820K87007
March 31, 1987
DICHLOROMETHANE
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-terra
(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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Dichloromethane March 31, 1987
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This Health Advisory is based upon information presented in the Office
of Health and Environment Assessment Criteria Document (CD) for Dichloromethane
(U.S. EPA, 1985a). The HA and CD formats are similar for easy reference.
Individuals desiring further information on the toxicological data base or
rationale for risk characterization should consult the CD. The CD is available
for a fee from the National Technical Information Service, U.S. Department of
Commerce, 5285 Port Royal Rd., Springfield, VA 22161, PB85 191559. The toll-
free number is (800) 336-4700; in the Washington, D.C. area: (703) 487-4650.
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 75-09-2
Structural Formula
Cl
I
H-C-C1
I
H
Synonyms^
0 Methylene chloride, methylene dichloride, methylene bichloride, DCM
Uses
0 Solvent for insecticides, paints, varnish and paint removers and in
food processing; degreasing and cleaning fluids.
Properties (Verschueren, 1977; Windholtz, 1983)
Chemical Formula CH2C12
Molecular Weight 84.94
Physical State Colorless liquid
Boiling Point 40°C (760 mm Hg)
Melting Point -95 to -97°C
Density 1.3255 (20/4°C)
Vapor Pressure 349 mm Hg (20°C)
Water Solubility 20 g/L (20°C)
Log Octanol/Water Partition —•
Coefficient
Odor Threshold —
Taste Threshold —
Conversion Factor —
Occurrence
0 Dichloromethane (DCM) is a synthetic chemical with no known natural
sources.
0 Production of DCM was approximately 600 million Ibs in 1983 (U.S.
ITC, 1984).
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Dichloromethane March 31, 1987
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The major sources of DCM released to the environment are from its
industrial uses where the majority of all DCM produced is released.
Most of the releases occur to the atmosphere by evaporation. However,
large amounts of DCM are disposed of by burial in landfills or dumping
on the ground or into sewers. Because DCM is involved in industrial
operations performed nationwide, releases occur in all urban areas.
Releases of DCM during its production are relatively minor in comparison
to releases during its use.
Dichloromethane released to the air is degraded in a matter of a few
days. Dichloromethane released to surface waters migrates to the
atmosphere in a few days or weeks where it also degrades. Volatiliza-
tion is the major transport process for its removal from aquatic
systems (U.S. EPA, 1979). Dichloromethane which is released to the
land does not sorb onto soil and migrates readily to ground water
where it is expected to remain for months to years. Dichloromethane,
unlike some other chlorinated compounds, does not bioaccumulate in
individual animals or food chains.
Because of the large and dispersed releases, DCM occurs widely in the
environment. It is ubiquitous in the air with levels in the ppt
range and is a common contaminant in ground and surface waters with
higher levels found in ground water.
Very limited information is available on the occurrence of dichloro-
methane in food. Dichloromethane has been reported to occur in fish.
It is used as an extraction solvent for the -decaffination of coffee
and other food processing operations. Low levels of DCM have been
reported to occur in some foods from these operations.
The major sources of exposure to DCM are from contaminated water.
Air and food are only a minor sources (U.S. EPA, 1980c).
III. PHARMACOKINETICS
Absorption
Dichloromethane is expected to be absorbed completely when ingested.
A single oral dose of 1 or 50 mgAg 14C-DCM administered to male rats
(3/dose) was exhaled as unchanged DCM (12.3 or 72.1%, respectively)
within 48 hours (McKenna and Zempel, 1981).
Distribution
Tissue distribution after administration of 1 or 50 mgAg of 14c-DCM
in water by gavage to male rats (3/dose) was measured by McKenna and
Zempel (1981). The highest concentration of radioactivity was present
in liver and the lowest in fat, 48 hours after either dose.
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Metabolism
0 The major metabolites of DCM are carbon monoxide and carbon dioxide.
McKenna and Zempel (1981) studied the metabolism of 14c-DCM after
gavage administration to groups of three male Sprague-Dawley rats
dosed at 1 or 50 mgAg« They metabolized about 88 or 28% of the
dose, respectively. The major metabolites exhaled after 48 hours
were carbon monoxide (30.9 and 11.9% of the 1 or 50 rag/kg doses,
respectively) and carbon dioxide (35.0 and 6.3% of the 1 or 50 mgAg
doses, respectively).
Excretion
Metabolites of DCM are excreted in urine. McKenna and Zempel (1981)
reported that, in rats given 1 or 50 mgAg 14C-DCM, 4.52 ±0.05% or
1.96 ±0.05% of the dose, respectively, was excreted in the urine
within 48 hours. The fecal elimination of DCM after oral or intra-
peritoneal administration of DCM is low (<1.0%) (DiVincenzo and
Hamilton, 1975; McKenna and Zempel, 1981).
IV. HEALTH EFFECTS
Humans
Bonventre et al. (1977) described a fatal intoxication with DCM
which was being used as a paint remover. Postmortem examination
revealed the presence of DCM in the liver (14.4 mg/100 g tissue),
blood (51 mg/dL or 510 mg/L) and brain (24.8 mg/100 g tissue).
The carboxyhemoglobin content was 3% saturated.
Animals
Short-term Exposure
0 Oral LD^gs for DCM were reported as 1,987 mgAg for mice and 2,121
mgAg for rats (Kimura et al. 1971; Aviado et al. 1977).
Kimura et al. (1971) administered single oral doses of DCM to young
adult Sprague-Dawley rats and determined that an approximate dose
of 1 .3 gAg body weight was the lowest dose to induce the first
observable signs of toxicity (dyspnea, ataxia, cyanosis and/or coma)..
Long-term Exposure
Bornmann and Loeser (1967) administered DCM in drinking water at
2.25 g/18L (or 125 mg/L) to 30 male and 30 female Wistar rats for 13
weeks. This is equivalent to a dose of about 15 mgAg/day assuming
that 1 0 mL of water is consumed daily. The animals were examined
for changes in behavior, body weight, blood and urine chemistries,
reproductive function, organ to body weight ratios and histology.
No treatment-related effects were observed, even though some rats
may have consumed as much as 250 mg DCM (36.6 mgAg/day ) during this
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Dichloromethane March 31, 1987
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experiment. The urine albumin test was frequently positive; however,
the authors did not attach any biological significance to this obser-
vation. From this study, a NOAEL of 125 mg/kg/day was identified.
0 Hazelton Labs (1982) reported on the toxicity and carcinogenicity of
DCM in a chronic two-year drinking water study in Fischer 344 rats.
Two control groups (85 and 50 rats/sex/group) received deionized
drinking water. Four groups of animals (85 rats/sex/group} were
given DCM in drinking water at target doses of 5, 50, 125 and 250
mg/kg/day. A high-dose recovery group (25 rats/sex) was given DCM
in drinking water at a target dose of 250 mg/kg/day for the initial
78 weeks and deionized drinking water subsequently for the remainder
of the study. At 26, 52 and 78 weeks of treatment, there were incre-
mental sacrifices of 5, 10 or 20 rats/sex/group, respectively. At
104 weeks of exposure, all survivors were sacrificed. Survival,
body weight gains, total food consumption, water consumption, clinical
observations, ophthalmoscopic findings, clinical pathology, absolute
and relative organ weights and gross and microscopic pathology were
examined to evaluate any compound-related effects. The dose of
5 mgAg was identified as the no-effect level based on the absence of
effects on body weight, hematological parameters and histopathological
changes in the liver (incidence of foci/areas of cellular alteration
and/or fatty changes).
Developmental Effects
Q No positive conclusion can be drawn regarding the potential for
developmental effects of DCM.
0 Maternal exposure of rats and mice to DCM (4337 mg/m3) on days 6
through 15 of gestation was associated with soft tissue abnormalities
in the offspring of rats and skeletal changes in the offspring of
both rats and mice (Schwetz et al., 1975).
0 Other workers have found no increased incidence of gross external,
skeletal or soft tissue anomalies in offspring after maternal exposure
of rats to DCM at 15,615 mg/m3 (6 hours/day, 7 days/wk) before and
during gestation. (Hardin and Manson, 1980).
Mutagenicity
0 DCM has been reported to be mutagenic in several bacterial and yeast
test systems, as well as in mammalian test systems. DCM was also
reported to be positive in a mammalian transformation test (U.S. EPA,
1985a).
Carcinogenic!ty
0 In a pulmonary tumor response assay, DCM administered intraperitoneally
did not produce an increased incidence of lung tumors in mice (Theiss
et al. 1977).
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0 An inhalation bioassay conducted in male and female F344/N rats and
B6C3F-] mice indicated clear evidence of carcinogenicity in male and
female mice as shown by increased incidences of lung (alveolar/
bronchiolar adenoma and/or carcinoma) and liver (hepatocellular
adenoma and carcinoma combined) tumors (NTP, 1985, as cited in U.S.
EPA, 1985c). Some evidence of carcinogenicity in male rats and
sufficient or clear evidence of carcinogenicity in female rats was
indicated by an increased incidence of benign neoplasms of the mammary
gland. These animals were exposed at concentrations of 0, 1,000,
2,000 and 4,000 ppm for rats and 0, 2,000 and 4,000 ppm for mice,
6 hours/day, 5 days/week for 102 weeks.
0 Hazelton Laboratories (1982) studied the carcinogenicity of DCM in a
chronic two-year drinking water study in Fischer 344 rats, using the
protocol as described under longer-term exposure. Hepatic histologicaJ
alteration detected in the 50 to 250 mgAg/day dose groups (both
sexes) included an increased incidence of foci/areas of cellular
alteration. Fatty liver changes were detected in the 125 and 250
mgAg/day groups after 78 and 104 weeks of treatment. The authors
stated that DCM did not induce carcinogenicity under the conditions
of the study.
0 The U.S. EPA (1985b) performed an independent assessment of the data
from the Hazelton Laboratories (1982) study and determined that
incidences of hepatic neoplastic nodules and carcinomas (combined
in females exposed to 50 mgA9/<3ay (4.8%), 250 mgAg/day (7.1%) and
250 mgAg/day, recovery group (8.0%) were significantly (P<0.05)
higher than that in matched controls (0%). No significant increase
in liver tumors was evident in any of the male dose groups. The U.S.
EPA (1985b) considered data on historical cbntrol values and concluded
that the 250 mgAg/day dose was borderline for carcinogenicity in
Fischer 344 rats.
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) = /L ( /L}
(UF) x ( L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effeet-Level
in mgAg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
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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 Health Advisory
The study by Kimura et al. (1971) has been selected to serve as the
basis for the One-day HA for the 10 kg child because no other acute oral
studies of appropriate duration or design were located in the literature.
This study identified a LOAEL in young adult Sprague-Dawley rats on the basis
of the first observable gross signs of toxicity (i.e., dyspnea, ataxia,
cyanosis and/or coma) following administration of a single oral dose of DCM
by gavage. The authors implied that multiple dose levels were administered
to define dose-response, although details were not reported. The calculations
for a One-day HA for a 10-kg child are given below:
One-day HA » 1,326 mg/kg/day) (10 kg) = 13.3 /L (13,300 ug/L)
(1,000) (1 L/day)
where:
1,326 mgAg/day = LOAEL, based on the first observable gross signs of
toxicity in rats.
10 kg = assumed body weight of a child. ~
1,000 = uncertainty factor, chosen in accordance with ODW/NAS
guidelines for use with a LOAEL from an animal study.
1 L/day = Assumed daily water consumption of a child.
Ten-day Health Advisory
The study by Bornmann and Loeser (1967) in which DCM was administered
in drinking water at 125 mg/L to Wistar rats for 13 weeks, has been selected
to serve as the basis for the Ten-day HA for the 10-kg child because it was
the most comprehensive short-term oral toxicity study located.
The Ten-day HA for a 10 kg child is calculated as follows:
Ten-day HA = <1S mg/kg/day)(10 kg) = , 5 /L (1 500 ug/L)
(100) (1 L/day)
where:
15 mg/kg/day = NOAEL, based on absence of effects on body weight gain,
blood and urine chemistries, reproductive function,
organ/body weight ratios, or histopathological changes
in Wistar rats.
10 kg = assumed body weight of a child.
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Dichloromethane March 31, 1987
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100 = uncertainty factor, chosen in accordance with ODW/NAS
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
Longer-term Exposure
There were no suitable data available from which to calculate Longer-Term
Health Advisories.
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
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 DWEL 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.
Dichloromethane may be classified in Group B2: Probable Human Carcinogen,
according to EPA's guidelines for assessment of carcinogenic risk (U.S. EPA,
1986). Because of this, caution must be exercised in making a decision on
how to deal with possible lifetime exposure to this substance. The risk
manager must balance this assessment of carcinogenic potential against the
likelihood of occurrence of health effects related to non-carcinogenic end-
points of toxicity. In order to assist the risk manager in this process,
drinking water concentrations associated with estimated excess lifetime cancer
risks over the range of one in ten thousand to one in a million for the 70-kg
adult, drinking 2 liters of water per day, are provided in the following
section. In addition, in this section, a Drinking Water Equivalent Level
(DWEL) is derived. A DWEL is defined as the medium-specific (in this case,
drinking water) exposure which is interpreted to be protective for non-
carcinogenic end-points of toxicity over a lifetime of exposure. The DWEL
is determined for the 70-kg adult, ingesting 2 liters of water per day. Also
provided is an estimate of the excess cancer risk that would result if exposure
were to occur at the DWEL over a lifetime.
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Neither the risk estimates nor the DWEL take relative source contribution
into account. The risk manager should do this on a case-by-case basis,
considering the circumstances of the specific contamination incident that has
occurred.
The study by Hazelton Laboratories (1982) is most appropriate from which
to derive the DWEL because it is an oral chronic (two year) study that admini-
stered DCM in drinking water in multiple dose levels to rats. This is the
most comprehensive chronic oral study available. There were sufficient
numbers of animals in the dose groups and a dose-response was demonstrated.
A NOAEL of 5 mg/kg/day was identified in this study.
The DWEL for a 70-kg adult is calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = 15 mg/kg/day) - 0.05 mgAg/day
where:
5 mg/kg/day = NOAEL based on the absence of liver and blood effects
in rats.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.05 mg/kg/dav)(70 kg) = , >75 mg/L (1f750 ug/L)
(2 L/day)
where:
0.05 mgAg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption by an adult.
Step 3: Determination of the Lifetime Health Advisory
Dichloromethane is classified in Group B2: Probable Human Carcinogen.
A Lifetime HA has not been calculated for DCM.
The estimated excess cancer risk associated with lifetime exposure to
drinking water containing DCM at 1,750 ug/L is approximately 3.7 x 10~4.
This estimate represents the upper 95% confidence limit from extrapolations
prepared by EPA's Carcinogen Assessment Group using the linearized, multistage
model. The actual risk is unlikely to exceed this value, but there is consid-
erable uncertainty as to the accuracy of risks calculated by this methodology.
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Dichloromethane March 31, 1987
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Evaluation of Carcinogenic Potential
0 IARC (1982) has classified DCM in group 3: Limited evidence of
carcinogenicity in animals.
0 Applying the criteria described in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986), DCM 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.
0 More recently, EPA's CAG (U.S. EPA, 1985c) estimated that the upper-
bound incremental unit carcinogenic risk for drinking water containing
1 ug/L DCM for a lifetime was 2.1 x 10-7 (ug/L)-1. This risk estimate
was the mean of the derived carcinogenic risk estimates based on the
finding of liver tumors (not based on lung tumors) in the NTP (1985)
draft inhalation study in female mice and the suggestively positive
finding of liver tumors in the Hazelton (1982) unpublished ingestion
study in male mice. Since the extrapolation model is linear at low
doses, additional lifetime cancer risk is directly proportional to
the water concentration of DCM. Thus, levels of 10~4, 10"5 and 10-6
are 0.48, 0.048 and 0.005 mg/L, respectively.
0 The linear multistage model is only one method of estimating carcino-
genic risk. Using the 10~6 risk level, the following comparisons in
micrograms/L may be made: Multistage, 4.8; Probit, 74,000; Logit,
4,000; Weibull, 10. Each model is based on differing assumptions.
No current understanding of the biological mechanism of carcinogenesis
is able to predict which of these models is more accurate than another.
While recognized as statistically alternative approaches, the range of
risks described by using any of these modeling 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.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 ACGIH (1984) has recommended a time-weighted average threshold limit
value (TWA-TLV) of 100 ppm ( 360 mg/m3) in the absence of occupa-
tional exposure to carbon monoxide and is based upon experimental
data obtained from nonsmoking males at rest. A short-term exposure
level (STEL) of 500 ppm is also recommended.
0 The Occupational Health and Safety Administration (OSHA, 1979) has
established occupational exposure standards as follows: an eight-hour
time-weighted-average (TWA) of 1,737 mg/m3; an acceptable ceiling
concentration of 3,474 mg/m3; and an acceptable maximum peak above
the ceiling of 6,948 mg/m3 (five minutes in any two hours).
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Dichloromethane
March 31, 1987
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0 Due to the metabolic formation of carboxyhemoglobin and the additive
toxicity with carbon monoxide, the National Institute of Occupational
Safety and Health (NIOSH, 1976) has recommended a ten-hour TWA exposure
limit of 261 mg/m3 and a 1737 mg/m3 peak (15 minute sampling), in the
presence of carbon monoxide concentrations less than or equal to 9.9
mg/m3 (TWA). Proportionately lower levels of DCM are required in the
workplace when carbon monoxide concentrations greater than 9.9 mg/m3
are present.
0 Based on noncarcinogenic risks, a water quality criterion of 12.4 mg/L
is the acceptable concentration of DCM in drinking water (U.S. EPA,
1980a). This calculation was performed by the U.S. EPA as part of the
overall process for developing a U.S. EPA Water Quality Criteria for
halomethanes as a group and uses a limit of 200 ppm (694 mg/m3) for
protection against excessive carboxy-hemaglobin formation. In that
calculation, the EPA assumed that the average person consumes approxi-
mately two liters of water and eats 6.5 g of contaminants in fish and
seafood per day, and that the estimated coefficient of absorption via
inhalation versus ingestion is 0.5.
0 The original U.S. EPA Suggested-No-Adverse-Response-Levels (SNARLs,
now referred to as Health Advisories) for DCM were set at 13, 1.5
and 0.150 mg/L in drinking water for One-day, Ten-day and Longer-term
exposures, respectively (U.S. EPA, 1980b). The U.S. EPA-SNARLs were
established for a 10 kg body weight child and did not consider the
possible carcinogenic risk that may result from exposure to a chemical.
0 The MAS (1980) calculated one-day and seven-day NAS-SNARLs for DCM
in drinking water based on the minimal-effect acute oral dose in rats
reported by Kimura et al. (1971). The NAS concluded that data on the
no-effect dose do not exist. Using the 1 ml/kg (1.3 gAg) minimal-
effect acute oral dose in the rat, assuming two liters/day of drinking
water as the only source (consumed by a 70 kg adult) and employing a
safety factor of 1,000, the NAS (1980) calculated the one-day SNARL.
Since no appropriate data were available for the seven-day SNARL, the
one-day SNARL was divided by a factor of seven (days). However, the
NAS (1980) erroneously reported a value of 35 mg/L for the one-day
and 5 mg/L for the seven-day calculation. Re-examination of calcula-
tions indicated that the one-day and seven-day adult NAS-SNARLs
should be 45.5 mg/L and 6.5 mg/L, respectively.
VII. ANALYTICAL METHODS
Analysis of DCM is by a purge-and-trap gas chromatographic procedure
used for the determination of volatile organohalides in drinking water
(U.S. EPA, 1985d). This method calls for the bubbling of an inert
gas through the sample and trapping DCM on an adsorbant material.
The adsorbant material is heated to drive off the DCM onto a gas
chromatographic column. This method is applicable to the measurement
of DCM over a concentration range of less than 1 to 1500 ug/L; however,
measurement of DCM at low concentrations is difficult due to problems
with contamination. Dichloromethane vapors readily penetrate tubing
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Dichloromethane March 31, 1987
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during the purge/trap procedure. Confirmatory analysis for DCM is
by mass spectrometry. (U.S. EPA 1985e). The detection limit for
confirmation by mass spectrometry is 0.3 ug/L.
VIII. TREATMENT TECHNOLOGIES
8 Limited information is available concerning the removal of dichloro-
methane from drinking water. However, evaluation of physical and
chemical properties and some experimental data suggest that adsorp-
tion by granular activated carbon (GAG) and aeration are feasible
technologies to remove this contaminant in drinking water supplies.
0 Dobbs and Cohen (1980) developed adsorption isotherms for several
organic chemicals, including DCM. This study reported that Filtrasorb*
300 exhibited adsorptive capacities of 1.3 mg and 0.09 mg DCM per gm
carbon at equilibrium concentrations of 1,000 mg/L and 100 mg/L,
respectively.
0 Another study reported activated carbon usage of 3.9 lb/1,000 gal of
treated water to maintain an effluent DCM concentration below 1 ug/L
from a raw water influent concentration above 20 mg/L (ESE, 1982).
This particular treatment scheme employed two activated carbon columns
operating in series with extremely long empty bed contact time (262
minutes).
0 The calculated Henry's Law constant for DCM is 2.5 x 10-3 atm-m3/mole
(ESE, 1982). In a bench-scale study, distilled water which was
spiked with 225 ug/L of DCM was passed through a diffused air aerator.
The results showed 82 percent reduction in DCM at an air-to-water
ratio of 15:1 (Love, 1983). Dichloronethane will, therefore, be
amenable to air stripping treatment. Actual field performance data,
however, have not been reported for this compound.
0 Air stripping is an effective, simple and relatively inexpensive
process for removing DCM 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
hazards associated with the chemical.
0 Treatment technologies for the removal of DCM from water have not
been extensively evaluated except on an experimental level. Selection
of individual or combinations of technologies to attempt DCM reduction
must be based on a case-by-case technical evaluation, and an assessment
of the economics involved.
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Dichloromethane March 31, 1987
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IX. REFERENCES
ACGIH. 1984. American Conference of Governmental Industrial Hygienists.
Documentation of the threshold limit values. 4th ed. 1980-1984 supplement.
pp. 275-276.
Aviado, D.M., S. Zakhari and T. Watanabe. 1977. Methylene chloride. In;
Non-fluorinated propellants and solvents for aerosols, L. Goldberg, ed.,
CRC Press, Inc., Cleveland, Ohio, pp. 19-45.
Bonventre, J., 0. Brennan, D. Jason, A. Henderson and M.L. Bastos. 1977.
Two deaths following accidental inhalation of dichloromethane and 1,1,1-
trichloroethane. J. Anal. Toxicol. 1:158-160.
Bornmann, G., and A. Loeser. 1967. Zur Frage einer chronisch-toxischen
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