c^
  Effect of^--'l>^~131-Ghlbrl3eth:ar^^ri--^lmOT^                     —
  Activation Through  Conjugation with Glutathione in vitro.
  Chem. Biol.  Interact.  20:1-


 Rapoport,  I.A.   1960.  The Reaction of Genie Proteins with  1,2-
   D-ichloroethane.   (Russ.).  Dokl. Akad. Nauk SSR.  134:1214-1217.
   [Translation  in  Dokl. Biol. Sci. (1960) 134:745-747.]

 Reitz,  R.H.,  Fox,  T.R., Doraoradzki, J.Y.f Quast, J.F.,  Langvardt,
   P.  and  P.G. Wanatabe.  1980.  Pharmacokinetics and Macromole-
   cular Interactions of Ethylene Dichloride: Comparison of  Oral
   and Molecular Exposures. In: Ethylene Dichloride: A Potential.
   Health  Risk?   Banbury Report 5.  Ames, B., Infante, P., Reitz,
   R., Eds.  Cold Spring  Harbor, NY:_Cold Spring Harbor Laboratory.
   pp. 135-144.

 Shakarnis,  V.F.  1969.   1,2-Dichloroethane Induced  Chromosome
   Non-Disjunction  and Recessive Sex-Linked Lethal Mutation  in
  " pro sop hi la- me 1 anbgasterv^sSe-ngtitea?r5 r 8-9*95 -* f RtrSs ; y?~ '*'-  ' •" •"  '

 Shakarnis,  V.F.  1970.   Effect-of-lr2^Dichloroethane^on-Chromo»«-«-
   some  Non-Disjunction  and Recessive Sex-Linked Lethals in  a
   Radio-Resistant  Strain~of"DrosbpRilia melanogaster; "Vestn."
   Leningrad Univ.  Ser..Biol. 25:153»-156-(Russ. )«—=----

 Spencer/  H.C.,  Rowe>  V.K., Adams, E.M., McCollister, D.D. and
   D.D.  Irish.   1951.   Vapor Toxicity of Ethylene Dichloride
   Determined-by .Experiments
   Occup.  Med. 4:482-493.
.Soreafico,  F.^..E.  Zuccato., — E^— Mar cue c i ,  M . -~Si
   lunga,  M.  Madonna and E.  Mussini.  1980.  Pharmacokinetics of
   Ethylene  Dichloride- in— Rats— Treated— by--Di£ferent Routes- and— - •-—•
   Its  Long-Term  Inhalation  Toxicity.  In: Ethylene Dichloride:
   A  Potential  Health Risk?   Banbury Report 5.  Ames, B. ,  Infante,
   P.,  Reite, R. , eds.   Cold Spring Harbor, -New- York^ - -Cold Spring .
   Harbor  Laboratory,  pp. 107-130.

Storey, C.L. ,  Kirks, L. D^ .and^G.C^-Mus taker-. — 1932. -Fate o.f---^.
   EDC-CC14  Residues During  Extraction of Soybeans.  J.  Econ.
   Entomol.  65 C4): 1126-1129^: ~~"-~
Stuhlert,  H^_ -1949.
   DLsch. Med. Wochenschr.  74:1542-1543 (Ger.)«~

Symons, . J.M. , T.M.  Bellar, J.K.  CarsA^ell-,u_J._DeMarca^- -K»L», Kropp,
   G.G.  Robeck,  D.R.  Seeger, C.J. Slocum, B.L. Smith and A. A.
 .. Stevens .   1975.   National - Organics~Reconnaissance:~Survey- for-  -
   Halogenated Organics.   J. AWWA 67(11) : 634-647.

U . S..  De-par tltren t-' O'f ^
   stration.   1972.   "Occupational Health and Environmental Con-
   trol."   Federal Register 37:22139.


U.S. EPA.  1980a.  Water Quality Criteria Documents; Avail-  -
  ability.  Federal Register 4j5(231):79318-79379.

U.S. EPA.  1980b.  U.S. Environmental Protection Agency.  The
  Determination of Halogenated Chemical Indicators of  Industrial
  Contamination in Water by the Purge and Trap Method  502.1.
  Organic Analyses Section, Environmental Monitoring and
  Support Laboratory, U.S. Environmental Protection Agency,
  Cincinnati, Ohio 45268.  September.

U.S. EPA.  1980c.  U.S. Environmental Protection Agency.  Memo
  from Gordon G. Robeck: Treatment for the Control of  Trichloro-
  ethylene and Other Related Industrial Solvents in Drinking

Urusova, T.P.  1953.  The Possible Presence of Dichloroethylene
  in Human Milk with Exposure in Industrial Conditions.  Gigiena
  i Sanitaryi 18:36-37.

Wirschafter, Z.T. and E.D. Schwartz.  1939.  Acute Ethylene
  Dichloride Poisoning.  J. Ind. Hyg. Toxicol. 21:126-131.

Yllner, S.  1971.  Metabolism of 1,2-Dichloroethane-14C in the
  Mouse.  Acta Pharmacol. Toxicol. 30:257-265.
Yodaiken, R.E. and J.R. Babcock.  1973.  .1,2-Dichloroethane
  Poisoning.  Arch. Environ. Health 26:281-284.

This health advisory is a preliminary draft.  It.has
not been released formally by the Office of Drinking
Water, U.S. Environmental Protection Agency, and.should
not at this stage be construed to represent the position
of the Office of Drinking Water.  It is being circulated
for comments on its technical merit.