Methylene chloride (EHC 164, 1996, 2nd edition)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 164

Methylene Chloride
Second Edition)

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization

World Health Organization
Geneva, 1996

The International Programme on Chemical Safety (IPCS) is a joint
venture of the United Nations Environment Programme, the International
Labour Organisation, and the World Health Organization. The main
objective of the IPCS is to carry out and disseminate evaluations of
the effects of chemicals on human health and the quality of the
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carried out by the IPCS include the development of know-how for coping
with chemical accidents, coordination of laboratory testing and
epidemiological studies, and promotion of research on the mechanisms
of the biological action of chemicals.

WHO Library Cataloguing in Publication Data

Methylene chloride.

(Environmental health criteria; 164)

1.Methylene chloride - adverse effects 2. Solvents
I.Series

ISBN 92 4 157164 0 (NLM Classification: QV 633)
ISSN 0250-863X

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR METHYLENE CHLORIDE

1. SUMMARY

1.1. Identity, physical and chemical properties, and analytical
methods
1.2. Sources of human and environmental exposure
1.3. Environmental transport, distribution and transformation
1.4. Environmental levels and human exposure
1.5. Kinetics and metabolism
1.6. Effects on organisms in the environment
1.7. Effects on laboratory mammals and in vitro test systems
1.7.1. Single exposure
1.7.2. Short- and long-term exposure
1.7.3. Skin and eye irritation
1.7.4. Developmental and reproductive toxicity
1.7.5. Mutagenicity and related end-points
1.7.6. Chronic toxicity and carcinogenicity
1.8. Effects on humans

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS

2.1. Identity
2.2. Physical and chemical properties
2.3. Conversion factors
2.4. Analytical methods

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. Production
3.2.2. Uses
3.2.3. Consumer applications
3.2.4. Sources in the environment

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION

Appraisal
4.1. Transport and distribution between media
4.1.1. Water/air
4.1.2. Soil/air
4.1.3. Water/soil
4.1.4. Multicompartment distribution
4.2. Abiotic degradation
4.2.1. Atmosphere
4.2.2. Water
4.2.3. Soil

4.3. Biotransformation
4.3.1. Aerobic
4.3.2. Anaerobic
4.3.3. Bioaccumulation
4.4. Interaction with other physical, chemical or biological
factors

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

Appraisal
5.1. Environmental levels
5.1.1. Atmosphere
5.1.1.1 Ambient air
5.1.1.2 Precipitation
5.1.2. Water
5.1.3. Aquatic organisms
5.1.4. Soil and sediment
5.2. Human exposure
5.2.1. General population
5.2.1.1 Indoor air
5.2.1.2 Drinking-water
5.2.1.3 Foodstuffs
5.2.1.4 Consumer exposure
5.2.2. Occupational exposure
5.2.2.1 Production
5.2.2.2 Paint stripping and related activities
5.2.2.3 Aerosol production and use
5.2.2.4 Use as a process solvent
5.2.2.5 Cleaning and degreasing
5.2.3. Occupational exposure limits
5.3. Human monitoring data
5.3.1. Body burden
5.3.2. Occupational exposure studies
5.3.3. Biological exposure indices

6. KINETICS AND METABOLISM

6.1. Absorption
6.1.1. Inhalation exposure
6.1.1.1 Human studies
6.1.1.2 Animal studies
6.1.2. Oral exposure
6.1.3. Dermal exposure
6.2. Distribution
6.2.1. Inhalation exposure
6.2.1.1 Human studies
6.2.1.2 Animal studies
6.2.2. Oral exposure
6.2.3. Dermal exposure

6.3. Metabolism
6.3.1. In vitro studies
6.3.2. In vivo studies
6.4. Elimination and excretion
6.4.1. Inhalation exposure
6.4.1.1 Human studies
6.4.1.2 Animal studies
6.4.2. Oral exposure
6.4.3. Dermal exposure

7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

7.1. Microorganisms
7.1.1. Bacteria
7.1.1.1 Aerobic bacteria
7.1.1.2 Anaerobic bacteria
7.1.2. Protozoa
7.1.3. Algae
7.2. Aquatic organisms
7.2.1. Plants
7.2.2. Invertebrates
7.2.2.1 Insects
7.2.2.2 Crustaceans
7.2.2.3 Molluscs
7.2.3. Fish
7.2.3.1 Acute toxicity
7.2.3.2 Chronic toxicity and reproduction
7.2.4. Amphibians
7.3. Terrestrial organisms
7.4. Population and ecosystem effects
7.4.1. Soil microorganisms
7.4.2. Sediment microorganisms
7.4.3. Microcosms and mesocosms

8. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS

8.1. Single exposure
8.1.1. Acute toxicity data
8.1.2. Oral administration
8.1.3. Inhalation administration
8.1.3.1 Rat
8.1.3.2 Mouse
8.1.3.3 Other animals
8.1.4. Dermal administration
8.1.5. Intraperitoneal administration
8.1.6. Intravenous administration
8.1.7. Subcutaneous administration
8.1.8. Appraisal
8.2. Short-term exposure
8.2.1. Oral administration
8.2.2. Subcutaneous administration

8.2.3. Inhalation administration
8.2.3.1 Rat
8.2.3.2 Other animals
8.3. Long-term exposure
8.3.1. Rat
8.3.1.1 Inhalation exposure
8.3.1.2 Oral exposure
8.3.2. Mouse
8.3.2.1 Inhalation exposure
8.3.2.2 Oral exposure
8.3.3. Other animals
8.3.4. Appraisal
8.4. Skin and eye irritation; skin sensitization
8.4.1. Skin irritation
8.4.2. Eye irritation
8.4.3. Sensitization
8.4.4. Appraisal
8.5. Developmental and reproductive toxicity
8.5.1. Developmental toxicity
8.5.2. Reproductive toxicity
8.5.3. Appraisal
8.6. Mutagenicity and related end-points
8.6.1. In vitro
8.6.1.1 Bacteria
8.6.1.2 Fungi and yeasts
8.6.1.3 Mutation in mammalian cells
8.6.1.4 Chromosomal effects
8.6.1.5 DNA damage
8.6.1.6 DNA binding in vitro
8.6.1.7 Cell transformation
8.6.2. In vivo
8.6.2.1 Chromosome damage
8.6.2.2 Drosophila
8.6.2.3 DNA damage
8.6.2.4 DNA binding
8.6.2.5 Dominant lethal assay
8.6.2.6 Replicative DNA synthesis
8.6.3. Appraisal
8.7. Chronic toxicity and carcinogenicity
8.7.1. Inhalation exposure
8.7.1.1 Rat
8.7.1.2 Mouse
8.7.1.3 Hamster
8.7.2. Oral administration
8.7.2.1 Rat
8.7.2.2 Mouse
8.7.3. Appraisal
8.8. Mechanistic studies
8.8.1. In vitro metabolic studies
8.8.2. In vivo metabolic studies

8.8.3. Pulmonary effects
8.8.4. Studies on oncogene activation
8.8.5. The use of mechanistic studies in extrapolation
8.8.6. Mammary tumour promotion
8.8.7. Appraisal
8.9. Interspecies and dose extrapolations by kinetic modelling

9. EFFECTS ON HUMANS

9.1. General population exposure
9.1.1. Environmental exposure
9.1.2. Oral exposure
9.2. Occupational exposure
9.2.1. Short-term exposure
9.2.1.1 Case studies
9.2.1.2 Skin and eye effects
9.2.1.3 Laboratory studies
9.2.2. Long-term exposure
9.2.2.1 Case studies
9.3. Appraisal of human effects

10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT

10.1. Evaluation of human health risks
10.2. Evaluation of effects on the environment

REFERENCES

RESUME

RESUMEN

NOTE TO READERS OF THE CRITERIA MONOGRAPHS

Every effort has been made to present information in the criteria
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A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Case postale
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This publication was made possible by grant number 5 U01 ES02617-
15 from the National Institute of Environmental Health Sciences,
National Institutes of Health, USA, and by financial support from the
European Commission.

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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR METHYLENE CHLORIDE

Members

Dr L.A. Albert, Consultores Ambientales Associados, Xalapa, Veracruz,
Mexico

Mr D. Farrar, ICI Chemicals and Polymers, Runcorn, Cheshire, United
Kingdom (Rapporteur)

Dr R. Fransson-Steen, Institute of Environmental Medicine, Karolinska
Institute, Stockholm, Sweden

Dr S. Henry, US Food and Drug Administration, Washington, DC, USA

Mr P. Howe, Institute of Terrestrial Ecology, Monks Wood Experimental
Station, Huntingdon, United Kingdom

Dr P. Standring, Health and Safety Executive, Bootle, Merseyside,
United Kingdom

Dr L. Stayner, Division of Standards Development and Technology
Transfer, National Institute for Occupational Safety and Health,
Cincinnati, Ohio, USA

Dr T. G. Vermeire, Toxicology Advisory Centre, National Institute of
Public Health and Environmental Hygiene, Bilthoven, The
Netherlands (Chairman)

Dr Ruqiu Ye, National Environmental Protection Agency, Beijing, China

Observers

Dr C. De Rooij, Solvay & Cie S.A., Brussels, Belgium

Dr T. Green, ICI Chemicals & Polymers Ltd., Runcorn, Cheshire, United
Kingdom

Secretariat

Dr M. Gilbert, International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland (Secretary)

Dr P. Demers, Unit of Analytical Epidemiology, International Agency
for Research on Cancer, Lyon, France

ENVIRONMENTAL HEALTH CRITERIA FOR METHYLENE CHLORIDE

A WHO Task Group on Environmental Health Criteria for Methylene
Chloride met at the Institute of Terrestrial Ecology, Monks Wood,
United Kingdom from 16 to 20 August 1993. Dr S. Dobson welcomed the
participants on behalf of the host institution, and Dr M. Gilbert
opened the meeting on behalf of the three cooperating organizations of
the IPCS (ILO/UNEP/WHO). The Task Group reviewed and revised the draft
monograph and made an evaluation of the risks for human health and the
environment from exposure to methylene chloride.

The first draft of this monograph was prepared by Mr D. Farrar,
ICI Chemicals and Polymers, Runcorn, United Kingdom.

Dr M. Gilbert, IPCS, was responsible for the overall scientific
content of this monograph. After his death in July 1994, this
responsibility was transferred to Dr P.G. Jenkins, IPCS, who also
dealt with the technical editing.

The efforts of all who helped in the preparation and finalization
of the monograph are gratefully acknowledged.

ABBREVIATIONS

ALT alanine aminotransferase

AST aspartate aminotransferase

BEI Biological Exposure Index

CO-Hb carboxyhaemoglobin

GST glutathione transferase

LEV local exhaust ventilation

MATC maximum acceptable toxicant concentration

NADPH reduced nicotinamide adenine dinucleotide phosphate

NIOSH National Institute for Occupational Safety and Health (USA)

SCE sister-chromatid exchange

SGOT serum glutamic-oxaloacetic transaminase

SGPT serum glutamic-pyruvic transaminase

TT toxicity threshold

TWA time-weighted average

UDS unscheduled DNA synthesis

1. SUMMARY

1.1 Identity, physical and chemical properties, and analytical methods

Methylene chloride (dichloromethane) is a clear, highly volatile,
non-flammable liquid with a penetrating ether-like odour. The pure dry
compound is very stable. Methylene chloride hydrolyses slowly in the
presence of moisture, producing small quantities of hydrogen chloride.
Commercial methylene chloride normally contains small quantities of
stabilizers to prevent decomposition.

Analytical methods are available for the determination of
methylene chloride in biological media and environmental samples. All
methods involve gas chromatography in combination with a suitable
detector. In this way, very low detection limits have been reached
(e.g., in food: 7 ng/sample; water: 0.01 µg/litre; air: 1.76 µg/m³
(0.5 ppb); blood: 0.022 mg/litre).

1.2 Sources of human and environmental exposure

World production of methylene chloride is estimated to be
570 000 tonnes/year. Most applications are based on its solvent
capacity for grease, plastics and paint binding agents, in combination
with its volatility and stability. The worldwide usage pattern
comprises aerosols (20-25%), paint remover (25%), process solvent in
the chemical and pharmaceutical industry (35-40%), miscellaneous uses
(e.g., polyurethane foam manufacturing) and metal cleaning (10-15%).
The usage of methylene chloride is tending to decrease, at least in
western Europe.

More than 99% of the atmospheric releases of methylene chloride
result from its use as an end-product by various industries and the
use of paint removers and aerosol products at home.

1.3 Environmental transport, distribution and transformation

Abiotic degradation in water is slow compared to evaporation.
Methylene chloride has been shown to disappear rapidly from soil and
ground water.

The aerobic and anaerobic degradation of methylene chloride has
been established by a variety of different test systems. Complete
biodegradation, especially by acclimated bacterial cultures under

aerobic conditions, is rapid (e.g., 49-66% mineralization in 50 h with
acclimated municipal sludge). In bioreactors, up to 10% degradation
per hour is achievable. There is no evidence of significant
bioaccumulation or biomagnification.

1.4 Environmental levels and human exposure

Methylene chloride has been detected in the ambient air of rural
and remote areas at concentrations of 0.07-0.29 µg/m³. In suburban
areas, the average concentration is < 2 µg/m³ and in urban areas
< 15 µg/m³. In the vicinity of hazardous waste sites up to
43 µg/m³ has been found. Precipitation may also contain methylene
chloride.

Methylene chloride enters the aquatic environment through waste
water discharge from various industries, and methylene chloride has
been found in surface water, ground water and sediment.

Exposure of members of the general public to methylene chloride
will occur from its use in consumer products such as paint removers,
which can result in relatively high levels being found in indoor air.
Occupational exposure during production arises primarily during
filling and packaging (manufacturing is in closed systems). Because of
its use in paint strippers, occupational exposure to methylene
chloride occurs during formulation of paint-remover, original
equipment manufacture, and in commercial furniture refinishing.
Methylene chloride is widely used as a process solvent in the
manufacture of a variety of products, in particular in the industries
mentioned in section 1.2.

Biological monitoring of methylene chloride exposure can be based
on measurement of the solvent itself in exhaled air or blood. However,
as production of carbon monoxide with exposure for more than 3-4 h/day
appears to be the limiting factor in regard to health risk, biological
monitoring based upon either analysis of carbon monoxide in exhaled
air or of carboxyhaemaglobin (CO-Hb) in blood is to be preferred.
However, this can only be used for non-smoking subjects. Sampling
should be done at about 0-2 h post-exposure, or after 16 h, i.e. on
the following morning.

Post-exposure CO-Hb levels 2 h after exposure ceases are not
expected to exceed 2-3%, and at 16 h 1%, in the case of an 8-h
exposure to less than 350 mg methylene chloride/m³ in non-smokers.

1.5 Kinetics and metabolism

Methylene chloride is rapidly absorbed though the alveoli of the
lungs into the systemic circulation. It is also absorbed from the
gastrointestinal tract, and dermal exposure results in absorption but
at a slower rate than via the other routes of exposure.

Methylene chloride is quite rapidly excreted, mostly via the lungs
in the exhaled air. It can cross the blood-brain barrier and be
transferred across the placenta, and small amounts can be excreted in
urine or in milk.

At high concentrations, most of the absorbed methylene chloride is
exhaled unchanged. The remainder is metabolized to carbon monoxide,
carbon dioxide and inorganic chloride. Metabolism occurs by either or
both of two pathways, whose relative contribution to the total
metabolism is markedly dependent on the dose and on the animal species
concerned. One pathway involves oxidative metabolism mediated by
cytochrome P-450 and leads to both carbon monoxide and carbon dioxide.
This pathway appears to operate similarly in all rodents studied and
in man. Whilst this is the predominant metabolic route at lower doses,
saturation occurs at a relatively low dose (around 1800 mg/m³).
Increasing the dose above the saturation level does not lead to extra
metabolism by this route.

The other pathway involves a glutathione transferase (GST), and
leads via formaldehyde and formate to carbon dioxide. This route seems
only to become important at doses above the saturation level of the
"preferred" oxidative pathway. In some species (e.g., the mouse) it
becomes the major metabolic pathway at sufficiently high doses. In
contrast, in other species (e.g., hamster, man) it seems to be used
very little at any dose.

Species difference in GST metabolism correlates well with the
observed species difference in carcinogenicity. The extent of
metabolism by this pathway in relevant species has been used as the
basis for a kinetic model to describe the metabolic behaviour of
methylene chloride in various species.

1.6 Effects on organisms in the environment

Algae and aerobic bacteria show no inhibition of growth below
500 mg/litre. Bacteria have been identified that are able to grow in
the presence of methylene chloride at much higher concentrations
including a saturated solution in water (section 4.2.4.1). Anaerobic
bacteria are more sensitive; growth inhibition has been observed at
1 mg/litre in anaerobic biological sludge.

In soil a concentration of 10 mg/kg strongly decreased the ATP
content of the biomass including fungi and aerobic bacteria, and
induced transient inhibition of enzyme activity. The no-observed-
effect level was 0.1 mg/kg. In earthworms methylene chloride is
moderately toxic (100-1000 µg/cm²) in the filter-paper contact
toxicity test. In sediment no toxic effects were observed even at very
high levels.

In higher plants no effects were found after exposure for 14 days
to 100 mg/m³.

Adult fish seem to be relatively insensitive to methylene chloride
even after prolonged exposure (14-day LC₅₀ > 200 mg per litre). The
effect of methylene chloride on Daphnia is difficult to assess given
the large variation in the outcome of the studies performed. The
lowest reported EC₅₀ was 12.5 mg/litre.

In the aquatic environment, fish and amphibian embryos have been
shown to be the most sensitive with effects on hatching from
5.5 mg/litre.

1.7 Effects on laboratory mammals and in vitro test systems

1.7.1 Single exposures

The acute toxicity of methylene chloride by inhalation and oral
administration is low. The inhalation 6-h LC₅₀ values for all
species are between 40 200 and 55 870 mg/m³. Oral LD₅₀ values of
1410-3000 mg/kg were recorded. Acute effects after methylene chloride
administration by various routes of exposure are primarily associated
with the central nervous system (CNS) and the liver, and these
occurred at high doses. CNS disturbances were found at concentrations
of 14 100 mg/m³ or more, with slight changes in EEG at 1770 mg/m³.
Slight histological changes in the liver were found at 17 700 mg/m³
or more. Occasionally other organs were affected such as the kidney or
respiratory system. In mice, effects on the lungs were restricted to
the Clara cells after exposure to 7100 mg/m³. Cardiac sensitization
to adrenaline-induced arrhythmia has been reported. Cardiovascular
effects have been seen but the effects were inconsistent.

1.7.2 Short- and long-term exposure

Prolonged exposure to high concentrations of methylene chloride
(> 17 700 mg/m³) caused reversible CNS effects, slight eye
irritation and mortality in several laboratory species. Body weight
reduction was observed in rats at 3500 mg/m³ and in mice from
17 700 mg/m³. Slight effects on the liver were noted in dogs
continuously exposed to 3500 mg/m³ for up to 100 days. After
intermittent exposure, effects on the liver were observed in rats at
3500 mg/m³ and in mice at 14 100 mg/m³.

Other target organs are the lungs and the kidneys.

No evidence of irreversible neurological damage was seen in rats
exposed by inhalation to concentrations up to 7100 mg/m³ for 13
weeks.

Oral administration of methylene chloride to rats caused effects
on the liver from about 200 mg/kg per day.

1.7.3 Skin and eye irritation

Methylene chloride is moderately irritant to the skin and eyes of
experimental animals.

1.7.4 Developmental and reproductive toxicity

Methylene chloride is not teratogenic in rats or mice at
concentrations up to 16 250 mg/m³. No evidence of an effect on the
incidence of skeletal malformations or other developmental effects
were observed in three animal studies. Small effects on either fetal
or maternal body weight were reported at 4400 mg/m³, and on
postnatal weight gain of male rats at 0.04% in the diet. A two-
generation reproductive toxicity study in rats exposed to methylene
chloride by inhalation at concentrations up to 5300 mg/m³, 6 h/day,
5 days/week for 17 weeks did not show evidence of an adverse effect on
any reproductive parameter, neonatal survival or neonatal growth in
either the F₀ or F₁ generation.

1.7.5 Mutagenicity and related end-points

Under appropriate exposure conditions, methylene chloride is
mutagenic in prokaryotic microorganisms with or without metabolic
activation (Salmonella or Escherichia coil). In eukaryotic systems
it gives either negative or, in one case, weakly positive results.
In vitro gene mutation assays and tests for unscheduled DNA
synthesis (UDS) in mammalian cells were uniformly negative. In vitro
assays for chromosomal aberrations using different cell types gave
positive results, whereas negative or equivocal results were obtained
in tests for sister chromatid exchange (SCE) induction.

The majority of the in vivo studies reported provided no
evidence of mutagenicity of methylene chloride (e.g., chromosome
aberration assay, micronucleus test or UDS assay). Marginal increase
in frequencies of SCEs and micronuclei in mice has been reported
following inhalation exposure to high concentrations of methylene
chloride.

There was no evidence of binding of methylene chloride to DNA or
DNA damage in rats or mice given high doses of methylene chloride.
These studies are potentially the most sensitive in vivo studies,
the best of which are capable of detecting one alkylation in 10⁶
nucleotides.

Within the limitations of the short-term tests currently
available, there is no conclusive evidence that methylene chloride in
genotoxic in vivo.

1.7.6 Chronic toxicity and carcinogenicity

Methylene chloride is carcinogenic in the mouse, causing both lung
and liver tumours, following exposure to high concentrations (7100 and
14 100 mg/m³) of methylene chloride. The incidence of both lung and
liver tumours was increased in mice exposed to 7100 mg/m³ for 26
weeks and maintained for a further 78 weeks. There was no substantial
evidence of associated toxicity or hyperplasia in the target organs.

Syrian hamsters exposed to methylene chloride by inhalation at
concentrations up to 12 400 mg/m³ for 2 years showed no evidence of
a carcinogenic effect related to exposure to methylene chloride.

Rats exposed to methylene chloride via various routes have shown
increased incidences of tumours at certain sites. An excess of tumours
in the region of the salivary gland was reported in female rats
exposed to either 5300 or 12 400 mg/m³ for 2 years. This excess was
only evident when the tumours, which were all of mesenchymal origin,
were grouped together for statistical analysis. As the tumours arose
from a variety of different cells, the statistical approach adopted
was inappropriate. Furthermore, it was reported that the rats in the
study had been infected with a common viral disease (sialoda-
cryoadenitis) early in the study, an infection that affects primarily
the salivary gland. It is likely that these tumours were not causally
related to exposure to methylene chloride but that the exposure had
exacerbated the response of the infection in the region of the
salivary gland. The response was not seen in a second study in which
rats were exposed to either 3500, 7100 or 14 100 mg/m³ for their
lifetime. A further inhalation study on rats exposed to methylene
chloride at concentrations up to 1770 mg/m³ for their lifetime
showed no evidence of carcinogenicity. Rats exposed to methylene
chloride via their drinking-water or by gavage similarly showed no
substantive evidence of carcinogenicity.

An increased incidence of benign mammary tumours in rats exposed
to methylene chloride has been reported in three studies, two
following exposure by inhalation and the third by gavage. There are no
reports of increases in mammary tumour incidence in hamsters or in
mice receiving methylene chloride at comparable dose levels. The
dependence of mammary tumours upon pituitary hormones in both male and
female rats has been established unequivocally. In the rat, prolactin
acts as both an initiator and promoter of mammary carcinogenesis.
There is good evidence that increased prolactin levels increase the
incidence of mammary tumours (e.g., the grafting of multiple pituitary
glands into Sprague-Dawley rats increases the incidence of mammary
tumours and there is a positive correlation between elevated blood
prolactin levels and mammary tumours in aged R-Amsterdam female rats).

Treatments that induce hyperprolactinaemia in female rats that have
received carcinogens produce a dramatic increase in tumour incidence.
These treatments include adrenalectomy, pituitary homografts and high
dietary fat.

The mechanism by which methylene chloride induces mammary adenomas
in the rat is important for human hazard assessment. Female Sprague-
Dawley rats receiving methylene chloride have a high blood level of
prolactin. In common with the response to other agents which act via
hyperprolactinaemia, the methylene chloride-induced response is of
benign neoplasms only. There is no evidence for the binding of
methylene chloride to the DNA of other tissues and hence it seems
unlikely that it will bind to mammary tissue when the primary site of
metabolism is the liver. It seems most likely, therefore, that the
increased incidence of mammary adenomas is the result of an indirect
mechanism operating via hyperprolactinaemia.

In humans, there is conflicting evidence on whether or not mammary
tumours are as responsive to prolactin as is the case in the rat. The
rat has elevated levels of prolactin when fed ad libitum in
comparison to a restricted dietary regimen and this may explain why
the mammary tumour incidence is so responsive to a variety of
environmental and other effects. In the rat, however, prolactin is
luteotrophic. An increase in the circulating levels of prolactin will
lead to an increase in progesterone and exogenous oestrogen levels. It
is the presence of all three factors that causes tubular-alveolar
growth of the mammary glands, which ultimately leads to tumour
development. Prolactin is not luteotrophic in primates. It is
unlikely, therefore, that this mechanism of tumour development is of
relevance to man.

The mechanism of production of mammary tumours in the rat
involving hyperprolactinaemia will occur only at doses of methylene
chloride which affect prolactin levels. There is no direct information
on prolactin levels in rats receiving low doses of methylene chloride,
but no increase in mammary adenomas has been observed following the
administration of low doses in either inhalation or drinking-water
studies (i.e. below 250 mg/kg body weight).

1.8 Effects on humans

Methylene chloride irritates the skin and eyes especially when
evaporation is prevented. In these circumstances, prolonged contact
may cause chemical burns. A case of serious pulmonary oedema has been
reported after excessive inhalation. Fatalities due to accidental
inhalation and skin contamination have been reported. The main toxic
effects of methylene chloride are reversible CNS depression and CO-Hb
formation. Liver and renal dysfunctions and effects on haematological
parameters have also been reported following exposure to methylene
chloride.

Neurophysiological and neurobehavioural disturbances have been
observed in human volunteers exposed to methylene chloride at
concentrations of 694 mg/m³ for 1.5-3.0 h. No evidence of
neurological effects was seen in men with exposure for several years
to methylene chloride at concentrations ranging from 260 to
347 mg/m³. Similarly, a group of retired airplane strippers with a
long history of exposure to methylene chloride (22 years) at high but
unspecified levels performed a battery of neurophysiological and
psychological tests within the "normal" range, when compared with a
control group who had a history of either no or only low exposure to
methylene chloride.

An increased rate of spontaneous abortion in employees in Finnish
pharmaceutical industries has been attributed to exposure to methylene
chloride. A causal relationship was not established because of
insufficiencies in the design of the study.

Several mortality studies in relevant cohorts show an inconsistent
pattern in the causes of death. Excesses in mortality from specific
diseases (e.g., pancreatic cancer, ischaemic heart disease) were not
consistently increased, but confined to single studies. These effects
cannot be attributed to exposure to methylene chloride.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS

2.1 Identity

Formula: CH₂CI₂

CI
'
Structure: CI - C - H
'
H

Relative molecular mass: 84.93

Common name: Methylene chloride

Synonyms: DCM; dichloromethane; methane
dichloride; methylene bichloride;
methylene dichloride; methylenum
chloratum

Tradenames: Aerothene MM; Freon 30; Narkotil;
Solaestin; Solmethine

CAS name (9 CI): Methane, dichloro-

CAS registry number: 75-09-2

EC registry number: 602-004-00-3

EINECS registry number: 200-838-9

RTECS registry number: PA 8050000

Purity of technical 99.9% (analytical grade)
product:

Impurities of technical Mostly C₁- and C₂-chlorinated
product hydrocarbons (up to 200 mg/kg)
(ECETOC, 1984)

Stabilizer: Typically 0.005-0.2% (w/w)
methanol, ethanol, amylene
(2-methyl-but-2-ene), cyclohexane
or tertiary butylamine (ECSA, 1989)

2.2 Physical and chemical properties

Methylene chloride is a clear, colourless, highly volatile, non-
flammable liquid with a penetrating ether-like odour. Pure dry
methylene chloride is a very stable compound and is non-corrosive. In
the presence of water, it undergoes very slow hydrolysis to produce
small quantities of hydrogen chloride, which can lead to corrosion,
e.g., to mild steel. This reaction is accelerated by elevated
temperatures and the presence of alkalis or metals. In the vapour
phase under abnormal conditions (elevated temperatures, high UV light
exposure, flame, sparks, red hot surfaces), methylene chloride may be
decomposed to give small amounts of hydrogen chloride, carbon monoxide
and phosgene (ECSA, 1989). Other physical and chemical properties are
given in Table 1.

Commercial methylene chloride is normally stabilized (section 2.1)
to prevent decomposition. Applications in aggressive conditions, such
as special metal cleaning operations may require more sophisticated
stabilizer technology. Poorly stabilized methylene chloride can react
violently with aluminium or other light metals.

2.3 Conversion factors

Conversion factor for methylene chloride concentrations in air,
calculated at 20°C and 1.013 hPa are:

1 mg/m³ = 0.28 ppm
1 ppm = 3.53 mg/m³

and for carbon monoxide:

1 mg/m³ = 0.86 ppm
1 ppm = 1.16 mg/m³

2.4 Analytical methods

Details of sampling and methods of analysis used in biological
media and environmental samples are given in Tables 2 and 3.

Table 1. Physical and chemical properties

Parameter, units Value Reference

Boiling temperature (°C at 1.013 hPa) 40 Weast et al. (1988)

Melting temperature (°C at 1.013 hPa) -95.1 Weast et al. (1988)

Relative density of liquid D (₂₀) 1.3266 Weast et al. (1988)
(water at 4°C = 1 kg/m³) ⁴

Vapour pressure (hPa at 20°C) 470 ECSA (1989)

Saturation concentration in air 1.7 Calculated
(kg/m³ at 20°C)

Vapour density at 20°C (air = 1) 2.93 IPCS (1984)

Threshold odour concentration 743 Leonardos et al.
(mg/m³) (1969)
(odour: ether-like) 700-1060 DFG (1983)
880 Amoore & Hautala
(1983)
540-2160 Ruth (1986)

Solubility in water (g/kg at 20°C) 20 Verschueren (1983)
13.0 Horvath (1982)

Solubility in alcohol, ether, acetone Weast et al. (1988)
and benzene

Partition coefficients, at 20°C 1.25 IPCS (1984)
log P_ow (octanol/water) 1.3 Hansch & Leo
(1979)
log K_oc 0.89
calculated from K_ow
(Karickhoff, 1981)
Henry's Law constant, Pa.m³/mol at 380
20°C Smith (1989)

Flash point, closed cup (°C) None ECSA (1989)

Explosion limits in air^a (%) 13-22 ECSA (1989)

Auto-flammability, ignition temp. (°C) 605 ECSA (1989)

^a This is with a high energy source; these conditions are unlikely
to arise in normal operations.

Table 2. Analytical methods for determining methylene chloride in biological monitoring (ATSDR, 1991)

Sample matrix Preparation method Analytical Sample detection Percentage Reference
method^a limit recovery

Blood Heat sample, collect GC/FID 0.022 mg/litre 49.8±1.33 Di Vincenzo et al.
headspace vapour (1971)

Urine Heat sample, collect GC/FID No data 59±2.75 Di Vincenzo et al.
headspace vapour (1971)

Breath Heat sample, inject into gas GC/FID 0.706 ± 0.353 No data Di Vincenzo et al.
sample loop mg/m³ (1971)
(0.2 ± 0.1 ppm)

Adipose tissue Hydrolyse with acid, heat GC/FID 1.6 mg/kg^b No data Engström & Bjurström
sample, collect headspace (1977)
vapour

Human milk Purge with helium, trap on GC/MS No data No data Pellizzari et al. (1982)
sorbent trap, desorb thermally

^a FID = flame ionisation detector; GC = gas chromatography; MS = mass spectrometry
^b Lowest reported concentration

Table 3. Analytical methods for determining methylene chloride in environmental samples (ATSDR, 1991)

Sample Preparation method Analytical Sample detection Percentage Reference
matrix method^a limit recovery

Air Adsorb on charcoal, desorb with GC/FID 88.25µg/m³ 90-110^c APHA (1977)
carbon disulfide (25 ppb)^b

Air Adsorb on charcoal, desorb with GC/FID 0.01 mg 95.3 NIOSH (1987)
carbon disulfide

Air Adsorb on charcoal, desorb with GC/ECD approx. 1.76 µg/m³ No data Woodrow et al.
benzyl alcohol (approx. 0.5 ppb) (1988)

Water Purge with inert gas, trap on sorbent GC/HSD No data 85 US EPA (1989c)
trap, desorb thermally

Water Purge with inert gas, trap on sorbent GC/ELCD 0.01 µg/litre 97-100 US EPA (1989)
trap, desorb thermally

Water Purge with inert gas, trap on sorbent GC/MS 1.0 µg/litre 99 US EPA (1989b)
trap, desorb thermally

Water Purge with inert gas, trap on sorbent HRGC/MS 0.03-0.09 µg/litre 95-97 US EPA (1989a)
trap, desorb thermally

Water Purge with inert gas, trap on sorbent HRGC/ELCD 0.01-0.05 µg/litre 97±28 APHA (1989a)
trap, desorb thermally

Table 3 (Cont'd)

Sample matrix Preparation method Analytical Sample detection Percentage Reference
method^a limit recovery

Water Purge with inert gas, trap on sorbent HRGC/MS 0.02-0.2 µg/litre 95±5 APHA (1989b)
trap, desorb thermally

Water Purge with helium, trap on sorbent GC/MS No data 99-105 Michael et al.
trap, desorb thermally (1988)

Waste Purge with inert gas, trap on sorbent GC/HSD 0.25 µg/litre 97.9±2.6 US EPA (1982a)
water trap, desorb thermally

Waste Purge with inert gas, trap on sorbent GC/MS 2.8 µg/litre 89±28 US EPA (1982b)
water trap, desorb thermally

Soil/solid Purge with inert gas, trap on sorbent GC/MS 5 µg/kg D-221 US EPA (1986a)
waste trap, desorb thermally

Soil/solid Purge with inert gas, trap on sorbent GC/HSD No data 25-162 US EPA (1986b)
waste trap, desorb thermally; or inject
directly into GC

Food Equilibrate in heated sodium sulfate GC/ELCD 0.05 ppm No data Page & Charbonneau
solution, collect headspace vapour (1984)

Food Isolate solvent by closed system GC/ELCD 7 ng 94 Page & Charbonneau
vacuum distillation with toluene as (1977)
carrier solvent

Table 3 (Cont'd)

Sample matrix Preparation method Analytical Sample detection Percentage Reference
method^a limit recovery

Food Isolate solvent by closed system GC/ECD 7 ng 100 Page & Charbonneau
vacuum distillation with toluene as (1977)
carrier solvent

Food Purge with nitrogen, trap on sorbent GC/ELCD 1.2 mg/kg^d 84-96 Heikes (1987)
trap, elute with hexane

Food Extract with acetone-water, back GC/ELCD 4 µg/kg 66 Daft (1987)
extract with iso-octane

^a ECD = electron capture detector; ELCD = electrolytic conductivity detector; FID = flame ionisation detector; GC = gas chromatography;
HRGC = high resolution gas chromatography; HSD = halogen-specific detector; MS = mass spectrometry
^b Lowest value for various compounds reported during collaborative testing of this method
^c Estimated accuracy of the method when the personal sampling pump is calibrated with a charcoal tube in the line
^d Lowest reported concentration

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1 Natural occurrence

Methylene chloride is not known to occur naturally in the
environment.

3.2 Anthropogenic sources

3.2.1 Production

Methylene chloride is produced almost exclusively by the Stauffer
process. Methyl chloride is first produced by the reaction of methanol
with hydrogen chloride and is then reacted with chlorine. Chloroform
and, to a lesser extent, carbon tetrachloride are also produced.
Historically the direct route to methylene chloride by chlorination of
methane was also used; this also produced the other three
chloromethanes in varying proportions depending on the conditions used
(CEC, 1986; ICI, personal communication to the IPCS).

World production of methylene chloride in 1980 was estimated to be
570 000 tonnes (Edwards et al., 1982); a similar figure is considered
to apply currently (ECSA, 1992). USA production was 229 000 tonnes in
1988, the demand being 207 000 tonnes. The total amount produced in
western Europe ranged from 331 500 tonnes in 1986 to 254 200 tonnes in
1991 (ECSA, 1992).

3.2.2 Uses

The usage of methylene chloride in Western Europe shows a decrease
from 200 000 tonnes/year in 1975-1985 (CEFIC, 1986) to
175 000 tonnes/year in 1989 and to 150 000 tonnes/year in 1992 (CEFIC,
1993).

Most of the applications of methylene chloride are based on its
considerable solvent capacity, especially for grease, plastics and
various paint-binding agents. Other important properties are its
volatility and stability; it is also non-flammable. Among its uses are
(CEFIC, 1983):

- a component of paint and varnish strippers, and adhesive
formulations

- a solvent in aerosol formulations

- an extractant in food and pharmaceutical industries

- a process solvent in cellulose ester production and fibre and
film forming

- a process solvent in polycarbonate production

- a blowing agent in flexible polyurethane foams

- the extraction of fats and paraffins

- plastics processing, and metal and textile treatment

- a vapour degreasing solvent in metal-working industries

An estimated breakdown of usage worldwide before 1985 is given in
Table 4.

Table 4. Estimated usage patterns (BUA, 1986)

USA (1985) Western Europe (1984)

Aerosols 25 10

Paint strippers 23 50

Degreasing agent 8 13

Film, electronics industries 7 15

Blowing agent 5

Others 35 12

It should be noted that these data apply to the situation
approximately 10 years ago and may have changed since. Reliable
reports on present trends are not available.

3.2.3 Consumer applications

The main use in consumer products is in paint strippers, where
methylene chloride is the main constituent (70-75%). The second
important use is in hairspray aerosols, where it acts as a solvent and
vapour pressure modifier. In the European Community (EC) it may be
used in such products at concentrations of up to 35% w/w (European
Council, 1982). The US Food and Drug Administration has banned the use
of methylene chloride in cosmetic products. It is also used in aerosol
paints. Other types of methylene chloride-containing products are
household cleaning products and lubricating, degreasing and automotive
products, some of which may be in aerosol form. Chemical products
containing methylene chloride were banned from sale or transfer to

consumers for their private use in 1993 according to the Swedish Code
of Statutes. Furthermore, it may not be used for working purposes
after 1st January 1996 (National Chemical Inspectorate, Sweden,
personal communication to the IPCS).

3.2.4 Sources in the environment

Most of the methylene chloride released to the environment results
from its use as an end-product by various industries, and the use of
paint removers and aerosol products in the home. Methylene chloride is
mainly released to the environment in air and, to a lesser extent, in
water and soil.

Methylene chloride is released to the atmosphere during its
production, storage and transport, but more than 99% of the
atmospheric releases result from industrial and consumer uses (US EPA,
1985). It has been estimated that 85% of the total amount of methylene
chloride produced in the USA is lost to the environment, of which 86%
is released to the atmosphere (US EPA, 1985). Data reported to the US
EPA for the 1988 Toxic Chemical Release Inventory indicate that
approximately 170 000 tonnes of the USA production volume for 1988
(230 000 tonnes) was lost to the atmosphere; of this, 60 000 tonnes
resulted from industrial methylene chloride emissions and 110 000
tonnes from the use of consumer products and from other sources such
as hazardous waste sites.

Estimates of annual global emissions of 500 000 tonnes have been
reported for methylene chloride (WMO, 1991). The short atmospheric
lifetime of methylene chloride (see section 4.2.1) implies that
emissions quantities given on a seasonal as well as on a regional
basis are more relevant for comparison with atmospheric measurements.
The total emission into the air in western Europe was estimated to be
173 000 tonnes for 1989 and 180 000 tonnes in 1991.

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION

Appraisal

Due to its high volatility, most of the methylene chloride
released to the environment will partition to the atmosphere, where
it will degrade by reaction with photochemically produced hydroxyl
radicals with a lifetime of 6 months. Given an intra-hemispheric
mixing time of approximately 1 month, transport can occur to regions
far removed from the emission source. The atmospheric lifetime is
fairly short relative to the inter-hemispheric transport time of 1 to
1.5 years, resulting in higher concentrations of methylene chloride
in the northern hemisphere, where most of the emissions occur at
present.

Methylene chloride is expected to have no significant impact on
stratospheric ozone depletion. It will not contribute significantly
to photochemical smog formation.

Hydrolysis and photolytically induced degradation in water are
slow compared to evaporation. Methylene chloride has been shown to
disappear rapidly from soil and ground water due to bio-
transformation.

The aerobic and anaerobic degradation of methylene chloride has
been proven by a variety of different test systems. Complete
biodegradation by acclimated bacterial cultures under aerobic
conditions is rapid. There is no evidence that significant
bioaccumulation or biomagnification of methylene chloride along the
food chain will occur.

4.1 Transport and distribution between media

4.1.1 Water/air

Methylene chloride enters the hydrosphere either directly, via
aqueous effluents, or indirectly from the atmosphere by dissolution in
sea water and in rain water. Due to its high volatility (Henry's Law
constant 380 Pa.m³/mol at 20°C) and low liquid-film transfer
coefficient (Kp = 0.005 m/h), methylene chloride is rapidly
transferred from the hydrosphere to the atmosphere.

Under laboratory conditions, the estimated half-life for
volatilization of methylene chloride from water at 25°C was 18-25 min
(when present at 1 mg/litre and stirred at 200 rpm). Removal of 90% of
the methylene chloride required 60-80 min. When stirring was minimal
(15 seconds every 5 min), the time required for 50% reduction in the
concentration was about 90 min. The presence of 3% sodium chloride (as
in sea water) decreased the evaporation rate by 10% (Dilling et al.,
1975; Dilling, 1977).

Various factors have been shown to affect the rate of
volatilization. For example, the half-life for volatilization of
methylene chloride from a depth of 1 m has been shown to be 3 h
(Lyman, 1982). The application of wind across the surface of the water
caused an increase of 17% in volatilization over a period of 20 min
compared to the presence of still conditions (Dilling et al., 1975). A
decrease in the water temperature decreased the rate of
volatilization. For example, over a period of 30 min, a 28% decrease
in rate was seen at 1-2°C compared to that at 25°C (Dilling et al.,
1975).

When measured under field conditions in experimental ponds, half-
lives for methylene chloride of 26-28 h have been reported (Merlin et
al., 1992). Its half-life for evaporation from the river Rhine has
been estimated to be 33-38 clays (Zoeteman et al., 1980). Further
estimates of the half-life for its evaporation are between 3 and 48 h
depending on wind and mixing conditions (Halbartschlager et al.,
1984). In a further study, methylene chloride was not detected at a
point 4-8 km from the point of release into an estuarine bay (Helz &
Hsu, 1978) or at 25 km below its discharge point in a river basin (De
Walle & Chain, 1978).

Rain-out is considered to be a limited process for removal of
methylene chloride from the troposphere. If it is assumed that its
aqueous-phase concentration is in equilibrium with the background
concentration in the northern hemisphere of about 123-134 ng/m³
(35-38 ppt) (Cox et al., 1976; WMO, 1991), the total amount of
methylene chloride rained out in the northern hemisphere will be
700 tonnes/year (assuming a rain fall of 2.5x10¹⁴ tonnes/year
containing 9.9 ng/m³ (2.8 ppt) at 10°C). The same calculation
performed at 20°C (Henry's constant is 1.57 times higher) would lead
to a value of 445 tonnes methylene chloride rained out annually in the
northern hemisphere. For the southern hemisphere, rainout quantities
of 390 and 248 tonnes methylene chloride can be calculated. The half-
life for removal by wet deposition is 550 years (Cupitt, 1980).

In 1978, it was estimated that 2.5% of releases at ground level
may reach the stratosphere (Derwent & Eggleton, 1978).

4.1.2 Soil/air

Methylene chloride present in the soil is predicted to evaporate
from the near-surface layer into the atmosphere because of its high
vapour pressure (470 hPa at 20°C).

4.1.3 Water/soil

The adsorption coefficient sediment/water for methylene chloride
is 8-10 (log K_oc = 0.89-1.05). Methylene chloride has a low tendency
to adsorb to soil (adsorption coefficient 0.25 for a soil containing
1% organic carbon, Giger et al., 1983). Therefore there is a potential
for it to leach to ground water.

The amount of adsorption of methylene chloride to dry granular
bentonite clay added at a concentration of 375-750 mg/litre was found
to be 10-22% within 10-30 min. In the presence of 500 mg/litre peat
moss, about 40% of methylene chloride was absorbed after 10 min. Some
adsorption by dry-powdered dolomitic limestone was observed, but not
with silica sand (Dilling et al., 1975).

4.1.4 Multicompartment distribution

The regional distribution of methylene chloride over water, soil
and air compartments may be estimated by means of the fugacity model
developed by MacKay (Slooff & Ros, 1988). Application of this model
suggests that over 98% of the total emissions of the chemical will be
found in air, 1 to 2% in water and far less than 1% in soil and ground
water (BUA, 1986; Slooff & Ros, 1988).

4.2 Abiotic degradation

4.2.1 Atmosphere

The principal process by which methylene chloride is scavenged
from the atmosphere is the reaction with hydroxyl rate of methylene
chloride can be calculated from the rate constant for the initiating
breakdown reaction with HO. and the varying concentration of these
radicals in the troposphere. Determination of the rate constant for
the reaction of methylene chloride with hydroxyl radicals has been the
subject of various investigations. WMO (1991) recommends the following
value:

k_OH = 5.8 × 10^-12 exp(-1100/T) cm³ molecule^-1 s^-1

Other reactive species (e.g., ozone, oxygen atoms, chlorine atoms
and nitrate radicals) are not thought to contribute significantly to
the primary attack on methylene chloride (Table 5). As methylene
chloride does not absorb in the visible or near ultraviolet light
region (> 290 nm), direct homogeneous gas-phase photolysis in the
troposphere is of negligible importance.

Table 5. Primary tropospheric reactions of methylene chloride (other than with .OH)

Reaction k (at 25°C) Global average [X] Lifetime
with: (cm³ molecule^-1 s^-1) (molecule cm^-3) (years)

.Cl 4.1 × 10^-13 10³ 77
(IUPAC, 1992) (estimated) (estimated)

.NO₃ <3.2 × 10^-17 1.2 × 10⁸ > 8.3

.O(³p) 6.44 × 10^-16 2.5 × 10⁴ approx. 2000
(Barassin & Cambourieu, 1973)

.O(¹D) < 5 × 10^-10 0.5 > 120
(estimated)

Carbon dioxide and hydrogen chloride are the major breakdown
products and minor quantities of carbon monoxide and phosgene are
formed (Sanhueza & Heicklen, 1975; Rayez et al., 1987). The breakdown
reaction can be described as follows:

CH₂Cl₂ + HO. --> .CHCl₂ + H₂O
.CHCl₂ + O₂ --> .CHCl₂O₂
.CHCl₂O₂ + NO --> .CHCl₂O + NO₂
.CHCl₂O --> .Cl + HCOCl or
.CHCl₂O + O2 --> COCl₂ + HO₂ (minor reaction)

Formyl chloride may be taken up by cloud droplets, hydrolysed to
formic acid and wet deposited as such, or dry deposited to the ocean
or land surfaces and then hydrolysed. The overall lifetime for wet or
dry deposition is unlikely to exceed a few months and may be much
shorter. On the other hand, degradation in the troposphere by
photolysis or reaction with HO. may possibly be a more rapid process.
The reaction products would be carbon oxides (CO, CO₂) and HCl
(Libuda et al., 1990).

Phosgene is known to hydrolyse slowly in the gas phase, but
rapidly once dissolved in liquid water, to give CO₂ and HCl.

HCl is removed from the troposphere by wet deposition (dissolution
in atmospheric water droplets and subsequent rain-out) or dry
deposition (direct uptake by the oceans, land surfaces, vegetation
etc.) with an average lifetime of about 1 week. The amount of chloride

deposited in this manner is completely negligible compared to the
natural atmospheric chloride flux of around 10¹⁰ tonnes/year
primarily from sea-salt aerosols (WMO, 1991).

In the stratosphere methylene chloride will rapidly degrade by
photolysis and reaction with chlorine radicals (Derwent et al., 1976).

4.2.2 Water

Sunlight absorption of water results in the formation of HO. and
hydrated electrons (e^-_aq). The near surface concentrations of HO.
and e^-_aq are 4 × 10^-16 mol/litre and 5 × 10^-17 mol/litre,
respectively, which corresponds to theoretical half-lives for
methylene chloride of 400 and 33 days. In water systems these
reactions are very limited, the reaction with hydroxyl radicals being
dominant. The total rate constant for the sunlight-induced
transformation in surface water (with a depth of 2.5 m, a DOC content
of 4 mg/litre, a chlorophyll a content of 10 µg/litre and a
suspended matter content of 40 mg/litre) was estimated to be
2.8 × 10^-5 day^-1 (half-life 68 years). The HO. causes 90% of this
transformation (Slooff & Ros, 1988). No direct photolysis of methylene
chloride was found after visible and UV irridiation for 5 days at 22°C
(Chodola et al., 1989).

The half-life of a 1 mg/litre aqueous solution of methylene
chloride was found to be about 1.5 years when measured in sealed glass
tubes in the dark at 25°C and pH 7 (Dilling et al., 1975). No
significant hydrolysis was found at 50°C and pH 4 or 9.2 after 7 days
in the dark (Chodola et al., 1989). Under acidic and basic conditions
in the temperature range of 80-150°C, the hydrolysis of methylene
chloride results in the formation of formaldehyde and HCl (Fells &
Moelwyn-Hughes, 1958). Extrapolation of these data to 25°C gives a
long half-life of about 680-704 years (Dilling et al., 1975; Radding
et al., 1977). As the activation energy for hydrolysis of methylene
chloride varies with temperature, the extrapolation of rate data from
80-150°C may not be valid.

No reductive dehalogenation of methylene chloride in water was
observed in the presence of sodium sulfide and haematein, a common
iron porphyrin (Klecka & Gonsior, 1984).

4.2.3 Soil

As is the case in aqueous systems, hydrolysis is probably not an
important process in the removal of methylene chloride from soil (see
section 4.2.2).

In a lysimeter experiment, a 90% decrease over 2.5 m soil column
was obtained (Nellor et al., 1985).

In the report of a spillage, the concentrations of methylene
chloride were up to 802 mg/m³ and 26 900 mg/m³ near the point of
leakage. In both cases, methylene chloride could not be detected some
hundred metres away from the points of contamination even in the
direction of the groundwater flow (ECSA, 1989). In the neighbourhood
of polluted areas, an increase of bacterial activity has been found.
In well-documented cases of accidental spills to soils, methylene
chloride disappeared rapidly from ground water, probably due to
(bio)degradation (Baldanf, 1981; Leitfaden für die Beurteilung, 1983).

4.3 Biotransformation

4.3.1 Aerobic

Negligible oxygen consumption was found in a biochemical oxygen
demand (BOD) test (Klecka, 1982), and methylene chloride was
considered to be degradation resistant in a degradation test following
the Japanese MITI standards (Kawasaki, 1980). However, complete
degradation occurred during a static-culture flask test (Tabak et al.,
1981).

In laboratory studies methylene chloride was almost completely
transformed within days by bacteria enriched from a primary sewage
sludge, municipal activated sludge (with or without acclimitization)
and industrial waste water (Rittmann & McCarty, 1980; Davis et al.,
1981; Klecka, 1982; Stover & Kincannon, 1983; Halbartschlager et al.,
1984).

In field studies it has been shown that methylene chloride is
efficiently removed from water treatment works (Namkung & Rittmann,
1987).

Certain strictly aerobic, facultative methylotrophic bacteria,
like Pseudomonas DMI and Hyphomicrobium DM2, both readily isolated
from contaminated soil and waste-water treatment plants, are capable
of using methylene chloride as a sole carbon source for growth
(Brunner et al., 1980; Stucki et al., 1981).

Secondary substrate utilisation of methylene chloride was
demonstrated by Pseudomonas sp. strain LP. This strain showed a
preference towards degrading methylene chloride over acetate, whether
it was the primary or the secondary substrate (Lapat-Polasko et al.,
1984).

In Hyphomicrobium DM2, a glutathione (GSH)-dependent, strongly
inducible enzyme (a glutathione S-transferase) was found to be
responsible for the degradation of methylene chloride. It converted
methylene chloride to formaldehyde via the nucleophilic displacement
of chloride and the formation of S-chloromethyl glutathione and

S-hydroxymethyl glutathione. This enzymic dehalogenation in extracts
of methylene-chloride-grown cells amounted to 1160 mg/g protein per h
under alkaline (pH 8-9) conditions (Stucki et al., 1981; Leisinger,
1983).

Eight other bacteria (mainly Pseudomonads ), capable of growing
on methylene chloride as their sole carbon source, were isolated from
enriched cultures. Maximum degradation rates for methylene chloride
(up to 860 mg/litre per h) were found for an initial saturated
solution of 14.5 g/litre in a pH-controlled fermenter (flow rate
10 ml/h). Further increases in degradation rate were limited by the
high salt concentration resulting from the neutralization of the
degradation products. In a fluidized bed reactor with bacteria
immobilized on silica, a degradation rate of methylene chloride of up
to 1600 mg/litre per h was observed (Gälli and Leisinger, 1985;
Stucki, 1990).

Ubiquitous soil- and water-dwelling nitrifying bacteria such as
Nitrosomonas europaea, which depends for growth on the oxidation of
ammonia, were able to degrade 1 mg methylene chloride/litre completely
within 24 h in the presence of ammonia and by 67% in the absence of
ammonia (Vannelli et al., 1990).

The removal of methylene chloride from aerobic soil was
significantly increased following exposure to methane (Henson et al.,
1988).

Flathman et al. (1992) described the remediation of ground water
contaminated with dichloromethane after a leak. Air stripping was used
initially on water pumped out from the contaminated site, and 97% of
the contamination was removed in this way. This was followed by the
first phase of bioremediation, in which contaminated water was
withdrawn from the site and added to a bioreactor containing bacteria
acclimated to DCM. The treated water was reinjected on the site
together with the bacteria. This phase decreased the concentration by
97% over a period of 40 days. A second phase of bioremediation
followed some 3 years later, dealing with a subsection of the original
site. In this case, the indigenous bacteria were used and nutrients
were added to the site. Concentrations before treatment were up to
5200 mg/litre; after 10 months these had reduced to < 2 mg/litre. At
this point active treatment ceased, but the levels of DCM continued to
decrease, falling below 10 µg/litre at all but one of the sampling
sites.

The biodegradation of methylene chloride in contaminated ground
water can be strongly inhibited in the presence of other contaminants
such as 1,2 dichloroethane, xylene and ethylbenzene (Scholz-Muramatsu
et al., 1988).

Aerobic biodegradation of methylene chloride was observed in a
variety of surface soils including sand, a sandy loam and a sandy clay
loam, as well as in subsurface clay soil. Degradation occurred over
concentrations ranging from approximately 0.1 to 5 mg/litre. The time
required for 50% disappearance of the parent compound varied between
1.3 and 191.4 days.

4.3.2 Anaerobic

Details of studies on the anaerobic biodegradation of methylene
chloride are given in Table 6.

Methylene chloride was degraded at a concentration of 200 µg/litre
in the aqueous phase of natural sediment. Degradation was observed to
proceed via methyl chloride, although accumulation was not observed
(Wood et al., 1981). After a varying acclimation period using
anaerobic digestion in waste water, 86-92% conversion to CO₂ will
occur (Gossett, 1985). The half-life of methylene chloride in an
anaerobic water/sludge system is 11 days (Bayard et al., 1985).

Methylene chloride degradation was observed under anaerobic
conditions in sandy loam soil (Davis & Madsen, 1991).

4.3.3 Bioaccumulation

The n-octanol/water partition coefficient for methylene chloride
is 18 (log P_ow = 1.25-1.3). As a consequence, its bioaccumulation is
not expected to be significant. Moreover, its high depuration and
degradation rate will reduce the probability of bioaccumulation.

No experimental bioconcentration factor (BCF) for methylene
chloride is available. Its theoretical BCF ranges between 0.91 and 7.9
(Veith et al., 1980; Lyman et al., 1982; Veith and Kosian, 1983;
Bayard et al., 1985). Further data indicative of bioaccumulation in
aquatic organisms and human breast milk can be found in sections 5.1.3
and 5.3.1, respectively.

There is no evidence of biomagnification.

4.4 Interaction with other physical, chemical or biological factors

The ozone-depletion potential (ODP) of methylene chloride, as
compared to the standard ODP of CFC11, can be estimated from the
numbers of chlorine atoms (2 as compared to 3 for CFC11) and the
atmospheric lifetime (0.7 years as compared to 60 years). This results
in an ODP for methylene chloride of 0.4% of that of CFC11.

Table 6. Aerobic biodegradation of methylene chloride

Test system Condition Duration Degradation Initial concentration Reference

Laboratory studies

Unknown aerobic, BOD 20 days none Klecka (1982)

Domestic waste aerobic 28 days none Kawasaki (1980)
water (MITI)

Domestic waste aerobic, static, 7 days for each 100% 5, 10 mg/litre, loss by Tabak et al. (1981)
water subcultures taken at days culture transformation volatilization 6.25%
14 and 21

Enriched primary aerobic, static, closed 24 h almost 25 mg/litre Rittmann & McCarty
sewage effluent complete (1980)
transformation

Industrial waste aerobic 6 h 92% 50 mg/litre Davis et al. (1981)
water, municipal transformation,
activated sludge no metabolites

Activated sludge aerobic, continuous-flow 2-6 days > 99% 180 mg/litre, loss by Stover & Kincannon
reactor volatilization 5% (1983)

Municipal activated aerobic 50 h 49-66% 1, 10, 100 mg/litre Klecka (1982)
sludge (9-11 days mineralization
acclimatization)

Activated sludge aerobic 20-28 mg//litre 264-1300 mg/litre Halbartschlager et al.
(6 weeks per hour (1984)
acclimatization) transformation

Table 6 (Cont'd)

Test system Condition Duration Degradation Initial concentration Reference

Field studies

Water treatment aerobic 30-55% removal 50-150 µg/litre Loehr (1987)
works

Conventional aerobic 5-6 h 96.0-96.3% Namkung & Rittmann
activated sludge transformation (1987)
plant

At the current estimated total emission rate of 500 000 tonnes per
year, the calculated tropospheric chlorine loading due to methylene
chloride is 35 ppt, i.e. approximately 1% of the total chlorine
loading of 3600 ppt (WMO, 1991).

As methylene chloride has a low photochemical ozone creation
potential in the troposphere (0.9), when compared with chemicals such
as ethanol (27) or ethylene (100), it will not contribute
significantly to photochemical smog formation (Derwent & Jenkin,
1991).

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

Appraisal

As a consequence of release during its production and use,
methylene chloride is found in biota, water and air. Levels in water
and air tend to be higher in industrial and urban areas than in rural
areas. Improved control of emissions has led to lower environmental
levels of methylene chloride.

For the general population, air is the major source of exposure
to methylene chloride. In indoor air, higher levels may result from
the use of consumer products which contain methylene chloride. High
levels of methylene chloride may occur for short periods of time when
paint strippers and aerosols are used.

Exposure to methylene chloride can occur during its production
and use as a paint stripper. cleaner, degreaser, process solvent and
as an aerosol.

5.1 Environmental levels

Environmental levels measured before 1980 were summarized in
EHC 32: Methylene Chloride (IPCS, 1984). This monograph therefore
focuses on levels measured after 1980.

5.1.1 Atmosphere

5.1.1.1 Ambient air

In the ambient air of rural and remote areas, mean background
levels of methylene chloride are 0.07-0.29 µg/m³ (Table 7). The
average concentrations in suburban and urban areas, respectively, are
reported to be < 2 µg/m³ and < 15 µg/m³. In the vicinity of
hazardous waste sites, up to 43 µg/m³ have been round.

5.1.1.2 Precipitation

Rain water sampled in Koblenz (Germany) in 1982-1983 was found to
contain up to 4 µg methylene chloride/litre (Hellmann, 1984).

5.1.2 Water

Data on the levels of methylene chloride in water are presented in
Table 8.

Table 7. Methylene chloride levels in ambient air

Country/ Location Year of Concentration Reference
region measurement (µg/m³)

Germany urban area: Frankfurt 1980 2.1-4.2 Arendt et al. (1982)

Italy northern part 1983-1984 < 14 De Bortoli et al. (1986)

Netherlands Delft, Vlaardingen (urban 1980-1981 14.1 (max. annual mean) Guicherit & Schulting (1985)
area)
Isle of Terschelling (rural, 1980-1981 1.4 (max. annual mean) Guicherit & Schulting (1985)
suburban area)
mean concentration in 1980-1981 9 Guicherit & Schulting (1985)
the country

USA rural, suburban areas - 0.18-2.1 Shah & Heyerdahl (1988)
San Francisco Bay area 1984 3.2-9.1 Levaggi et al. (1988)
urban areas 1980 0.8-6.7 Shah & Heyerdahl (1988)
Shikiya et al. (1984)
1980-1981 1.35-6.76 Singh at al. (1982)
1981 0.8-2.5 Harkov (1984)
1982 2.4-4.2 Harkov (1984)
1987 0.95-1.64 Pleil & McClenny (1990)
1988 0.62-1.80 Pleil & McClenny (1990)
1989 0.48-1.68 Pleil & McClenny (1990)
hazardous waste sites 1983-1984 0.3-43 Harkov et al. (1985)

Arctic Spitzbergen July 1982 0.26±0.04 Hov et al, (1984)
March 1983 0.29±0.06 Hov et al. (1984)

Northern eastern Pacific 1981 0.12±0.15 Singh et al. (1983)
hemisphere

Southern eastern Pacific 1981 0.07 Singh et al, (1983)
hemisphere

Table 8. Methylene chloride levels in water

Country Location Year of Concentration Reference
measurement (µg/litre)

Ground water

Italy Milan 1983 4.5 CEFIC (1986)

USA Iowa 128 wells 1984-1985 1-5 (4 wells) Kelley (1985)

Surface water

Germany Mosel 1983 1.5-2.0 Hellmann (1984)

Neckar 1983 0.6-1.0 Hellmann (1984)

Elbe 1983 0.7-2.1 Hellmann (1984)

Elbe 1988 11 (max) LWA (1990)

Weser 1982-1983 < 0.5 Hellmann (1984)

Weser 1988 6 (max) LWA (1990)

Rhine at various sites 1981-1983 < 1 LWA (1981,1982,1983)

Rhine at Koblenz 1983 5.35-171 (monthly mean) Hellmann (1984)

Rhine at the Wesel 1983 < 2.0 Hellmann (1984)

Rhine at Duisburg 1984 1.5 (max) LWA (1984)

Rhine at various sites 1988 3.3 (max) LWA (1989)

Table 8 (Cont'd)

Country Location Year of Concentration Reference
measurement (µg/litre)

1989 1.0 (max) LWA (1990)

1990 1.1-3.9 (90th percentile) LWA (1991)

1991 < 0.1 (max) LWA (1992)

1986 0.1 (mean) BUA (1986)

Main 1985 ± 0.2 Van de Graaff (1986)

Emscher 1988 8.5 (max) LWA (1989)

1989 2.5 (max) LWA (1990)

1990 3.9 (max) LWA (1991)

1991 < 0.1 (max) LWA (1992)

Lippe 1988 5.5 (max) LWA (1989)

1989 < 1 (max) LWA (1990)

1990 2.4 (90th percentile) LWA (1991)

1991 < 0.1 (max) LWA (1992)

Wupper 1988 2.3 (max) LWA (1989)

1989 13.6 (90th percentile) LWA (1990)

1990 3.0 (90th percentile) LWA (1991)

Table 8 (Cont'd)

Country Location Year of Concentration Reference
measurement (µg/litre)

USA Susquehanna river, 1987 10 (mean) Smith (1989)
Columbia

Lancaster 1987 4.7 (mean) Smith (1989)

Ohio river basin (11 1980-1981 > 1 (238 samples) Howard et al. (1990)
stations, 4972 samples) > 10 (19 samples)

Sea and estuarine East Pacific Ocean 1981 0.002 (mean) Singh et al. (1983)
water (30 samples)

East Sea (German Coast) 1983 1.3-2.6 Hellmann (1984)

North Sea (German 1983 0.06-0.20 Hellmann (1984)
Coast)

In surface water, levels of methylene chloride have been reported
to vary from not detectable to 10 µg/litre. According to data recorded
in the US EPA STORET database, 30% of the samples showed methylene
chloride levels above the detection limits. A median concentration of
0.1 µg/litre was estimated (Staples et al., 1985).

Limited information concerning the contamination of sea water and
estuaries by methylene chloride is available. It appears that
methylene chloride can be found at up to 2.6 µg/litre in coastal
waters of the Baltic Sea. Levels of up to 0.20 µg/litre have been
found in North Sea coastal waters. Methylene chloride is generally not
detected in open oceans. A mean concentration of 2.2 ng/litre has been
reported in the South Pacific Ocean.

Methylene chloride enters the aquatic environment primarily
through waste water discharge. An estimated amount of 0.2% of the
total methylene chloride production is released in waste water
(Dequinze et al., 1984). The input from air rain-out has been
estimated for the northern and southern hemisphere (section 4.1.1).

Waste water from certain industries has been reported to contain
methylene chloride at average concentrations in excess of
1000 µg/litre, these being coal mining, aluminium forming,
photographic equipment and supplies, pharmaceutical manufacture,
organic chemical/plastics manufacture, paint and ink formulation,
rubber processing, foundries and laundries. The maximum concentration
measured was 210 mg/litre in waste water from the paint and ink
industry and the aluminium-forming industry (US EPA, 1981).

In the US EPA STORET database on industrial effluents, 38.8% of
the samples recorded contained methylene chloride with a median
concentration of 10 µg/litre (Staples et al., 1985).

Samples from the outfalls of four municipal treatment plants in
Southern California, USA, with both primary and secondary treatment,
contained < 10 to 400 µg methylene chloride/litre (Young et al.,
1983). In 30 Canadian water-treatment facilities, average
concentrations of methylene chloride in summer and winter were found
to be 10 µg/litre and 3 µg/litre, respectively (maximum, 50 µg/litre)
(Otson et al., 1982).

In leachate from industrial and municipal landfills, methylene
chloride concentrations were reported to range from 0.01 to
184 000 µg/litre (Sabel & Clark, 1984; Brown & Donnelly, 1988;
Sawhney, 1989).

Background data on ground water contamination by methylene
chloride are limited. It is the sixth most frequently detected organic
contaminant in ground water at hazardous waste disposal sites in the
CERCLA database (178 sites), the detection frequency being 19% (Plumb,
1987). In contaminated ground water in Minnesota, USA, up to

250 µg/litre has been detected (Sabel & Clark, 1984). Levels of up to
110 µg/litre were found in percolation water from a waste-disposal
site in Germany. However, methylene chloride was not found
(< 1 µg/litre) in the ground water below the site (Heil et al.,
1989).

5.1.3 Aquatic organisms

Concentrations of methylene chloride in freshwater organisms have
been reported for oyster and clams from Lake Ponchartrain, Louisiana,
USA. Levels ranging from 4.5 to 27 µg/kg (wet weight) could be
detected (Ferrario et al., 1985).

No methylene chloride was detected in fish taken from the River
Rhine in 1981 (Binnemann et al., 1983).

Levels of methylene chloride up to 700 µg/kg wet weight were found
in marine bottom fish taken from Commencement Bay in the state of
Washington, USA (Nicola et al., 1987).

Data on biota collected in the US EPA STORET data base show an
average level of 660 µg/kg in the 28% of the samples in which
methylene chloride was detected (Staples et al., 1985).

5.1.4 Soil and sediment

No data are available on the levels of methylene chloride in soil.

The levels of methylene chloride found in sediment from Lake
Pontchartrain, Louisiana ranged from not detectable to 3.2 µg/kg wet
weight (Ferrario et al., 1985).

Data recorded in the US EPA STORET database revealed a median
concentration of 13 µg/kg in 20% of 338 sediment sampling data
(Staples et al., 1985).

The levels of methylene chloride found in sediments from the river
Rhine in 1987-1988 varied from non-detectable to 30-40 µg/kg. At one
site maximum concentrations of 220-2200 µg/kg were measured (BUA,
1993, personal communication to the IPCS).

5.2 Human exposure

5.2.1 General population

5.2.1.1 Indoor air

In buildings where products containing methylene chloride are
used, air levels of methylene chloride much higher than outdoor levels
(< 15 µg/m³, see section 5.1.1.1) may be found (Table 7).

Relatively high levels (mean 670 µg/m³, peak level 5000 µg/m³)
have been found in the indoor air of residential houses (De Bortoli et
al., 1986).

5.2.1.2 Drinking-water

Methylene chloride has been detected in drinking-water supplies
(estimations made before 1980) in numerous cities in the USA (Dowty et
al., 1975; Coleman et al., 1976; Kopfler et al., 1977; Kool et al.,
1982), the mean concentrations reported being generally less than
1 µg/litre. An average of 3-10 µg/litre and a maximum of 50 µg/litre
were observed in a Canadian study of 30 drinkable water treatment
facilities (Otson et al., 1982).

Samples from 128 drinking-water wells in the USA showed that 3.1%
of them had methylene chloride levels of 1-5 µg/litre (Kelley, 1985).

Rodruigez Rojo et al. (1989) sampled the drinking-water of
Santiago de Compostela, Spain, in 1987. Methylene chloride was found
in 98.4% of the samples; the average concentration was 14.1 µg/litre,
with a range of 1.2-93.2 µg/litre. Other halomethanes were also found
and measured in the samples at average concentrations ranging from
9 to 25 µg/litre.

A wide sampling exercise involving 630 public community water
supplies (serving 6.9 million people in New Jersey, USA) was carried
out in 1984 and 1985 by McGeorge et al. (1987). The percentage of
positive results for methylene chloride ranged from 2.6 to 7.1%. The
median concentration ranged from 1.1 to 2.0 µg/litre and the range for
the whole sampling period was 0.5 to 39.6 µg/litre.

5.2.1.3 Foodstuffs

Although methylene chloride is used in food processing (solvent
extraction of coffee, spices, hops), there is little information on
its residual levels in food. In the USA, residues of methylene
chloride were found in decaffeinated coffee beans (0.32 to 0.42 mg/kg)
whilst a major coffee processor reported levels of 0.01 to 0.1 mg/kg
(ATSDR, 1992).

No methylene chloride was detected in ice-cream and yoghurt (BUA,
1986).

In seven types of decaffeinated ground coffee the methylene
chloride content ranged from < 0.05 to 4.04 mg/kg; in eight instant
coffee samples <0.05 to 0.91 mg/kg was found (Page & Charbonneau,
1984).

Heikes & Hopper (1986) analysed samples of grains and intermediate
grain-based foods for a range of fumigants using a purge-and-trap
method. Methylene chloride was not found in any of the grain samples,
nor in uncooked rice or dried lima beans. It was found in some of the
intermediate foods such as bleached flour (30 µg/kg), yellow corn meal
(4.7 µg/kg), lasagne noodles (5.4 µg/kg) and yellow cake mix
(4.6 µg/kg).

One of the authors (Heikes, 1987) investigated levels of methylene
chloride in table-ready foods, taken from the US Food and Drug
Administration's Total Diet Study. Of the 19 foods examined, eight
contained methylene chloride above the quantification limit (not
given). Detailed results for six of the foods are given in Table 9.

Table 9. Dichloromethane content of table ready foods
(Heikes, 1987)

Food Number of Number Range of
samples positive concentration
(µg/kg)

Butter 7 7 1.1-280
Margarine 7 7 1.2-81
Ready-to-eat cereal 11 10 1.6-300
Cheese 8 8 3.9-98
Peanut butter 7 4 26-49
Highly processed foods^a 12 10 5-310

^a e.g., frozen chicken dinner, fish sticks, pot pie

5.2.1.4 Consumer exposure

Consumers are exposed to methylene chloride via the use of a
number of formulated products such as aerosols or paint strippers. A
USA survey found that 78% of paint removers and 66% of aerosol spray
paints sold as household products contained methylene chloride (US
EPA, 1987). Over 100 consumer products in Sweden contain methylene
chloride (National Chemical Inspectorate, Sweden, personal
communication to the IPCS). In Norway the number is around 140,
including 45 paint removers (AKZO, personal communication to the
IPCS).

Methylene chloride does not appear to be subject to widespread
volatile substance abuse. Statistics on deaths resulting from
substance abuse in the United Kingdom were collected over the period
1971-1991 and analysed by product type. Of the 1221 deaths recorded,
five were assigned to the group "paint thinners and paint strippers".

Methylene chloride is used only in the latter products, the former
containing solvents such as toluene and xylene which are known to be
substances of abuse (Flanagan et al., 1990).

A large do-it-yourself consumer population uses paint strippers
containing methylene chloride on furniture and woodwork. Formulations
are available mainly in liquid form, but also, occasionally, as an
aerosol. Exposures have been estimated on the basis of USA
investigations of household solvent products. The estimated levels
ranged from less than 35 mg/m³ to a few short-term exposures of 14
100 to 21 200 mg/m³. The majority of the concentration estimates
were below 1770 mg/m³ (US EPA, 1990).

Methylene chloride exposure was estimated while using a number of
formulations of paint stripper in a small room. Various ventilation
conditions were evaluated and a worst possible case was simulated,
with doors and windows closed. In one test, involving furniture
stripping in a room with through ventilation, the operator exposure
was found to be 289 mg/m³ on a 2-h TWA. Peaks of exposure were
observed during application (460 mg/m³) and during scraping-off
(710-1410 mg/m³) (ICl, 1988, personal communication to the IPCS).

A series of paint-stripping exercises were performed in a small
room. Various ventilation conditions were evaluated while using a
number of formulations of paint stripper. A worst possible case was
simulated with doors and windows closed. Concentrations of methylene
chloride in the room rose to 14.1-17.6 g/m³ (4000-5000 ppm),
although it is questionable whether anyone could work in such
conditions without breathing apparatus. Further exercises with the
door and windows open (as recommended by