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EPA 749-F-94-018a
CHEMICAL SUMMARY FOR METHYLENE CHLORIDE (DICHLOROMETHANE)
prepared by
OFFICE OF POLLUTION PREVENTION AND TOXICS
U.S. ENVIRONMENTAL PROTECTION AGENCY
August 1994
This summary Is based on Information retrieved from a systematic
search limited to secondary sources (see Appendix A). These sources
Include online databases, unpublished EPA Information, government
publications, review documents, and standard reference materials. No
attempt has been made to verify Information In these databases and
secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical Identity and physical/chemical properties of methylene
chloride are summarized In Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL
PROPERTIES OF METHYLENE CHLORIDE
Characteristic/Property
Data
Reference
CAS No.
Common Synonyms
Molecular Formula
Chemical Structure
Physical State
Molecular Weight
Melting Point
Boiling Point
Water Solubility
Density
Vapor Density (air
KOC
Log KOW
Vapor Pressure
= 1)
75-09-2
MC, dlchloromethane,
DCM, methylene bichloride,
methylene dlchloride
CH2C12
Cl
H - C - H
Cl
colorless liquid
84.94
-950C
39.750C at 760 mm Hg
1.32 x 104 mg/L at 200C
d20/4, 1.3255 g/mL
2.93
25
1.25
400 mm Hg at 24.10C
Budavarl et al
Budavarl et al
Budavarl et al
Budavarl et al
1989
1989
1989
1989
U.S. Air Force 1989
Budavarl et al. 1989
NIOSH 1986
ATSDR 1993
U.S. Air Force 1989
HSDB 1994
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Reactivity
Flash Point
Henry's Law Constant
Fish B1 concentration Factor
Odor Threshold
Conversion Factors
Nonflammable
2.57 x 10-3 atm m3/mol
2 (estimated)
214 ppm (In air)
1 ppm = 3.48 mg/m3;
1 mg/m3 = 0.288 ppm
U.S. Air Force 1989
U.S. Air Force 1989
U.S. EPA 1984
U.S. Air Force 1989
U.S. Air Force 1989
II. PRODUCTION, USE. AND TRENDS
A. Production
There are 3 manufacturers with 5 plants producing methylene chloride
In the United States: Dow Chemical, Occidental Chemical, and Vulcan
Chemicals. Annual capacity Is about 527 million pounds. In 1992,
approximately 350 million pounds of methylene chloride were produced
In the US. Since 1988, production of methylene chloride has fallen
at an average rate of 8.6 percent per year. Imports do not account
for much of U.S. methylene chloride consumption. In 1992, it was
estimated that 13 million pounds of methylene chloride were Imported
Into the US (Mannsville, 1993).
B. Use
Methylene chloride Is used In many applications. Its largest use Is
as the principal active Ingredient In organic-based paint strippers,
accounting for approximately 125 million pounds (35 percent of all
U.S. methylene chloride production In 1992). It Is used In both
consumer and Industrial paint removers, where It Is commonly present
In 60-80$ concentration. The second largest application (88 million
pounds) of methylene chloride Is in chemical processing. Table 2
presents the estimated 1992 end use pattern for methylene chloride.
C. Trends
Methylene chloride demand is expected to continue to decline by over
30$ by 1995 because of environmental and occupational concerns. Users
of methylene chloride have been under strong pressure to limit usage,
restrict emissions, maximize recycling, and reduce worker exposure
(Mannsville, 1993).
III. ENVIRONMENTAL FATE
A. Environmental Release
Of the total methylene chloride released to the environment, about
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Q6% is released to the atmosphere, 12% to land, and 2% to water
(ATSDR 1993). The highly volatile methylene chloride [vapor
pressure, 400 mm Hg at 24.10C (HSDB 1994)] Is released Into the
atmosphere from Industrial and consumer uses (ATSDR 1993). The
principal releases of methylene chloride to land are from the
disposal of methylene chloride products and containers In landfills
(ATSDR 1993). The principal releases to surface water and
potentially to groundwater are via Industrial effluents and
underground Injections, respectively (ATSDR 1993). In 1992,
releases of methylene chloride to environmental media, as reported
to the Toxic Chemical Release Inventory by certain types of U.S.
Industries, totaled about 74 million pounds to the atmosphere,
221 thousand pounds to surface water, 1 million pounds to under-
ground Injection, and 79 thousand pounds to land (TRI88 1990).
In addition, an estimated 243 million pounds of methylene chloride
were released to the atmosphere In 1988 from consumer products and
other sources, such as hazardous waste sites (ATSDR 1993).
Maximum levels of methylene chloride measured In environmental
media are 6.7 m1crograms/m3 (urban U.S. air), 39 m1crograms/m3
(air around hazardous waste sites), 743 aeg/L (New Jersey surface
water), 3600 mlcrograms/L (groundwater), and 13 micrograms/L
(sediment) (ATSDR 1993).
TABLE 2. ESTIMATED 1992 U.S. END USE PATTERN OF METHYLENE CHLORIDE
Use of Methylene Chloride 1992 US Consumption Percentage of US
[typical Standard Industrial (In millions of pounds) Methylene Chloride
[Classification (SIC) code] Use
(see end note 1)
Paint Removers
(production, SIC 2851;
use, various Industries) 125 35
Chemical Processing
(SIC 2821, 2823) 88 25
Foam Blowing
(various Industries) 49 14
Metal Cleaning & Finishing
(various industries) 28 8
Aerosols
(various Industries) 25 7
Adheslves and Coatings
(production, SIC 2851; use,
various Industries) 14 4
Electronics
(SIC 3672) 11 3
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Miscellaneous (see end note 2)
TOTAL
14
354
4
100
Source: Mannsville 1993
B. Transport
Methylene chloride tends to volatilize to the atmosphere from the
water and soil (ATSDR 1993; U.S. Air Force 1989). With an organic
carbon partitioning coefficient (KOC) of 25, methylene chloride is
expected to be highly mobile in soils, and leaching of the chemical
into groundwater is likely (ATSDR 1993). In deep, saturated soils
that contain no soil air and negligible soil organic carbon, as much
as 96% of environmental methylene chloride may be present in the
soil-water phase and transported with flowing groundwater (U.S. Air
Force 1989).
C. Transformation/Persistence
1. Air - The main degradation pathway for methylene chloride in the
atmosphere is reaction with photochemically produced hydroxyl
radicals (ATSDR 1993). The estimated lifetime for the chemical
in the atmosphere is 130 days. The small amount of methylene
chloride reaching the stratosphere (about 1%) would probably
undergo direct photolysis (ATSDR 1993).
2. Soil - In surface soil, volatilization to air is an important
fate process for methylene chloride (U.S. Air Force 1989;
ATSDR 1993). The biodegradation of methylene chloride has been
demonstrated in the laboratory and may occur in subsurface
soils (ATSDR 1993); however, biodegradation (except, perhaps
in landfills with active microbial populations) is probably not
a significant degradation pathway in the soil-groundwater system
(U.S. Air Force 1989). It has been suggested that microorganisms
used in biological sewage treatment can degrade the chemical
with suitable acclimatization (U.S. Air Force 1989).
3. Water - An important fate process for methylene chloride is
volatilization; in the laboratory, the volatility half-life was
estimated to be 21 minutes (ATSDR 1993). Methylene chloride has
been shown to hydrolyze slowly (experimental half-life in
water at 250C, -18 months) (ATSDR 1993).
4. Biota - The estimated fish bioconcentration factor (BCF) for
methylene chloride of 2 (U.S. EPA 1984) suggests that
biomagnification of the chemical in the aquatic and terrestrial
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food chains Is not likely.
IV. HEALTH EFFECTS
A. Pharmacoklnetics
1. Absorption - Studies In humans and animals have demonstrated
that methylene chloride Is readily absorbed via the lungs and
the gastrointestinal tract (U.S. EPA 1984; ATSDR 1993). Limited
animal data Indicate some skin absorption (ATSDR 1993).
2. Distribution - In studies with animals exposed to radlolabeled
methylene chloride, radioactivity was detected In the liver,
kidneys, lungs, brain, muscle, adipose tissues, and adrenals
about 1 hour after Inhalation exposure; and In the liver,
kidneys, lungs, brain, epldidymal fat and testes 48 hours after
single oral doses (ATSDR 1993).
3. Metabolism - The major metabolites of Inhaled and Ingested
methylene chloride are carbon dioxide probably via glutathione
transferase and carbon monoxide probably via mixed function
oxldases (ATSDR 1993). Elevated levels of carboxyhemoglobln
(COHb) have been observed In exposed human subjects and
animals (ATSDR 1993).
4. Excretion - Methylene chloride and Its metabolites are excreted
primarily In expired air. Small amounts are also eliminated In
the urine and feces. Following Inhalation exposure, exhaled air
contained 58 to 19% of a dose of radlolabeled methylene chloride.
B. Acute Effects
Humans acutely exposed to methylene chloride experience adverse
effects of the central nervous system and the heart. Animal studies
Indicate acute exposures to high levels of methylene chloride can
adversely affect the liver and the kidney.
1. Humans - Direct contact with methylene chloride causes corneal
burns and erythema and burning of the skin (ATSDR 1993). The
lowest lethal Ingested dose of methylene chloride reported for
humans Is 357 mg/kg (RTECS 1993). Occupational overexposure to
methylene chloride (concentrations were not reported) has resulted
In worker deaths (ATSDR 1993). Exposure to 500 ppm methylene
chloride for 8 hours produced euphoria In humans (RTECS 1994).
The concentration of 500 ppm Is roughly equivalent to a total of
248 mg/kg over an 8-hour period (see end note 3). Methylene
chloride Is metabolized to carbon monoxide In humans, resulting
In the formation of carboxyhemoglobln (COHb) and subsequent oxygen
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deprivation (U.S. Air Force 1989). The formation of COHb Is
concentration-dependent and saturable. Human subjects exposed to
100 ppm for 7.5 hours developed COHb levels of >5$, subjects
exposed
to 500 ppm for 1 hour had COHb levels of 1-4$, and subjects
exposed
to 1000 ppm for 2 hours had COHb levels of 10$ (saturation) (ATSDR
1993). A concentration of 2.5$ COHb Is associated with Impairment
of time-Interval discrimination, whereas levels of 65$ COHb are
associated with other psychomotor effects and cardiovascular
changes (Amdur et al. 1991). The cardiovascular changes Include
Increased cardiac output, A-V oxygen difference, and coronary
blood flow In patients without coronary disease. Patients with
coronary heart disease and elevated COHb levels may experience
decreased coronary sinus blood P02 and impaired oxidative
metabolism of the myocardium, producing an added burden on the
patient (Amdur et al. 1991).
2. Animals - LD50/LC50 values for rats, reported In the literature
searched, are as follows for the various routes of exposure:
2100 mg/kg (oral) (ATSDR 1993), 25,287 ppm for 30 mln
(respiratory),
and 916 mg/kg [intraperltoneal (i.p.) injection] (RTECS 1994).
LD50/LC50 values for mice are slightly lower. Signs and symptoms
of the acute toxicity of methylene chloride Include (a) liver
damage In mice exposed orally to 133 to 665 mg/kg (IARC 1986),
In rats exposed by inhalation to 552 ppm, 6 hours/day for 5 days,
and In guinea pigs exposed by Inhalation to 5200 ppm for 6 hours;
and (b) kidney damage In dogs and mice Injected i.p. with
"near-lethal doses" and in rats injected i.p. with 1330 mg/kg
(IARC 1986). In animals, as in hurnans, methylene chloride is
metabolized to carbon monoxide, resulting in the formation of
carboxyhemoglobin (COHb) and subsequent oxygen deprivation (U.S.
Air Force 1989). The formation of COHb is concentration-dependent
and saturable. COHb levels reached 13$ in rats exposed to
500 ppm methylene chloride for 6 hours, but no further increase
in COHb occurred after 6 hours' exposure to higher concentrations
up to 1500 ppm (U.S. Air Force 1989).
C. Subchronic/Chronic Effects
Humans chronically exposed to methylene chloride experience adverse
effects of the central nervous system and the heart. Animal studies
indicate chronic exposures to high levels of methylene chloride
adversely affects the liver and the kidney. EPA has derived an
oral RfD (reference dose) (see end note 4) of 0.06 mg/kg/day for
methylene chloride.
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1. Humans - Available Information suggests that the central nervous
system and the cardiovascular system are affected by subchromc
or chronic exposure to methylene chloride. Two workers were
exposed intermittently for 13 to 20 years; one reported leg and
arm pain, dizziness, fatigue, loss of appetite, and poor night
vision; and the other reported drowsiness, headache, and tingling
of hands and feet (U.S. Air Force 1989). Deaths occurring
following chronic Inhalation exposure have been attributed to
cardiac Injury and heart failure (U.S. EPA 1984). No other
target organs were Identified.
2. Animals - The major target organs for the subchronlc/chronlc
toxlclty of methylene chloride are the liver and kidney.
Methylene chloride, administered to F344 male and female rats
In their drinking water for 2 years. Induced hlstologlcal
alterations of the liver at doses 650 mg/kg/day; the no-observed-
adverse effect level (NOAEL) for the study was 5 mg/kg/day
(U.S. EPA 1994). Based on these data, the U.S. EPA (1994)
calculated an oral RfD of 0.06 mg/kg/day for methylene chloride.
In Inhalation studies with methylene chloride, cytoplasmlc
vacuollzatlon and fatty Infiltration of the liver and tubular
degeneration and regenerative changes of the kidneys were observed
In rats exposed continuously to 25 or 100 ppm of the chemical
for 100 days (ATSDR 1993). Rats exposed to 500 ppm methylene
chloride, 6 hours/day, 5 days/week for 2 years developed
multinucleated hepatocytes (the liver was not affected at .200
ppm), and Increased hemoslderosls, cytomegaly, and cytoplasmlc
vacuollzatlon of the liver after exposure to 1000 ppm, 6 hours/
day, 5 days/week for 2 years (ATSDR 1993). IARC (1986) reported
that Sprague-Dawley rats exposed to 6500 ppm methylene chloride
for 2 years exhibited pathological changes In the liver and kidney
more frequently than did control animals.
D. Cardnogenlcity
There Is Inadequate evidence of carclnogenlclty of methylene chloride
In humans. There Is sufficient evidence of Its carclnogenlclty In
animals. EPA has classified methylene chloride as a probable human
carcinogen.
1. Humans - Epidemiology studies revealed no Increased risk for cancer
among workers who were exposed to methylene chloride for up to 22
years (IARC 1986; HSDB 1994). Exposure levels of the chemical
ranged (for several studies) from 26 to 475 ppm.
2. Animals - Various Inhalation bloassays conducted In rodents,
exposed to methylene chloride concentrations up to 3500 or 4000
ppm 6 hours/day, 5 days/week for approximately 2 years, showed
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statistically significant Increases In the following types of
tumors: benign mammary tumors and sarcomas In rats; alveolar/
bronchiolar adenomas, alveolar/bronchiolar carcinomas, and
hepatocellular adenomas In mice; and lymphosarcomas In hamsters
(IARC 1986). Hepatocellular carcinoma and neoplastlc nodules were
observed In female rats and male mice In the 2-year drinking water
study described In the Suchronlc/Chronlc Section. Based on
Inadequate human data and sufficient evidence for cardnogenlcity
In animals, the U.S. EPA classification for methylene chloride
Is B2, probable human carcinogen (U.S. EPA 1994). The oral slope
factor (see end note 5) for methylene chloride Is 0.0075 per
(mg/kg)/day (U.S. EPA 1994). The Inhalation unit risk (see end
note 6) for methylene chloride Is 4.7 x 10-7 per (m1crograms/m3)
(U.S. EPA 1994). IARC (1987) classifies the chemical as 2B,
possibly carcinogenic to humans, and the National Toxicology
Program (NTP 1994) concluded that methylene chloride shows some
evidence of carclnogenlclty In male rats and clear evidence of
carclnogenlclty In female rats and In male and female mice.
E. Genotoxlclty
In the EPA GENETOX Program, methylene chloride was positive for cell
transformation In rat embryo cells, mitotic recombination or gene
conversion In Saccharomyces cerevlslae, reverse gene mutation In
S. cerevlslae, and hlstldlne reversion In the Ames assay; the
chemical was negative In the mlcronucleus test and the sex-linked
recessive lethality assay In D. melanogaster (GENETOX 1994).
USEPA (1994) reports methylene chloride as mutagenlc In Salmonella
and negative In gene mutation and chromosome aberration tests
In mammalian cells.
F. Developmental/Reproductive Toxlclty
There Is no Information on the developmental toxlclty or reproductive
system effects of methylene chloride In humans. Information on these
effects In animals Is limited; no conclusions on the can be made on
the developmental toxlclty or reproductive system effects of methylene
chloride from this Information.
1. Humans - No Information was found in the secondary sources
searched to indicate that methylene chloride is a developmental/
reproductive toxicant in humans.
2. Animals - No compound-related effects were observed in Charles
River CD male and female rats or their offspring, given oral
doses of up to 225 mg methylene chloride/kg/day in a two-
generation reproductive toxicity study (HSDB 1994). In inhalation
studies, the offspring of pregnant mice and rats exposed to
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1250 ppm (7 hours/day) or 4500 ppm (exposure details not given)
of methylene chloride during gestation exhibited treatment-related
reductions In fetal weight, skeletal anomalies and/or alterations
In spontaneous locomotor activities (IARC 1986; ATSDR 1993).
There was no Indication of fetal malformations In these studies,
even at maternally toxic concentrations. No compound-related
effects were observed In Fischer 344 male and female rats or their
offspring exposed to methylene chloride concentrations of up to
1500 ppm (exposure details not given) In a two-generation
reproductive toxicity study (HSDB 1994).
G. Neurotoxlclty
Human and animal studies Indicate that methylene chloride adversely
affects the central nervous system.
1. Humans - Inhalation of 300 to 800 ppm for 4 hours has caused
Impairment of visual, auditory, and psychomotor functions; the
effects were reversible at lower concentrations (ATSDR 1993).
Inhalation of 515 ppm for 1 to 2 hours and 1000 ppm for 1 to
2 hours resulted In decreased visual evoked response; exposure to
<500 ppm for 1-2 hours had no effect on visual evoked response
(ATSDR 1993). In an additional case study of longer-term
exposure, a chemist who breathed 660 to 3600 ppm (mean, 900 ppm
In the breathing zone) for 5 years experienced forgetful ness,
Insomnia, and auditory and visual hallucinations (U.S. EPA 1984).
2. Animals - Various Inhalation studies with methylene chloride In
cats have demonstrated various effects ranging from slight
narcosis (6000 ppm for 3 to 4 hours) to deep CNS depression
(10,000 ppm for 293 mln) (HSDB 1994). Gerbils exposed to 210 ppm
for 7 to 16 weeks (exposure details not given) exhibited decreased
hippocampal DNA concentration and alterations in brain amino acids
(ATSDR 1993).
V. ENVIRONMENTAL EFFECTS
A. Toxicity to Aquatic Organisms
Methylene chloride has low acute toxicity to aquatic organisms;
lethal concentrations are generally greater than 100 mg/L. Ninety-
six-hour LC50 values for fish are 193 mg/L for Pimephales promelas
(fathead minnow; flowthrough conditions) and 220 mg/L for Lepomis
macrochirus (bluegill; static conditions) (AQUIRE 1993). The 14-day
LC50 for Poecilia reticulata (guppy) is 294 mg/L (AQUIRE 1993).
In Scenedesmus quadricauda (green algae), the toxicity threshold
for cell multiplication inhibition test (TT) and for mortality
(static conditions) is 1,450 mg/L (AQUIRE 1993).
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B. Toxicity to Terrestrial Organisms
No information was found In the secondary sources searched for
terrestrial organism toxicity. The oral LD50 in the rat, 2100 mg/kg
(ATSDR 1993), suggests that the chemical would not be acutely toxic
to terrestrial animals unless present in very high concentrations.
Studies in laboratory animals also suggest that methylene chloride
would not cause developmental/reproductive effects in terrestrial
species at expected environmental levels (see section IV.F).
C. Abiotic Effects
The reaction of methylene chloride with ozone in the upper atmosphere
is not expected to be significant. Most methylene chloride in the
lower atmosphere is removed by reaction with hydroxyl radicals
(ATSDR 1993).
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
Voluntary reduction of methylene chloride environmental releases has
occurred since 1991, as a result of a joint industry/EPA pollution
prevention initiative known as the 33/50 program. The 1990 Clean
Air Act Amendments list methylene chloride as a hazardous air
pollutants.
Workplace exposure to methylene chloride is primarily regulated by the
Occupational Safety and Health Administration (OSHA); it has proposed
a reduction of the permissible exposure limit (PEL) to 25 ppm. Other
federal agencies and groups (listed in Table 4) have developed
recommendations to assist in controlling workplace exposure.
Regarding consumer exposure, the Consumer Product Safety Commision
(CPSC) requires that all consumer products containing more than
1% methylene chloride carry a label warning that the contents may
cause cancer. Also, the Food and Drug Administration (FDA) in 1989
banned the use of the chemical in hairspray and other cosmetic
products.
Federal agencies and other groups that can provide additional
information on methylene chloride are listed in Tables 3 and 4.
TABLE 3. EPA OFFICES AND CONTACT NUMBERS
FOR INFORMATION ON METHYLENE CHLORIDE
EPA OFFICE LAW PHONE NUMBER
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Pollution Prevention
& Toxics
Air
Solid Waste &
Emergency Response
Water
Toxic Substances Control Act
(Sec. 8A/8D/8E)
Emergency Planning and Community
Right-to-Know Act (EPCRA)
Regulations (Sec. 313)
Toxics Release Inventory data
Clean Air Act
Comprehensive Environmental
Response, Compensation, and
Liability Act (Superfund)/
Resource Conservation and Recovery
Act / EPCRA (Sec. 304/311/312)
Clean Water Act
Safe Drinking Water Act (Drinking
Water Standard: 0.005 mg/L)
(202) 554-1404
(800) 535-0202
(202) 260-1531
(919) 541-0888
(800) 535-0202
(202) 260-7588
(800) 426-4791
Agency for Toxic Substances and Disease Registry
American Conference of Governmental Industrial
Hygienists
Consumer Product Safety Commission
Food and Drug Administration
National Institute for Occupational Safety
and Health (NIOSH)
Occupational Safety and Health Administration
(404) 639-6000
(513) 742-2020
(301) 504-0994
(301) 443-3170
(800) 356-4674
(Check your local phone book under U.S. Department of Labor)
TABLE 4. OTHER FEDERAL OFFICE/OTHER GROUP CONTACT
NUMBERS FOR INFORMATION ON METHYLENE CHLORIDE
Other Agency/Department/Group
Contact Number
Agency of Toxic Substances & Disease Registry (404) 639-6000
American Conference of Governmental Industrial Hygienists
(Recommended Exposure Limit (see end note 7): 50 ppm) (513) 742-2020
Consumer Product Safety Commission
Food & Drug Administration
National Institute for Environmental Health Sciences
(EnvlroHealth Clearinghouse)
National Institute for Occupational Safety & Health
(301) 504-0994
(301) 443-3170
(800) 643-4794
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(Recommended Exposure Limit (see end note 8):
Lowest Feasible Concentration)
Occupational Safety & Health Administration
(Proposed Permissible Exposure Limit
(see end note 9): 25 ppm)
(800) 356-4674
Check local phone
book for phone
number under
Department of
Labor
VII. END NOTES
1. The Standard Industrial Classification (SIC) code Is the statistical
classification standard for all Federal economic statistics. The code
provides a convenient way to reference economic data on Industries of
Interest to the researcher. SIC codes presented here are not intended to
be an exhaustive listing; rather, the codes listed should provide an
indication of where a chemical may be most likely to be found in commerce.
2.Miscellaneous uses of methylene chloride include use as an extraction
solvent (including the extraction of heat-sensitive substances such as
caffeine, cocoa, and edible fats); and processing of cellulose triacetate
fiber.
3. Calculated using the factor, 3.48 (U.S. Air Force 1989). to convert
500 ppm to 1740 mg/m3 which is multiplied by 0.143 (the standard
occupational 8-hour breathing rate, 10 m3, divided by the assumed adult
body weight, 70 kg) to obtain the dose in mg/kg (U.S. EPA 1988).
4. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable
risk of deleterious effects during the time period of concern.
5. The slope factor is a plausible upper-bound estimate of the probability
of a response per unit intake of a chemical over a lifetime. The slope
factor is used in risk assessments to estimate an upper-bound lifetime
probability of an individual developing cancer as a result of exposure
to a particular level of a potential carcinogen.
6. The unit risk is a quantitative estimate in terms of risk per unit
intake of a chemical. The unit risk for methylene chloride incorporates
information on pharmacokinetics and metabolism.
7. The ACGIH exposure limit is a time-weighted average (TWA) concentration
for an 8-hour workday during a 40-hour workweek.
8. Exposure should be reduced to the lowest feasible limit; use of only the
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most reliable and protective respirators Is recommended.
9. The OSHA exposure limit Is a time-weighted average (TWA) concentration
that must not be exceeded during any 8-hour workshlft during a 40-hour
workweek.
VIII. CITED REFERENCES
Amdur MO, Doull J, Klaassen CD, Eds.. 1991. Casarett and Doull's
Toxicology, 4th ed. Pergamon Press, New York, p. 868.
AQUIRE. 1993. Aquatic Information Retrieval online data base. Chemical
Information Systems, Inc., a subsidiary of Feln-Marquart Assoc. Retrieved
June, 1993.
ATSDR. 1993. Agency for Toxic Substances and Disease Registry.
Toxicologlcal Profile for Methylene Chloride. Update. ATSDR, Chamblee,
GA, 111 pp.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck
Index, llth ed. Merck & Co., Inc., Rahway, NJ, p. 954.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. Retrieved
September, 1993.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information
Retrieval System, National Library of Medicine. Retrieved June, 1994.
IARC. 1986. International Agency for Research on Cancer. Dichloromethane.
In: IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to
Man, Vol. 41. IARC, Lyon, pp. 43-85.
IARC. 1987. International Agency for Research on Cancer. IARC Monographs
on the Evaluation of Carcinogenic Risk of Chemicals to Man. Overall
evaluations of carclnogenlclty. An updating of Vols. 1 to 42. IARC, Lyon,
p. 62.
Mannsvllle. 1993. Chemical Products Synopsis, Methylene Chloride.
Mannsvllle Chemical Products Corporation, January, 1993.
NIOSH. 1986. National Institute for Occupational Safety and Health.
Current Intelligence Bulletin 46, April 18, 1986. NIOSH, U.S. Department
of Health and Human Services, Cincinnati, OH, 18 pp.
NTP. 1994. National Toxicology Program. Management Status Report.
Produced from NTP Chemtrack system. April 8, 1994. National Toxicology
Program, Research Triangle Park, NC.
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http://www.epa.gov/opptintr/chemfact/s-dcm.txt
RTECS. 1994. Registry of Toxic Effects of Chemical Substances. MEDLARS
Online Information Retrieval System, National Library of Medicine.
Retrieved July, 1994.
TRI92. 1994. Toxic Chemical Release Inventory. National Library of
Medicine, National Toxicology Program, Bethesda. MD. (Cited in ATSDR 1993)
U.S. Air Force. 1989. Methylene Chloride: In: The Installation
Restoration Toxicology Guide, Vol. 1. Wright-Patterson Air Force Base,
OH, pp. 1-1 through 1-37.
U.S. EPA. 1984. U.S. Environmental Protection Agency. Health Effects
Assessment for Methylene Chloride. Office of Research and Development,
U.S. EPA, Washington, D.C., 48 pp. EPA/540/1-86-028.
U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for
Evaluating Potential Carcinogenicity in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group,
Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C.,
pp. 21, 22. OHEA-C-073.
U.S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk
Information System (IRIS) Online. Coversheet for Dichloromethane.
Office of Health and Environmental Assessment, U.S. EPA. Cincinnati, OH,
Retrieved 7/94.
APPENDIX A. SOURCES SEARCHED FOR FACT SHEET PREPARATION
AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical
Information Systems, Inc., a subsidiary of Fein-Marquart Assoc.
ATSDR. 1989-1994.' Agency for Toxic Substances and Disease Registry.
Toxicological Profiles. Chamblee. GA: ATSDR.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck
Index, llth ed. Rahway, N.J.: Merck & Co., Inc.
Clayton GD, Clayton FE. 1981-1982. Patty's Industrial Hygiene and
Toxicology, 3rd ed., Vol. 2C. New York: John Wiley & Sons.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information
Retrieval System. National Library of Medicine.
IARC. 1979-1994. International Agency for Research on Cancer. IARC
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man.
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Lyon: IARC.
NIOSH (National Institute for Occupational Safety and Health). 1992.
NIOSH Recommendations for Occupational Safety and Health. Compendium of
Policy Documents and Statements. Cincinnati, OH: NIOSH.
NTP. 1994. National Toxicology Program. Toxicology and Carclnogenesls
Studies. Tech Rep Ser.
NTP. 1994. National Toxicology Program. Management Status Report.
Produced from NTP Chemtrack system. April 8, 1994. National Toxicology
Program, Research Triangle Park, NC.
OSHA. 1994. Occupational Safety and Health Administration. Table Z-2.
Limits for Air Contaminants.
RTECS. 1994. Registry of Toxic Effects of Chemical Substances. MEDLARS
Online Information Retrieval System, National Library of Medicine.
U.S. Air Force. 1989. The Installation Restoration Toxicology Guide,
Vols.
1-5. Wright-Patterson Air Force Base, OH.
U.S. EPA (U.S. Environmental Protection Agency). 1991. Table 302.4 List
of Hazardous Substances and Reportable Quantities 40 CFR, part 302.4:3-271.
U.S. EPA. Most current. Drinking Water Regulations and Health Advisories.
Office of Drinking Water, U.S. Environmental Protection Agency, Washington,
D.C.
U.S. EPA. Most Current. Health Effects Assessment Summary Tables.
Cincinnati, OH: Environmental Criteria and Assessment Office, U:S.EPA.
U.S. EPA reviews such as Health and Environmental Effects Documents,
Health and Envlornmental Effect Profiles, and Health and Environmental
Assessments.
U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online.
Cincinnati, OH: Office of Health and Environmental Assessment.
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