Vinyl Chloride (EHC 215, 1999)

UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 215

Vinyl Chloride

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, and produced within the framework of the
Inter-Organization Programme for the Sound Management of Chemicals.

World Health Organization
Geneva, 1999

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environment.

WHO Library Cataloguing in Publication Data

Vinyl chloride.

(Environmental health criteria ; 215)

1.Vinyl chloride - analysis 2.Vinyl chloride - toxicity
3.Vinyl chloride - adverse effects 4.Environmental exposure
5.Occupational exposure I.International Programme on
Chemical Safety II.Series

ISBN 92 4 157215 9 (NLM Classification: QV 633)
ISSN 0250-863X

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR VINYL 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 in laboratory animals and
humans
1.6. Effects on laboratory mammals and in vitro test
systems
1.7. Effects on humans
1.8. Effects on other organisms in the laboratory and
field

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
2.4.1. General analytical methods and
detection
2.4.2. Sample preparation, extraction and analysis
for different matrices
2.4.2.1 Air
2.4.2.2 Water
2.4.2.3 PVC resins and PVC products
2.4.2.4 Food, liquid drug and cosmetic
products
2.4.2.5 Biological samples
2.4.2.6 Human monitoring
2.4.2.7 Workplace air monitoring

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. Production levels and processes
3.2.1.1 Production of VC
3.2.1.2 Production of PVC from VC
3.2.1.3 PVC products
3.2.2. Emissions from VC/PVC plants
3.2.2.1 Sources of emission during the
production of VC
3.2.2.2 Emission of VC and dioxins from VC/PVC
plants during production

3.2.3. Accidental releases of VC
3.2.3.1 PVC plant and transport accidents
3.2.3.2 Leakage and discharge from VC/PVC
plants
3.2.4. VC residues in virgin PVC resin and products
3.2.4.1 VC residues in different PVC samples
3.2.4.2 VC residues in PVC products
3.2.4.3 VC formation as a result of heating PVC
3.2.5. Other sources of VC
3.2.5.1 VC as a degradation product of
chlorinated hydrocarbons
3.2.5.2 VC formation from tobacco
3.3. Uses

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION

4.1. Transport and distribution between media
4.1.1. Air
4.1.2. Water and sediments
4.1.3. Soil and sewage sludge
4.1.4. Biota
4.2. Transformation
4.2.1. Microbial degradation
4.2.2. Abiotic degradation
4.2.2.1 Photodegradation
4.2.2.2 Hydrolysis
4.2.3. Other interactions
4.3. Bioaccumulation
4.4. Ultimate fate following use
4.4.1. Waste disposal
4.4.2. Fate of VC processed to PVC

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

5.1. Environmental levels
5.1.1. Air
5.1.1.1 Outdoor air
5.1.1.2 Indoor air
5.1.2. Water and sediment
5.1.3. Soil and sewage sludge
5.1.3.1 Soil
5.1.3.2 Sewage sludge
5.1.4. Food, feed and other products
5.1.5. Terrestrial and aquatic organisms
5.2. General population exposure
5.2.1. Estimations
5.2.2. Monitoring data of human tissues
or fluids
5.3. Occupational exposure

6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS

6.1. Absorption
6.1.1. Oral exposure
6.1.2. Inhalation exposure
6.1.3. Dermal exposure
6.2. Distribution and retention
6.2.1. Oral exposure
6.2.2. Inhalation exposure
6.2.3. Partition coefficients in vitro
6.3. Metabolic transformation
6.4. Elimination and excretion
6.4.1. Oral exposure
6.4.2. Inhalation exposure
6.5. Reaction with body components
6.5.1. Formation of DNA adducts
6.5.2. Alkylation of proteins
6.6. Modelling of pharmacokinetic data for
vinyl chloride

7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS

7.1. Acute toxicity
7.2. Short-term toxicity
7.2.1. Oral exposure
7.2.2. Inhalation exposure
7.2.3. Dermal exposure
7.3. Long-term toxicity - effects other than tumours
7.3.1. Oral exposure
7.3.2. Inhalation exposure
7.4. Skin and eye irritation; sensitization
7.5. Reproductive toxicity, embryotoxicity and
teratogenicity
7.5.1. Male reproductive toxicity
7.5.2. Embryotoxicity and teratogenicity
7.6. Special studies
7.6.1. Neurotoxicity
7.6.2. Immunotoxicity
7.6.3. Cardiovascular effects
7.6.4. Hepatotoxicity
7.7. Carcinogenicity
7.7.1. Oral exposure
7.7.2. Inhalation exposure
7.7.2.1 Short-term exposure
7.7.2.2 Long-term exposure
7.7.3. The effect of age on susceptibility to
tumour induction
7.7.4. The effect of gender on susceptibility to
tumour induction
7.7.5. Carcinogenicity of metabolites

7.8. Genotoxicity
7.8.1. In vitro studies
7.8.2. In vivo studies
7.8.3. Genotoxicity of VC metabolites
7.8.4. Other toxic effects of VC metabolites
7.8.5. Mutagenic and promutagenic properties of DNA
adducts formed by VC metabolites
7.8.6. Mutations in VC-induced tumours
7.9. Factors modifying toxicity
7.10. Mechanisms of toxicity - mode of action
7.10.1. Mechanisms of VC disease
7.10.2. Mechanism of carcinogenesis

8. EFFECTS ON HUMANS

8.1. General population
8.2. Controlled human studies
8.3. Occupational exposure
8.3.1. Overview
8.3.2. Non-neoplastic effects
8.3.2.1 Acute toxicity
8.3.2.2 Effects of short- and long-term
exposure
8.3.2.3 Organ effects
8.3.3. Neoplastic effects
8.3.3.1 Liver and biliary tract cancers
8.3.3.2 Brain and central nervous
system (CNS)
8.3.3.3 Respiratory tract
8.3.3.4 Lymphatic and haematopoietic
cancers
8.3.3.5 Malignant melanoma
8.3.3.6 Breast cancer
8.3.3.7 Other cancer sites
8.4. Genotoxicity studies
8.4.1. Cytogenetic studies of VC-exposed
workers
8.4.2. Mutations at the hypoxanthine guanine
phosphoribosyltransferase (hprt) locus
8.4.3. Mutations in ASL from VC-exposed
workers
8.4.3.1 p53 gene
8.4.3.2 ras genes
8.5. Studies on biological markers
8.5.1. Excretion of metabolites
8.5.2. Genetic assays
8.5.3. Enzyme studies
8.5.4. von Willebrand factor
8.5.5. p53 and ras proteins
8.6. Susceptible subpopulations
8.6.1. Age susceptibility
8.6.2. Immunological susceptibility
8.6.3. Polymorphic genes in VC metabolism

9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD

9.1. Laboratory experiments
9.1.1. Microorganisms
9.1.1.1 Water
9.1.1.2 Soil
9.1.2. Aquatic organisms
9.1.2.1 Invertebrates
9.1.2.2 Vertebrates
9.2. Field observations
9.2.1. Aquatic organisms

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

10.1. Evaluation of human health effects
10.1.1. Hazard identification
10.1.1.1 Non-neoplastic effects
10.1.1.2 Neoplastic effects
10.1.2. Dose-response analysis
10.1.2.1 Non-neoplastic effects
10.1.2.2 Neoplastic effects
10.1.3. Human exposure
10.1.3.1 General population
10.1.3.2 Occupational exposure
10.1.4. Risk characterization
10.2. Evaluation of effects on the environment

11. RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH

11.1. Public health
11.2. Occupational health

12. FURTHER RESEARCH

13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

REFERENCES

ANNEX 1. REGULATIONS CONCERNING VINYL CHLORIDE

ANNEX 2. PHYSIOLOGICAL MODELLING AND RECENT RISK ASSESSMENTS

ANNEX 3. EXECUTIVE SUMMARY OF VINYL CHLORIDE PANEL REPORT

RESUME

RESUMEN

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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR VINYL CHLORIDE

Members

Dr A. Barbin, International Agency for Research on Cancer, Lyon,
France

Professor V.J. Feron, TNO Nutrition and Food Research Institute, HE
Zeist, Netherlands

Ms P. Heikkilä, Uusimaa Regional Institute of Occupational Health,
Helsinki, Finland

Dr J. Kielhorn, Chemical Risk Assessment, Fraunhofer Institute for
Toxicology and Aerosol Research, Hanover, Germany (Co-Rapporteur)

Professor M. Kogevinas, Respiratory and Environmental Health Research
Unit, Municipal Institute of Medical Investigation (IMIM), Barcelona,
Spain

Mr H. Malcolm, Institute of Terrestrial Ecology, Monks Wood, Abbots
Ripton, Huntingdon, Cambridgeshire, United Kingdom (Co-Rapporteur)

Dr W. Pepelko, National Center for Environmental Assessment, Office of
Research and Development, US EPA, Washington DC, USA

Dr A. Pintér, National Institute of Environmental Health, Budapest,
Hungary (Vice-Chairman)

Dr L. Simonato, Department of Oncology, University of Padua, Venetian
Tumours Registry, Padua, Italy

Professor H. Vainio, Division of Health Risk Assessment, National
Institute of Environmental Medicine, Karolinska Institute, Stockholm,
Sweden (Chairman)

Dr E.M. Ward, Division of Surveillance Hazard, Evaluation and Field
Studies, National Institute for Occupational Safety and Health
(NIOSH), Robert Taft Laboratory, Cincinnati, Ohio, USA (Contact
address: Environmental Cancer Epidemiology, International Agency for
Research on Cancer, Lyon, France

Dr J.M. Zielinski, Biostatistics and Research Coordination Division,
Ottawa, Ontario, Canada

Secretariat

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

Dr I. Mangelsdorf, Chemical Risk Assessment, Fraunhofer Institute for
Toxicology and Aerosol Research, Hanover, Germany

Dr C. Melber, Chemical Risk Assessment, Fraunhofer Institute for
Toxicology and Aerosol Research, Hanover, Germany

Dr U. Wahnschaffe, Chemical Risk Assessment, Fraunhofer Institute for
Toxicology and Aerosol Research, Hanover, Germany

WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR VINYL CHLORIDE

A WHO Task Group on Environmental Health Criteria for Vinyl
Chloride met at the Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany, from 25 to 29 January 1999. Professor H.
Muhle welcomed the participants on behalf of the Institute and its
Director, Professor U. Heinrich. Dr A. Aitio, IPCS, welcomed the
participants on behalf of the Director, IPCS, and the three IPCS
co-operating organisations (UNEP, ILO, and WHO). The Group reviewed
and revised the draft and made an evaluation of the risks for human
health and the environment from exposure to vinyl chloride.

The first and second drafts of this monograph were prepared,
under the co-ordination of Dr I. Mangelsdorf, by the authors
Dr J. Kielhorn, Dr C. Melber and Dr U. Wahnschaffe. In the preparation
of the second draft, the comments received from the IPCS contact
points were carefully considered.

Dr A. Aitio of the IPCS Central Unit was responsible for the
scientific aspects of the monograph, and Dr P.G. Jenkins for the
technical editing.

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

* * *

The Federal Ministry for the Environment, Nature Conservation and
Nuclear Safety, Germany, contributed financially to the preparation of
this Environmental Health Criteria monograph, and the meeting was
organised by the Fraunhofer Institute for Toxicology and Aerosol
Research.

ABBREVIATIONS

Epsilon A 1, N ⁶-ethenoadenine
Epsilon C 3, N ⁴-ethenocytosine
Epsilon dA 1, N ⁶-etheno-2'-deoxyadenosine
Epsilon dC 3, N ⁴-etheno-2'-deoxycytidine
Epsilon G ethenoguanine
7-OEG 7-(2'-oxoethyl)guanine
ALAT alanine aminotransferase
ASAT aspartate aminotransferase
ASL angiosarcoma of the liver
BCF bioconcentration factor
CA chromosomal aberration
CAA chloroacetaldehyde
CEO chloroethylene oxide
CI confidence interval (95% unless otherwise stated)
CNS central nervous system
CYP2E1 cytochrome P-450 isozyme 2e1
ECD electron capture detection
EDC 1,2-dichloroethane
FDA Food and Drug Administration (USA)
FID flame ionization detector
GC gas chromatography
GST glutathione S-transferase
HCC hepatocellular carcinoma
HLA human-leukocyte-associated antigen
HPLC high performance liquid chromatography
HWD hazardous waste dump
IR infrared
LOAEL lowest-observed-adverse-effect level
MN micronuclei
MOR morbidity odds ratio
MS mass spectrometry
MSW municipal solid waste
NER non-extractable residue
NOAEC no-observed-adverse-effect concentration
NOAEL no-observed-adverse-effect level
NOEL no-observed-effect level
PCDD polychlorinated dibenzodioxin
PCDF polychlorinated dibenzofuran
PCE tetrachloroethene (perchloroethene)
PID photoionization detector
PVC polyvinyl chloride
SCE sister chromatid exchange
SIR standardized incidence ratio
SLRL sex-linked recessive lethal
SMR standardized mortality ratio
TCE trichloroethene
TEQ toxic equivalent quantity
UV ultraviolet
VC vinyl chloride
VOC volatile organic compound

1. SUMMARY

This monograph deals with vinyl chloride (VC) monomer itself and
is not an evaluation of polyvinyl chloride (PVC), the polymer of VC.
Exposures to VC in mixtures are not addressed.

1.1 Identity, physical and chemical properties, and analytical
methods

Under ambient conditions, VC is a colourless, flammable gas with
a slightly sweet odour. It has a high vapour pressure, a high value
for Henry's Law constant and a relatively low water solubility. It is
heavier than air and is soluble in almost all organic solvents. It is
transported in liquid form under pressure.

At ambient temperatures in the absence of air, dry purified VC is
highly stable and non-corrosive but above 450°C, or in the presence of
sodium or potassium hydroxide, partial decomposition can occur.
Combustion of VC in air produces carbon dioxide and hydrogen chloride.
With air and oxygen, very explosive peroxides can be formed,
necessitating a continuous monitoring and limitation of the oxygen
content, particularly in VC recovery plants. In the presence of water,
hydrochloric acid is formed.

Polymerization reactions to PVC are technically the most
important reactions from an industrial view, but addition reactions
with other halogens at the double bond, e.g., to yield
1,1,2-trichloroethane or 1,1-dichloroethane, are also important.

The concentration of VC in air can be monitored by trapping it on
adsorbents and, after liquid or thermal desorption, analysis by gas
chromatography. In ambient air measurements, several adsorbents in
series or refrigerated traps may be needed to increase the efficiency
of trapping. Peak concentrations at workplaces can be measured with
direct-reading instruments based on, for instance, FID or PID. In
continuous monitoring, IR and GC/FID analysers combined with data
logging and processing have been used. In analysis of VC in liquids
and solids, direct injection, extraction and more increasingly head
space or purge-and-trap techniques are applied. Also in these samples,
VC is analysed by GC fitted to, for instance, FID or MS detectors.

1.2 Sources of human and environmental exposure

VC is not known to occur naturally although it has been found in
landfill gas and groundwater as a degradation product of chlorinated
hydrocarbons deposited as solvent wastes in landfills or in the
environment of workplaces using such solvents. VC is also present in
cigarette smoke.

VC is produced industrially by two main reactions: a) the
hydrochlorination of acetylene; and b) thermal cracking (at about
500°C) of 1,2-dichloroethane (EDC) produced by direct chlorination
(ethylene and chlorine) or oxychlorination (ethylene, HCl and air/O₂)
of ethylene in the "balanced process". The latter process is the most
usual nowadays.

The world production of PVC (and therefore VC) in 1998 was about
27 million tonnes. PVC accounts for 20% of plastics material usage and
is used in most industrial sectors. About 95% of the world production
of VC is used for the production of PVC. The remainder goes into the
production of chlorinated solvents, primarily 1,1,1-trichloroethane
(10 000 tonnes/year).

Three main processes are used for the commercial production of
PVC: suspension (providing 80% of world production), emulsion (12%)
and mass or bulk (8%). Most of the case studies describing adverse
effects of VC concern plants using the suspension (also called
dispersion) process.

There have been reports of VC release through accidents in PVC
plants or during transportation. VC recovery has been introduced in
many countries to recover residual non-converted VC from
polymerization and other sources of the process such as in off-gas and
water effluents. Where special precautions are not taken, VC can be
detected in PVC resins and products.

The level of residual VC in PVC has been regulated since the late
1970s in many countries. Since then, release of VC from the thermal
degradation of PVC is either not detectable or is at very low levels.

Dioxins can be formed as contaminants in VC production. The
levels of dioxins emitted into the environment are controversial.

1.3 Environmental transport, distribution and transformation

Owing to its high vapour pressure, VC released to the atmosphere
is expected to exist almost entirely in the vapour phase. There are
indications for wet deposition.

VC has a relatively low solubility in water and has a low
adsorption capacity to particulate matter and sediment. Volatilization
of VC is the most rapid process for removal of VC introduced into
surface waters. Half-lives reported for volatilization from surface
waters range from about 1 to 40 h.

Volatilization half-lives from soil were calculated to be 0.2-0.5
days. Estimated losses of VC (after one year under a 1 m soil cover)
ranged from 0.1-45%, depending on soil type. Soil sorption
coefficients estimated from physicochemical data indicate a low
sorption potential and therefore a high mobility in soil. Another
important distribution route is leaching through the soil into
groundwater where VC may persist for years.

Laboratory experiments with aquatic organisms showed some
bioaccumulation, but no biomagnification within the foodchain.

With few exceptions, VC is not easily degraded by unadapted
microbial consortia under environmental conditions. Maximum
unacclimated biodegradation half-lives of VC were estimated to be in
the order of several months or years. However, special enrichment or
pure (e.g., Mycobacterium sp.) cultures are capable of degrading VC
under optimal culture conditions. The main degradation products were
glycolic acid or carbon dioxide after aerobic conversion and ethane,
ethene, methane or chloromethane after anaerobic transformation.
Frequently, the degradation reaction of VC proceeded faster with
aerobes than with anaerobes.

Reaction with photochemically produced OH radicals is the
dominant atmospheric transformation process, resulting in calculated
tropospheric half-lives of 1 to 4 days. Several critical compounds,
such as chloroacetaldehyde, formaldehyde and formyl chloride, are
generated during experimental photolysis reactions.

Photolytic reactions as well as chemical hydrolysis are thought
to be of minor importance in aqueous media. However, the presence of
photosensitizers may enhance the transformation of VC.

There are indications for reactions of VC with chlorine or
chloride used for water disinfection, thus leading to
chloroacetaldehyde and other undesirable compounds. Another
possibility for interaction is with salts, many of which have the
ability to form complexes with VC, perhaps resulting in increased
solubility.

Methods employed (with differing success) for removal of VC from
contaminated waters include stripping, extraction, adsorption and
oxidation. Some in situ bioremediation techniques (for groundwater
or soil) couple evaporative and other methods with microbial
treatment. VC in waste gases can be recycled, incinerated or
microbially degraded. Most of the VC produced industrially is bound in
PVC articles. Their incineration involves a risk of formation of
PCDDs/PCDFs and other unwanted chlorinated organic compounds.

1.4 Environmental levels and human exposure

There is very little exposure of the general population to VC.

Atmospheric concentrations of VC in ambient air are low, usually
less than 3 µg/m³. Exposure of the general population may be higher
in situations where large amounts of VC are accidentally released to
the environment, such as in a spill during transportation. However,
such exposure is likely to be transient. Near VC/PVC industry and
waste disposal sites, much higher concentrations (up to 8000 µg/m³
and 100 µg/m³, respectively) have been recorded.

Indoor air concentrations in houses adjacent to land fills
reached maximal concentrations of 1000 µg/m³.

The main route of occupational exposure is via inhalation and
occurs primarily in VC/PVC plants. Occupational exposures to VC
amounted to several thousands of mg/m³ in the 1940s and 1950s, and
were several hundreds of mg/m³ in the 1960s and early 1970s. After
the recognition of the carcinogenic hazards of VC, occupational
exposure standards were set at approximately 13-26 mg/m³ (5-10 ppm)
in most countries in the 1970s. Compliance with these guidelines has
considerably lowered workplace VC concentrations, but even in the
1990s higher concentrations have been reported and may still be
encountered in some countries.

VC has occasionally been detected in surface waters, sediment and
sewage sludges, with maxima of 570 µg/litre, 580 µg/kg, and
62 000 µg/litre, respectively. Soil samples near an abandoned chemical
cleaning shop contained very high VC concentrations (up to 900 mg/kg).
Maximal VC concentrations in groundwater or leachate from areas
contaminated with chlorinated hydrocarbons amounted to 60 000 µg/litre
(or more). High concentrations (up to 200 mg/litre) were detected in
well water in the vicinity of a PVC plant 10 years after leakages.

The few data available show that VC can be present in tissues of
small aquatic invertebrates and fish.

In the majority of drinking-water samples analysed, VC was not
present at detectable concentrations. The maximum VC concentration
reported in finished drinking-water was 10 µg/litre. There is a lack
of recent data on VC concentrations in drinking-water, but these
levels are expected to be below 10 µg/litre. If contaminated water is
used as the source of drinking-water, higher exposures may occur. Some
recent studies have identified VC in PVC-bottled drinking-water at
levels below 1 µg/litre. The frequency of occurrence of VC in such
water is expected to be higher than in tap water.

Packaging with certain PVC materials can result in VC
contamination of foodstuff, pharmaceutical or cosmetic products,
including liquors (up to 20 mg/kg), vegetable oils (up to 18 mg/kg),
vinegars (up to 9.8 mg/kg) and mouthwashes (up to 7.9 mg/kg). Owing to
the legislative action of many countries, a significant reduction in
VC levels and/or in the number of positive samples has been achieved
since the early 1970s.

Dietary exposure to VC from PVC packages used for food has been
calculated by several agencies and, based upon estimated average
intakes in the United Kingdom and USA, an exposure of < 0.0004 µg/kg
per day was estimated for the late 1970s and early 1980s. An early
study identified VC in tobacco smoke at the ng/cigarette range.

1.5 Kinetics and metabolism in laboratory animals and humans

VC is rapidly and well absorbed after inhalation or oral
exposure. The primary route of exposure to VC is inhalation. In animal
and human studies, under steady-state conditions, approximately 40% of
inspired VC is absorbed after exposure by inhalation. Animal studies
showed an absorption of more than 95% after oral exposure. Dermal
absorption of VC in the gaseous state is not significant.

Data from oral and inhalation studies on rats indicate rapid and
widespread distribution of VC. Rapid metabolism and excretion limits
accumulation of VC in the body. Placental transfer of VC occurs
rapidly in rats. No studies on distribution after dermal exposure have
been reported.

The main route of metabolism of VC after inhalation or oral
uptake involves oxidation by cytochrome P-450 (CYP2E1) to form
chloroethylene oxide (CEO), a highly reactive, short-lived epoxide
which rapidly rearranges to form chloroacetaldehyde (CAA). The primary
detoxification reaction of these two reactive metabolites as well as
chloroacetic acid, the dehydrogenation product of CAA, is conjugation
with glutathione catalysed by glutathione S-transferase. The
conjugation products are further modified to substituted cysteine
derivatives (S-(2-hydroxyethyl)-cysteine, N-acetyl- S-
(2-hydroxyethyl)cysteine, S-carboxymethyl cysteine and
thiodiglycolic acid) and are excreted via urine. The metabolite
carbon dioxide is exhaled in air.

CYP2E1 and glutathione S-transferase isoenzymes are known to
have large inter-species and inter-individual variation in activity.

After inhalative or oral exposure to low doses, VC is
metabolically eliminated and non-volatile metabolites are excreted
mainly in the urine. Comparative investigations of VC uptake via
inhalation revealed a lower velocity of metabolic elimination in
humans than in laboratory animals, on a body weight basis. However,
when corrected on a body surface area basis, the metabolic clearance
of VC in humans becomes comparable to that of other mammalian species.
With increasing oral or inhalative exposure, the major route of
excretion in animals is exhalation of unchanged VC, indicating
saturation of metabolic pathways. Independently of applied dose, the
excretion of metabolites via faeces is only a minor route. No studies
were located that specifically investigated excretion via the bile.

CEO is thought to be the most important metabolite in vivo,
concerning the mutagenic and carcinogenic effects of VC. CEO reacts
with DNA to produce the major adduct 7-(2'-oxoethyl)guanine (7-OEG),
and, at lower levels, the exocyclic etheno adducts,
1, N⁶-ethenoadenine (Epsilon A), 3, N⁴-ethenocytosine (Epsilon C)
and N²,3-ethenoguanine (Epsilon G). The etheno DNA adducts exhibit
pro-mutagenic properties, in contrast to the major adduct 7-OEG.
7-OEG, Epsilon A, Epsilon C and Epsilon G have been measured in

various tissues from rodents exposed to VC. Physiologically based
toxicokinetic (PBTK) models have been developed to describe the
relationship between target tissue dose and toxic end-points for VC.

1.6 Effects on laboratory mammals and in vitro test systems

VC appears to be of low acute toxicity when administered to
various species by inhalation. The 2-h LC₅₀ for rat, mouse,
guinea-pig and rabbit were reported to be 390 000, 293 000, 595 000
and 295 000 mg/m³, respectively. No data are available on acute
toxicity after oral or dermal application. VC has a narcotic effect
after acute inhalation administration. In rats, mice and hamsters,
death was preceded by increased motor activity, ataxia and
convulsions, followed by respiratory failure. In dogs, severe cardiac
arrythmias occurred under narcosis after inhalative exposure to
260 000 mg/m³. After acute inhalation exposure to VC in rats,
pathological findings included congestion of the internal organs,
particularly lung, liver and kidney, as well as pulmonary oedema.

No studies or relevant data are available for assessing effects
of dermal exposure, skin irritation or sensitizing property of VC.

Short-term oral exposure to VC for 13 weeks in rats resulted in a
no-observed-effect level (NOEL), based on increase in liver weight, of
30 mg/kg.

In various species, the main target organ for short-term (up to
6 months) inhalation exposure to VC was the liver. Increases in
relative liver weights and hepatocellular changes were noted in rats
at 26 mg/m³ (the lowest dose level tested); at higher levels
(> 260 mg/m³) more pronounced liver changes occurred in a
dose-related manner. Other target organs were the kidney, lung and
testis. Rats, mice and rabbits seem to be more sensitive than
guinea-pigs and dogs.

Long-term exposure to VC by inhalation resulted in statistically
significant increases in mortality in some strains of rats at a dose
of as low as 260 mg/m³, in mice at 130 mg/m³ and in hamsters at
520mg/m³ for various lengths of exposure. Rats exposed to
130 mg/m³ showed reduced body weight and increased relative spleen
weight, hepatocellular degeneration and proliferation of cells lining
the liver sinusoids. Exposure to higher levels produced degenerative
alteration in the testis, tubular nephrosis and focal degeneration of
the myocardium in rats. For rats and mice exposed via inhalation, the
no-observed-adverse-effect level (NOAEL) concerning non-neoplastic
effects is below 130 mg/m³.

Chronic feeding studies showed increased mortality, increased
liver weights and morphological alteration of the liver.

After oral exposure, liver cell polymorphism (variation in size
and shape of hepatocytes and their nuclei) could be seen in rats at
levels as low as 1.3 mg/kg body weight. The NOAEL was 0.13 mg/kg body
weight.

Long-term feeding studies in rats with VC in PVC granules yielded
significantly increased tumour incidences of liver angiosarcoma (ASL)
at 5.0 mg/kg body weight per day and neoplastic liver nodules
(females) and hepatocellular carcinoma (HCC) (males) at 1.3 mg/kg body
weight per day.

In inhalation studies with VC in Sprague-Dawley rats, a clear
dose-response relationship was observed for ASL and, at high
concentrations, Zymbal gland carcinomas. No clear dose-dependency for
hepatoma or extrahepatic angiosarcoma, nephroblastomas,
neuroblastomas, or mammary malignant tumours was observed. In mice,
the spectrum of tumours induced by long-term inhalation exposure is
similar to that observed in rats but an increase in lung tumours was
only observed in mice. In hamsters, an increased tumour incidence of
ASL, mammary gland and acoustic duct tumours, melanomas, stomach and
skin epithelial tumours was reported.

The mutagenic and genotoxic effects of VC have been detected in a
number of in vitro test systems, predominantly after metabolic
activation. VC is mutagenic in the Ames test in S. typhimurium
strains TA100, TA1530 and TA1535 but not in TA98, TA1537 and TA1538,
indicating mutations as a result of base-pair substitutions
(transversion and transition) rather than frameshift mutations. This
is in agreement with the finding that etheno-DNA adducts formed by the
reactive metabolites CEO and CAA convert to actual mutations by
base-pair substitutions.

Other gene mutation assays in bacteria, yeast cells and mammalian
cells have revealed positive results exclusively in the presence of
metabolic activation. Mutagenic effects were also reported in a human
cell line containing cloned cytochrome P-450IIE1, which is capable of
metabolizing VC. Gene mutation was also detected in plant
( Tradescantia ) cuttings exposed to VC. In gene conversion assays,
positive results were reported with Saccharomyces cerevisiae in the
presence of a metabolic activation system. VC exposure induced
unscheduled DNA synthesis in rat hepatocytes and increased
sister-chromatid exchange (SCE) in human lymphocytes after addition of
exogenic activation system. No growth inhibition was detected in DNA
repair-deficient bacteria without metabolic activation. Cell
transformation assays revealed positive results both with and without
metabolic activation.

VC exposure induced gene mutation and mitotic recombination in
Drosophila melanogaster but not gene mutation in mammalian germ
cells. VC showed clastogenic effects in rodents, increased SCE in
hamsters and induced DNA breaks in mice. In host-mediated (rat)
assays, VC induced gene conversion and forward mutations in yeast.

CEO and CAA were found to be mutagenic in different test systems.
CEO is a potent mutagen, whereas CAA is highly toxic. CEO and CAA were
found to be carcinogenic in mice, CEO being much more active than CAA.

Mutations of the ras and p53 genes were analysed in liver
tumours induced by VC in Sprague-Dawley rats: base-pair substitutions
were found in the Ha- ras gene in hepatocellular carcinoma (HCC) and
in the p53 gene in ASL. These mutations are in agreement with the
observed formation and persistence of etheno adducts in liver DNA,
following exposure of rats to VC, and with the known pro-mutagenic
properties of etheno adducts.

Studies into the mechanism of carcinogenicity of VC suggest that
the reactive epoxide intermediate CEO interacts with DNA to form
etheno adducts, which result in a base-pair substitution leading to
neoplastic transformation.

1.7 Effects on humans

Concentrations of VC in the region of 2590 mg/m³ (1000 ppm),
which were not unusual prior to 1974, over periods ranging from 1
month to several years, have been reported to cause a specific
pathological syndrome found in VC workers called the "vinyl chloride
illness". Symptoms described were earache and headache, dizziness,
unclear vision, fatigue and lack of appetite, nausea, sleeplessness,
breathlessness, stomachache, pain in the liver/spleen area, pain and
tingling sensation in the arms/legs, cold sensation at the
extremities, loss of libido and weight loss. Clinical findings
included scleroderma-like changes in the fingers with subsequent bony
changes in the tips of the fingers described as acroosteolysis,
peripheral circulatory changes identical with the classical picture of
Raynaud's disease and enlargement of the liver and spleen with a
specific histological appearance, and respiratory manifestations.

Studies in humans have not been adequate to confirm effects on
the reproductive system. A few morbidity studies have reported
elevated incidence of circulatory diseases among vinyl chloride
workers. However, large cohort studies have found lower cardiovascular
disease mortality.

There is strong and consistent evidence from epidemiological
studies that VC exposure causes the rare tumour, angiosarcoma of the
liver. Brain tumours and hepatocellular carcinoma of the liver may
also be associated with VC, although the evidence cannot be considered
definitive. Other cancer sites reported to be in excess, but less
consistently, include lung, lymphatic and haematopoietic tissue, and
skin.

VC is mutagenic and clastogenic in humans. Frequencies of
chromosomal aberrations (CA), micronuclei (MN) and SCE in the
peripheral blood lymphocytes of workers exposed to high levels of VC
have been shown to be raised compared to controls. Although in many

studies the exposure concentrations and duration of exposure were only
estimated, a dose-response relationship and a "normalization" of
genotoxic effects with time after reduction of exposure can be seen.

Point mutations have been detected in p53 and ras genes in
tumours from highly exposed (before 1974) autoclave workers with liver
angiosarcoma (ASL) and another VC worker with hepatocellular
carcinoma.

Biological markers that have been investigated as indicators for
VC exposure or VC-induced effects include a) excretion of VC
metabolites (e.g., thiodiglycolic acid), b) genetic assays (e.g.,
chromosomal abnormalities or micronucleus assay), c) levels of enzymes
(e.g., in liver function tests), d) serum oncoproteins (p21 and p53)
and/or their antibodies as biomarkers of VC-induced effects.

Children living near landfill sites and other point sources may
be at increased risk based on suggested evidence of early life
sensitivity in animal studies. However, there is no direct evidence in
humans.

In epidemiological studies, a clear dose-response is only evident
for ASL alone or in combination with other liver tumours. Only one
epidemiological study has sufficient data for quantitative
dose-response estimation.

1.8 Effects on other organisms in the laboratory and field

There is a lack of standard toxicity data on the survival and
reproduction of aquatic organisms exposed to VC. Care must be taken
when interpreting the data that are available, as most of it was
generated from tests where the exposure concentration was not measured
and therefore losses due to volatilization were not taken into
account.

The lowest concentration of VC that caused an effect in
microorganisms was 40 mg/litre. This was an EC₅₀ value based upon
inhibition of respiration in anaerobic microorganisms in a batch assay
over 3.5 days.

The lowest concentration that caused an effect in higher
organisms was 210 mg/litre (48-h LC₅₀ for a freshwater fish); with a
corresponding no-observed-adverse-effect concentration (NOAEC) of 128
mg/litre. Effects due to VC have been reported at lower concentrations
in other species, but the ecological significance of these effects was
not verified.

VC concentrations predicted to be non-hazardous to freshwater
fish were calculated to range from 0.088 to 29 mg/litre.

There is a paucity of data concerning the effects of VC on
terrestrial organisms.

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

This monograph deals with vinyl chloride (VC) monomer itself and
is not an evaluation of polyvinyl chloride (PVC), the polymer of VC.

2.1 Identity

Chemical formula: C₂H₃Cl

Chemical structure: H₂C=CHCl

Relative molecular mass: 62.5

Common names: Vinyl chloride

CAS chemical name: Ethene, chloro-

IUPAC name: Chloroethene

CAS Registry 75-01-4
number:

EC Number: 602-023-007

EINECS Number: 2008310

Synonyms: vinyl chloride monomer,
monochloroethene;
monochloroethylene;
1-chloroethylene, chloroethene,
chloroethylene

Purity 99.9% (by weight); water: max.
120 mg/kg; HCl: max. 1 mg/kg
(BUA, 1989)
Up to the 1960s the purity was not
so high (Lester et al., 1963)

Typical trace 10-100 mg/kg range: chloromethane,
components chloroethane; 1-10 mg/kg range:
ethyne
(acetylene), 1,3-butadiene, butene,
1,2-dichloroethane, ethene,
propadiene
(allene), propene, 1-butyne-3-ene
(vinyl acetylene) (BUA, 1989)

2.2 Physical and chemical properties

Some physical properties of VC are given in Table 1. Under
ambient conditions, vinyl chloride is a colourless, flammable gas with
a slightly sweet odour. It is heavier than air and has relatively low
solubility. There are discrepancies in the literature with regard to
Henry's Law constant (air-water partition coefficient, Hc). Whereas
some authors give a value between 1 and 3 kPa.m³/mol, other sources
quote a value two orders higher. Large uncertainties in the absolute
aqueous solubility in older studies probably contribute most to these
discrepancies (Ashworth et al., 1988). It is an azeotrope with water:
0.1 parts water/100 parts vinyl chloride (Bönnighausen, 1986; Rossberg
et al., 1986). VC is soluble in almost all organic solvents.

Since it is a gas that is heavier than air, VC can spread over
the ground creating an exposure long distances away from the original
source and can form explosive mixtures. The odour threshold value is
very subjective (see Table 1) and is far above the present accepted
occupational safety threshold values (see Annex 1).

VC is transported as a compressed liquid. As it does not tend to
polymerize easily, liquid VC (in the absence of oxygen and water) can
be stored and transported without polymerization inhibitors
(Bönnighausen, 1986).

At ambient temperatures in the absence of air, dry purified VC is
highly stable and non-corrosive. Above 450°C, partial decomposition
occurs yielding acetylene, hydrogen chloride and trace amounts of
2-chloro-1,3-butadiene (chloroprene) (Rossberg et al., 1986). This
reaction also occurs by lower temperatures (at 30°C and under) in the
presence of sodium or potassium hydroxide (Bönnighausen, 1986).

Combustion of VC in air produces carbon dioxide and hydrogen
chloride. Under oxygen deficient conditions, traces of phosgene may be
formed (Rossberg et al., 1986). In chlorine-atom-initiated oxidation
of VC, the vinyl chloride peroxide formed decomposes to formaldehyde,
hydrogen chloride and carbon monoxide (Bauer & Sabel, 1975; Sanhueza
et al., 1976).

With air and oxygen, very explosive peroxides can be formed
(Rossberg et al., 1986). There are reports of explosions in vinyl
chloride plants (Terwiesch, 1982). In VC recovery plants there is a
higher chance of explosion, which necessitates continuous monitoring
and limitation of the oxygen content.

Table 1. Some physical and chemical properties of vinyl chloride

Melting point -153.8 °C Bönnighausen (1986);
Dreher (1986)

Boiling point -13.4 °C Bönnighausen (1986);
(at 101.3 kPa) Dreher (1986)

Flash point -78 °C Bönnighausen (1986);
(open cup) Dreher (1986)

Autoignition 472 °C Bönnighausen (1986);
temperature Dreher (1986)

Critical temperature 156 °C Bönnighausen (1986);
Dreher (1986)

Critical pressure 5600 kPa Bönnighausen (1986);
Dreher (1986)

Explosion limits in air 3.8-29.3 vol% Bönnighausen (1986)
in air (20 °C);
4-22 vol% Dreher (1986)

Decomposition 450 °C Bönnighausen (1986)
temperature

Density (20 °C) 0.910 g/cm3 Bönnighausen (1986)

Vapour pressure at -20 °C 78 kPa Dreher (1986)
0 °C 165 kPa
20 °C 333 kPa

Solubility of VC in 0.95 wt% (9.5 g/litre) DeLassus & Schmidt
water; extrapolated over temperature (1981)
from low pressure range
experiments 1.1 g/litre Euro Chlor (1999)
over range 15-85 °C
at 20 °C

Solubility of water 0.02 ml (-20 °C) Bönnighausen (1986)
in 100 g VC 0.08 ml (+20 °C)

Henry's Law Constant 1.96 at 17.5 °C Gossett (1987)
(Hc) (kPa.m³/mol) 2.0-2.8 at 25 °C Ashworth et al. (1988)
18.8 at 20 °C Euro Chlor (1999)

Table 1. (cont'd)

Solubility in organic soluble in most Dreher (1986)
solvents organic liquids and
solvents;
insoluble in lower Bönnighausen (1986)
polyalcohols

log n-octanol/water 1.58 (measured; BUA (1989)
partition coefficient 22 °C)
(log K_ow) 1.36 (calculated) BUA (1989)
1.52 Gossett et al. (1983)

Odour threshold value 26-52 mg/m³ by Hori et al. (1972)
some, but by all at
2600 mg/m³
650 mg/m³ Baretta et al. (1969)
10 700 mg/m³ Patty (1963)

Polymerization reactions to form PVC are the most important
reactions from an industrial view (see section 3.2.1.2).

nH₂C = CHCl -> (- H₂C - CHCl -)_n; Delta H_R = -71.2 kJ/mol

The reaction is exothermic. Addition reactions with other halogens at
the double bond, for instance, to yield 1,1,2-trichloroethane or
1,1-dichloroethane, are also important. Catalytic halogen exchange by
hydrogen fluoride gives vinyl fluoride (Rossberg et al., 1986). In the
presence of water, hydrochloric acid is formed which attacks most
metals and alloys. This hydrolysis probably proceeds via a peroxide
intermediate (Lederer, 1959).

Vinyl chlorine reacts with chlorine to form trichloroethane.
1,1-Dichloroethane is formed from the exothermal reaction of VC with
hydrogen chloride in the presence of iron compounds.

2.3 Conversion factors

1 ppm = 2.59 mg/m³ at 20°C and 101.3 kPa
1 mg/m³ = 0.386 ppm

2.4 Analytical methods

2.4.1 General analytical methods and detection

Stringent regulations for the production, use and handling of
carcinogenic VC have been made in several countries (see Annex 1)
necessitating the usage of reliable methods to detect trace amounts of

this compound in air, water and in PVC articles in such human contact
applications as food packing, medical equipment and potable water
transport.

VC in air has been monitored by trapping it on different
adsorbents, e.g., activated charcoal, molecular sieve and carbotrap.

VC can be removed from adsorbents by liquid or thermal desorption
and analysed by GC fitted with FID, PID or MS detection. In ambient
air measurements, several adsorbents in sieves or refrigerated traps
have been used to increase the efficiency of trapping. In continuous
monitoring of workplace and ambient concentration, IR and GC/FID
analysers can be used.

Direct injection, extraction and more increasingly head space or
purge and trap techniques have been applied for analysis of liquids
and solids. VC can be detected by GC fitted to, for instance, FID,
PID, MS or Hall detectors.

A pre-concentration step and chemical derivatization may increase
sensitivity.

An overview of analytical methods for detecting VC in various
matrices is given in Table 2.

2.4.2 Sample preparation, extraction and analysis for different
matrices

2.4.2.1 Air

Most methods are based on that of Hill et al. (1976a), using
adsorption on activated charcoal, desorption with carbon disulfide and
analysis by GC/FID. Kruschel et al. (1994) used a three-stage carbon
molecular sieve adsorbent cartridge to collect a wide range of
selected polar and non-polar VOCs. After purging with helium prior to
analysis, levels of water and other interfering compounds were reduced
sufficiently to allow cryogenic preconcentration and focusing of the
sample onto the head of the analytical column. VC was detected at
levels below the detection limit of former methods.

Landfill gas monitoring has been carried out by trapping VC on a
molecular sieve, and samples have been analysed using, for instance,
GC/MS (Bruckmann & Mülder, 1982) or GC/ECD with prior conversion to
the 1,2-dibromo derivative (Wittsiepe et al., 1996).

Table 2. Analytical methods^a

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

Air

Expired air collected in 50 ml GC FID 50 ppb Baretta et al. (1969)
pipettes; direct (packed (130 µg/m³)
injection column)

Expired air multistage cryogenic GC FID; MS low ppb low reproducibility; Conkle et al. (1975)
trapping; thermal (packed & cap.) long sampling time
desorption

Expired air 500 ml charcoal tubes GC 0.3 mg/m³ Krajewski & Dobecki
(1978, 1980)

Expired air 1 litre canister; capGC MS n.g. for collecting Pleil & Lindstrom
pressurized with alveolar samples; e.g., (1997)
neutral gas; cryogenic 16 and 25 µg/m³
concentration

Air in car charcoal tube, CS₂ GC FID 10 ppb Going (1976); Hedley
interior desorption (26 µg/m³) et al. (1976)

Ambient air activated charcoal/CS₂ GC FID 2.6 mg/m³ Hill et al. (1976a)

Ambient air silica gel at -78°C, GC FID 2.6 mg/m³ IARC (1978)
thermal desorption

Ambient air activated charcoal GC n.g. 0.5 ppb Dimmick (1981)
column; 24-h sampling (1.3 µg/m³)

Ambient air sampling (1 to 10 HRGC MS 1 ng VOCs Kruschel et al.
litre) on carbon trap; FID (0.3 µg/m³) (1994)
thermal desorption

Table 2. (cont'd)

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

Ambient air solid phase sample capGC IMS 2 mg/m³ new method for Simpson et al.
trap preconcentration field monitoring (1996)

Landfill gas (20 litre) carbon capGC ECD 82 ng/m³ Wittsiepe et al.
molecular sieve; CS₂ (1996)
desorption;
conversion to
1,2,-dibromo
derivative

Tobacco charcoal tube, CS₂ GLC ECD 15 pg per Hoffmann et al.
smoke extraction; injection (1976)
conversion to
1,2,-dibromo
derivative

Workplace CS₂ desorption GC (packed FID 0.04 µg working range NIOSH (1994)
air column) (5 litre 0.4 to 40 mg/m³ (based on Hill
sample) et al., 1976a)

Workplace charcoal sorbent GC (packed FID 5 mg/m³ Kollar et al.
air tube; extraction column) (3 dm³ sample) (1988)
with
nitro-methane

Workplace carbon trap, GC FID 2.6 mg/m³ Hung et al. (1996)
air thermal desorption

Workplace activated charcoal, GC FID 0.1 mg/m³ working range HSE (1987);
air CS₂ desorption 0.07-25 mg/m³ for ASTM (1993)
30-litre samples

Workplace continuous process GC FID n.g. Pau et al. (1988)
air sampling

Table 2. (cont'd)

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

Workplace continuous pyrolysis detection 1 mg/m³ Nakano et al.
air sampling of HCl (1996)

Water

Water purge & trap GC MC n.g. in PVC pipes Dressman &
McFarren (1978)

Water purge & trap GC MS 0.05 µg/litre Schlett &
Pfeifer (1993)

Water headspace capGC MS 1 µg/litre Gryder-Boutet &
Kennish (1988)

Water purge & trap capGC PID-ELCD n.g. modification of US Driscoll et al.
EPA Methods 601 (1987)
& 602 for VOC

Water purge & trap capGC PID-ELCD 0.1 µg/litre VOC Ho (1989)

Water purge & trap; capGC ECD 1.6 ng/litre Wittsiepe et al.
CS₂ desorption; (1990, 1993)
1,2-dibromo
derivatization

Water GC PID and n.g. VCM loss during Soule et al.
Hall laboratory holding (1996)
detector time

Water purge & trap GC FID n.g. VOC Lopez-Avila et
al. (1987a)

Table 2. (cont'd)

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

Water CS₂ desorption; capGC ECD 1.6 ng/litre Wittsiepe et al.
conversion to (1990, 1996)
1,2,-dibromo
derivative

Bottled headspace with GC MS 10 ng/litre Benfenati et al.
drinking- thermal desorption (1991)
water cold-trap
injector (TCT)

Water solid phase capGC FID n.g. Shirey (1995)
micro-extraction MS

Food, liquids, biological fluids and tissues

Liquid headspace GC FID 0.1 ppb Watson et al.
drugs; (1979)
cosmetics

Food; headspace GLC confirmation 10 ppb Williams (1976a)
liquids with MS

Liquids derivatization to GLC ECD 15 µg/litre Williams (1976b)
1-chloro-1,2- (vinegar);
dibromoethane 50 µg/litre oil

Food direct injection GC FID 2-5 µg/kg detection limit UK MAFF (1978)
depends on medium

Food headspace GC FID 1 µg/kg IARC (1978)

Table 2. (cont'd)

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

Oil GC FID 5 µg/litre Rösli et al.
(1975) based on
Williams & Miles
(1975)

Food headspace GC n.g. 2-5 µg/kg UK MAFF (1978)

Intravenous headspace capGC FID 1 µg/litre Arbin et al.
solutions (1983)

Blood (rat) headspace GC FID 5 µg/litre Zuccato et al.
ethanol-water (1979)
extraction

Tissues freezing, GC FID 30 µg/kg Zuccato et al.
(rat) homogenization (1979)
then as above

Urine dry; dissolution GC MS 50 µg/litre TDGA Müller et al.
in methanol; (1979)
methylation with
diazomethane

Urine extraction and GC FID 10 mg/litre TDGA; standard: Draminski &
silylation o-phthalic acid Trojanowska
(1981)

Urine conversion to GC MS < 0.5 TDGA; standard: Pettit (1986)
dibutyl ester µmol/litre pimelic acid

PVC

PVC products charcoal tube, GC FID 10 ppb Going (1976)
CS₂ desorption (26 µg/m³)

Table 2. (cont'd)

Matrix Sampling/preparation Separation Detector Detection Comments References
limit^b

PVC headspace packed column 5 ppb ASTM (1985)
GC

PVC headspace capGC FID update suggestion for Wright et al.
FID-PID ASTM (1985) (1992)

PVC extraction/headspace GC FID 0.1 mg/kg Puschmann (1975);
IARC (1978)

PVC HPLC < 1 ppm for temperatures Kontominas et al.
packaging simulating storage (1985)
of foods conditions (8 to 27 °C)

PVC dynamic headspace GC FID low ppb Poy et al. (1987)
with a sparging and
focusing step
before thermal
desorption

PVC film or GC FID 2.2 ng Gilbert et al.
resin (5 ppb (w/w)) (1975)

Packaging MS 8.7 pg
materials

PVC bags purge/trap GC FID/ECD 0.3 ppb Thomas & Ramstad
(Tenax/charcoal) (1992)

Table 2. (cont'd)

^a Abbreviations: capGC = capillary gas chromatography; ECD = electron capture; ELCD = electrolytic conductivity detector;
FID = flame ionization detector; GC = gas chromatography; GLC = gas-liquid chromatography; HRGL = high-resolution gas
chromatography; IMS = ion mobility spectrometry; MC = microcoulometric titration detector; MS = mass spectrometry;
PID = photoionization detector; SPME = solid-phase microextraction; TDGA = determination of the metabolite, thiodiglycolic
acid; VOC = volatile organic chemical (a general method); n.g. = not given

^b The % recovery was not given in most cases

2.4.2.2 Water

VC is first purged from the water and then collected for GC
analysis by headspace/purge and trap. VC is highly volatile and has a
low specific retention volume on Tenax-GC, the most commonly used
trapping medium in purge/trap analysis. Combination traps such as
Tenax/silica gel/charcoal (Ho, 1989) or Tenax/OV-1/silica (Lopez-Avila
et al., 1987b) have been used. Another approach is to bypass the trap
altogether by purging directly onto a cryocooled capillary column
(Gryder-Boutet & Kennish, 1988; Pankow & Rosen, 1988; Cochran, 1988;
Cochran & Henson, 1988), but here there are complications due to the
need to remove water when stripping from an aqueous solution. A more
recent adaptation of the headspace method uses solid-phase
microextraction (SPME) in which a stationary phase, usually
poly(dimethylsiloxane), coated on a fused-silica fibre is used to
extract aqueous samples in completely filled sealed vials (Shirey,
1995).

It should be noted when measuring VC content in water or
groundwater that samples should be analysed as soon as possible, as
the VC content decreases with holding time (Soule et al., 1996).

2.4.2.3 PVC resins and PVC products

For the quantification of residual VC in PVC, a solid and a
solution approach have been used. The former involves the
equilibration of a solid polymer sample at 90°C in a sealed system,
followed by headspace analysis with single or multiple extraction
(Berens et al., 1975; Kolb, 1982). The solution approach involves the
equilibration of a 10% solution of PVC in dimethylacetamide in a
sealed system, followed by analysis of the headspace gas (Puschmann,
1975). A automatic dynamic headspace method involving a sparging and a
focusing step before desorption into the GC column has been developed
to increase the sensitivity of the solution approach method (Poy et
al., 1987).

2.4.2.4 Food, liquid drug and cosmetic products

For monitoring VC in foods in contact with PVC packaging,
headspace GC is the usual method. Before the levels of VC allowed in
PVC was regulated in the 1970s (see Annex I), many of the VC levels
observed were high enough to be determined by direct injection
methods. Limits of detection are given as 2, 5 and 5 µg/kg for
aqueous, ethanolic, and oleaginous medium respectively using
headspace-GC-FID (UK MAFF, 1978). Williams (1976a,b) reported a
gas-liquid chromatographic method using subsequent GC-MS confirmation,
and a further GC/ECD method requiring derivatization to
1-chloro-1,2-dibromoethane for determination of VC content in liquid
foods.

Methods for VC levels in liquid drug and cosmetic preparations
were described by Watson et al. (1979). A weighed aliquot of the
commercial product in a tightly septum-sealed vial with accurately
known headspace volume is heated to 50°C for 30 min. A portion of the
warm headspace gas is then injected into a GC equipped with FID and a
styrene-divinylbenzene porous polymer column.

2.4.2.5 Biological samples

There are few data on VC analysis in biological tissues. The only
report available was on rat blood and tissues (Zuccato et al., 1979).

2.4.2.6 Human monitoring

Methods for measuring VC concentrations in exhaled air (breath)
have been described (see Table 2) but, although useful for studying
metabolism, they are not well suited for biological monitoring due to
the short half times in the body and the saturable metabolism of VC.

Metabolites of vinyl chloride have been identified in the urine
of rats (Müller et al., 1976; Green & Hathway, 1977) and humans
(Müller et al., 1979) using GC-MS. As there is a strong correlation
between VC exposure in humans and increased excretion of
thiodiglycolic acid (Müller et al. 1978), this metabolite has been
using for monitoring purposes. It is, however, not specific for VC as
certain drugs and other C₂ compounds also have thiodiglycolic acid as
a urinary metabolite (Müller et al., 1979). Since thiodiglycolic acid
is also detected in unexposed subjects (Müller et al., 1979; van
Sittert & de Jong, 1985) and even premature babies (Pettit, 1986),
this approach can only be used to demonstrate high levels of exposure.
A discussion of biological markers for VC exposures and VC-induced
liver cancer is presented in section 8.5.

Thiodiglycolic acid has been determined by dissolving the dried
urine residue in methanol, methylating with diazomethane and analysing
with GC-MS (Müller et al., 1979), analysing the metabolite as its
dibutyl ester by GC-MS using selected ion monitoring (Pettit, 1986),
and by using GC/FID (Draminski & Trojanowska, 1981). Care must be
taken with methods which analyse for VC metabolites, as these
metabolites are not specific to VC.

A specific and sensitive new method has been reported for the
quantification of the VC metabolite N-acetyl- S-(2-hydroxyethyl)
cysteine by exchange solid-phase extraction and isotope dilution
HPLC-tandem mass spectrometry (Barr & Ashley, 1998). This method may
prove useful for monitoring occupational VC exposure, as the detection
limit of 0.68 µg/litre is low enough to detect this metabolite even in
people with no overt exposure to VC, ethylene oxide or ethylene
dibromide.

2.4.2.7 Workplace air monitoring

Before the 1960s, when it was established that VC was a
carcinogenic substance, halogen detectors and explosimeters were used,
non-specific for VC, with detection limits of 518-1295 mg/m³ (200-500
ppm). Gradually more sophisticated techniques became available for
detection of low ppm levels of VC, such as IR analysers, FID, PID
(ECETOC, 1988) and more recently mass spectrometry. In order to check
for leaks or for control measurements during cleaning and repair work,
detector tubes or direct-reading instruments with FID or PID can be
used, although they are not specific for VC and regular calibration is
necessary (Depret & Bindelle, 1998).

Continuous analyses based on, for instance, IR, GC/FID or HCl
detection have been developed (IARC, 1978; Pau et al., 1988; Nakano et
al., 1996). Analysers can be equipped for computerized data logging
and processing. The detection limit of an IR analyser depends on, for
instance, path length and is about 1.3 mg/m³ (IARC, 1978). The
analyser detecting HCl from VC pyrolyzed in a quartz tube was reported
to have a detection limit of 1 mg/m³ when the sampling time was 40
seconds (Nakano et al., 1996).

Breathing zone concentrations can be measured by sampling VC with
portable pumps or diffusion on activated charcoal (Nelms et al., 1977;
Heger et al., 1981; ASTM, 1993; NIOSH, 1994; Du et al., 1996). By
using thermosorption tubes (carbotrap 110-400), detection limits can
be decreased and the use of carbon disulfide in desorption avoided
(Hung et al., 1996).

Passive monitors for occupational personal monitoring of exposure
to VC are commercially available.

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1 Natural occurrence

VC is not known to occur naturally.

3.2 Anthropogenic sources

Anthropogenic sources of VC include the intentional manufacture
of the compound for further processing, primarily to PVC, and
unintentional formation of VC in, for instance, sanitary landfills, as
a degradation product of chlorinated hydrocarbons such as those used
as solvents, and the subsequent presence of VC in emitted gases and
groundwater. VC is also found in tobacco smoke.

3.2.1 Production levels and processes

VC was first synthesized by Regnault in 1835. It was not until
the 1930s that techniques were devised to polymerize VC into stable
forms of PVC.

VC production methods were altered in 1974 in many countries
after the confirmation that VC was a human carcinogen. Manufacturers
developed closed production methods to reduce exposure of the
workforce.

Annual total world production of VC, which is approximately equal
to PVC production, was about 17 million tonnes in 1985 and over 26
million tonnes in 1995 (see Table 3). More than half the world's
capacity (64%) in 1985 was concentrated in Western Europe and the USA.
Since that time many new VC/PVC plants have been opened or are under
construction in SE Asia, Eastern Europe, the Indian subcontinent and
developing and oil-producing countries. Thus there has been a
geographical shift of VC/PVC production.

The leading producers of PVC and therefore also of VC are the
USA, Japan, Germany, France and SE Asian countries such as Taiwan and
China (CHEM-FACTS, 1992). The capacity has only increased moderately
in the USA and Western Europe in recent years. Significant increases
in production have been reported for Japan and Taiwan. All the
countries of Eastern Europe have PVC plants and have exported PVC to
Western European countries. The PVC capacity and imports and exports
for each country are given in CHEM-FACTS (1992).

VC is produced in Western Europe by 14 companies. The plants are
in Belgium (3 plants), France (3 plants), Germany (8 plants), Italy (4
plants), the Netherlands (1 plant), Spain (2 plants), Sweden (2
plants), United Kingdom (1 plant) (Euro Chlor, 1999).

Table 3. World PVC (and therefore VC) production/capacity 1980-1998

Region Production/capacity in 1000 tonnes/year

1980^a 1985^a 1990^a 1995^b 1998^c

World capacity 16 000 17 000 20 700 26 400 approx. 27 000
World production 11 750 14 200 18 300

North America total 3200 3390 4700 6070
Suspension and mass 2810 2990
Vinyl acetate copolymer 200 210
Emulsion 190 190

Western Europe total 3900 4330 4800 5750 approx. 5600
Suspension and mass 33 350 3700
Vinyl acetate copolymer 130 130
Emulsion 420 500

Eastern Europe 925 1100 1200 2700^d
Former Soviet Union 370 700 760

China 150 400 790
Japan 1400 1550 2070 8200^e
SE Asia 330 600 900

South America 400 540 780
Rest of the world 1075 1590 2300 3680

^a Allsopp & Vianello (1992)
^b Rehm & Werner (1996)
^c Although exact figures are not available, an increase in world production
was seen in 1998 but no great increase in Western Europe (personal
communication, European Council of Vinyl Manufacturers, 1999)
^d Including former Soviet Republics
^e Total Asia

The manufacture of VC/PVC is one of the largest consumers of
chlorine.

3.2.1.1 Production of VC

VC is produced industrially by two main reactions, the first is
hydrochlorination of acetylene, which proceeds via the following
reaction:

C₂H₂ + HCl -> CH₂=CHCl

This route was used in the past when acetylene, produced via calcium
carbide from coal, was one of the important basic feedstocks for the
chemical industry (Rossberg et al., 1986). Today all USA and most
Western European manufacturers use the "balanced process" described
below. However, many Eastern European countries such as Poland and the
countries of the former Soviet Union still use acetylene to
manufacture VC because of relatively cheap raw materials such as
calcium carbide and natural gas. Mercury has been used as a catalyst,
although a new catalyst has now been developed in Russia, based on
platinum metal salts instead of mercury, which has increased yields
with acetylene conversion from 95 to 99% (Randall, 1994).

The second major production process involves thermal cracking
[reaction iii] (at about 500°C) of 1,2-dichloroethane (EDC), produced
by direct chlorination [reaction i] of ethylene or oxychlorination
[reaction ii] of ethylene in the "balanced process".

[i] CH₂=CH₂ + Cl₂ -> Cl CH₂-CH₂ Cl

[ii] CH₂=CH₂ + 2 HCl + 5 O₂ -> Cl CH₂-CH₂ Cl + H₂O

[iii] Cl CH₂-CH₂ Cl -> CH₂=CHCl + HCl

After the cracking (pyrolysis), HCl and unconverted EDC are separated
from VC by two steps of distillation and recycled. The VC is stored
either under pressure at ambient temperature or refrigerated at
approximately atmospheric pressure (European Council of Vinyl
Manufacturers, 1994). More than 90% of the VC produced today is based
on this route (Rossberg et al., 1986; Allsopp & Vianello, 1992).

Other methods of industrial production include:

a) VC from crack gases, where unpurified acetylene and ethylene are
chlorinated together, acetylene being first chlorinated to
1,2-dichloroethane.

b) VC from ethane, which is readily available in some countries. The
major drawback is that ethane must first be functionalized by
substitution reactions giving rise to a variety of side chain
reactions and therefore the reaction must be kinetically
controlled to obtain maximal VC yield.

3.2.1.2 Production of PVC from VC

Many PVC plants are fully integrated beginning with ethylene and
chlorine (or sodium chloride).

VC is a gas at ambient temperatures but is handled as a
compressed volatile liquid in all polymerization operations. PVC
polymerization reactors are thick-walled jacketed steel vessels with a
pressure rating of 1725 kPa. The polymerization of VC is strongly
exothermic. The explosive limits of VC in air are 4-22 vol%, and the
plant must be designed and operated with this in mind, particularly
when handling unreacted VC in the recovery system (Allsopp & Vianello,
1992).

Three main processes are used for the commercial production of
PVC: suspension (providing 80% of world production), emulsion (12%)
and mass or bulk (8%). In Western Europe, the proportion of PVC
produced by the different processes is: 80% suspension; 13% mass; 5%
emulsion and 2% copolymers (Wrede, 1995).

In the suspension (also called dispersion) process,
polymerization takes place at 40-70°C (depending on the type of PVC
being produced) in a reactor (autoclave) of 25-150 m³ capacity fitted
with a jacket and/or condenser for heat removal, as the reaction is
strongly exothermic. Precautions have to be taken in order to avoid
explosive mixtures with air. Liquid VC under its autogenous vapour
pressure is dispersed in water by vigorous stirring to form droplets
of average diameter 30-40 µm. The polymerization takes place within
these droplets and is started by addition of initiators dissolved in
the monomer. Stabilizers are added to prevent the drops rejoining and
to prevent the already polymerized PVC particles from agglomerating.
The reaction conditions can be exactly controlled and the properties
of the product, such as relative molecular mass, can be controlled
exactly. Once polymerization has ended, the autoclave charge is
emptied into degassing tanks, and the non-polymerized VC is degassed,
compressed and stored for reuse (ECETOC, 1988; Allsopp & Vianello,
1992).

During the polymerization process, the PVC is dispersed in the
aqueous phase and it cannot be prevented that a film of PVC forms on
the inside wall of the reactor. This film interferes with the transfer
of heat between the reactor and contents, and the process has to be
interrupted periodically to allow the reactor to be cleaned. The
autoclave, after being emptied, is opened, rinsed and washed either
with solvents or more usually by means of automatic high-pressure jets
(ECETOC, 1988). The latest development in this area is the use of
proprietary build-up suppressants, which are applied before every PVC
batch. After each batch, low pressure rinse with water can remove
loose polymers and the batch cycle is ready to restart. The reactor
needs then to be opened for a thorough cleaning only after 500 or more
batches (Randall, 1994).

Before awareness of the toxicity of VC, it was the autoclave
cleaning personnel who were primarily highly exposed to the compound.
In the past autoclaves were cleaned manually; the inside had to be
scraped with a spatula, or sometimes hammer and chisel to remove the
encrusted polymer adhering to the walls of the vessel and mixing
devices. Lumps of polymer often released monomer when broken,
resulting in high concentrations of VC in the autoclave. Before about
1970, it was usual to check that the level was below 1036 mg/m³ (400
ppm), i.e. two orders of magnitude below the lower explosion limit of
VC. Occupational exposure limits are now 18 mg/m³ (7 ppm) or less
(see Annex I). Further details of workplaces with a former high
exposure to VC are given in section 5.3 and Jones (1981).

Once polymerization has ended, the polymerization batch is
transferred to the stripping unit and then to the slurry tank. The
slurry is a suspension of PVC in water that has to be permanently
stirred; it is then dewatered in a centrifuge decanter and dried. The
resulting dried powder is either stored in silos or bagged. PVC is
then further processed into ready-to-use resins (Depret & Bindelle,
1998).

3.2.1.3 PVC products

PVC is a polymer of VC with 700-1500 monomeric units. It is
relatively inexpensive and is used in a wide range of applications.
PVC is a generic name. Each producer makes a range of PVC polymers,
which vary in morphology and in molecular mass according to the
intended use. PVC resins are rarely used alone but can be mixed with
heat stabilizers, e.g., lead, zinc and tin compounds (Allsopp &
Vianello, 1992), lubricants, plasticizers (e.g., diethylhexyl
phthalate) fillers and other additives, all of which can
influence its physical and mechanical properties (Williamson &
Kavanagh, 1987; Allsopp & Vianello, 1992). Such additives may
constitute up to 60% of the total weight in some finished PVC plastics
(Froneberg et al., 1982). These plastics are formed into a multitude
of consumer products by extrusion, thermoprocessing and rotational
moulding, and into rigid or flexible film by extrusion or calendering.

PVC accounts for 20% of plastic material usage and is used in
most industrial sectors (ECETOC, 1988; European Council of Vinyl
Manufacturers, 1994).

* Packaging

* bottles (produced by blow-moulding) for containing liquid
foods, beverages, cooking oils, vinegar, etc.

* rigid film (calendered or extruded) which is converted into
tubes and shaped containers by subsequent vacuum or
pressure-forming for packaging of various foodstuffs

* flexible film (made by blowing or calendering) for wrapping
solid foods such as cheese, meat, vegetables, fresh fruit,
etc.

* coatings in metal cans

* Building - floor coverings, wall coverings, windows, roller
shutters, piping; 58% of the water supply network and 80% of the
waste water disposal systems in Europe use pipes and fittings
made from PVC.

* Electrical appliances - wires and cables insulation

* Medical care - equipment such as blood bags and gloves;
pharmaceutical and cosmetic packaging. Worldwide, more than 25%
of all plastic-based medical devices used in hospitals are made
from PVC (Hansen, 1991)

* Agriculture - piping; drainage; tubing in dairy industry

* Automobiles - car dash boards and lateral trimming

* Toys

At present, the largest use of PVC is in the building sector
(Rehm & Werner, 1996).

3.2.2 Emissions from VC/PVC plants

3.2.2.1 Sources of emission during the production of VC

Process waste, by-products and unreacted material from a balanced
process and from a PVC plant include (Randall, 1994): a) light/heavy
ends from EDC purification (from direct chlorination and
oxychlorination reactors); b) heavy ends from VC purification (from
pyrolysis reactor); c) pyrolysis coke/tars (from thermal reactions in
the pyrolysis reactor); d) spent catalyst (from direct chlorination,
oxychlorination); e) recovery of unreacted VC (from PVC reactor); f)
offspec batches (from PVC reactor); g) aqueous streams (from EDC
washing, vent scrubbing, oxychlorination water; from centrifuge, VC
stripping, slurry tanks); h) vent gases (from distillation columns,
flash drums, reactor vents, storage tanks, vessel openings; from VC
recovery systems, dryer stacks, centrifuge vent, blending, storage
facilities); i) spills and leaks (sampling, pumps, flanges, pipes,
loading/unloading, valves; bag filling, agitator seals); and j)
equipment cleaning (tanks, towers, heat exchangers, piping; PVC
reactor, product dryer, recovery system).

a) Strategies for minimizing emissions

During the sixties, some control of exposure levels was
introduced resulting in an important decrease of estimated ambient
levels of VC.

In the 1970s, efforts were focused on controlling emissions at
the most significant emission points: reactors, filters and storage
tanks. Elementary modifications of equipment, room and local
ventilation by fans, provisional operation procedures, etc., enabled
the reduction of exposure levels in working areas.

Technical developments have achieved further reductions:

* removal of residual VC from the PVC suspension by stripping
between polymerization and drying with a flow of steam or in
closed-loop systems;

* appropriate collection of residual vents to thermal oxidizers or
other abatement systems;

* reduction of all sources of fugitive emission by maintenance and
upgraded equipment;

* high pressure internal cleaning of the autoclaves to remove PVC
crusts;

* intensive removal of VC before opening or a closed process
design.

Appropriate working procedures, personnel awareness and high
standard equipment, associated with good maintenance practices, are
the recommended ways to reduce fugitive emission to very low levels
(Depret & Bindelle, 1998).

b) Disposal of by-products

The main waste streams of EDC/VC production process in Europe are
light ends (gases: VC, EDC, HCl, ethylene, dioxins; aqueous effluents:
EDC, copper, dioxins) and heavy ends (viscous tars). According to the
PVC Information Council the total amount produced is approximately
0.03 tonnes of by-products per tonne of VC produced (European Council
of Vinyl Manufacturers, 1994). The fractions are either used as
feedstocks for other processes or combusted under controlled
conditions (> 900°C) or by catalytic oxidation to produce CO₂, CO,
HCl and water which can be recycled (see above). Exit gases should be
treated using HCl absorbers and gas scrubbers. Spent catalyst, metal
sludges and coke from EDC cracking should be disposed of in controlled
hazardous waste dumps (HWD) or incinerated under controlled
conditions. Sludges from effluent purification should be either
combusted under controlled conditions or deposited in HWD (European
Council of Vinyl Manufacturers, 1994).

3.2.2.2 Emission of VC and dioxins from VC/PVC plants during
production

a) VC

An estimated 550 tonnes of VC was released into air, 451 kg to
water and 1554 kg to soil from manufacturing and processing facilities
in the USA in 1992, although this was not an exhaustive list (ATSDR,
1997). From a VC capacity of 6 200 000 tonnes, an average emission of
80 g/tonne can be calculated (Depret & Bindelle, 1998).

Euro Chlor (1999) reported emissions of VC from suspension PVC
plants in Europe to be 448 tonnes/year, 22 tonnes/year being released
in waste water. An estimated emission value of 300 tonnes VC/year was
provided by German producers (BUA, 1989), i.e., about 55 g VC/tonne
PVC. Total VC emissions in England and Wales were reported to be
3800 tonnes in 1993 and 18 990 tonnes in 1994 (HMIP, 1996).

An estimated 200 000 tonnes of VC was released into the worldwide
atmosphere during 1982 (based on a worldwide PVC production of
17 million tonnes), i.e., 12 kg/tonne of PVC produced (Hartmans et
al., 1985). In 1974, a VC emission of 0.5 kg/tonne PVC was estimated
(Kopetz et al., 1986).

b) Dioxins

PCDDs/PCDFs, some of which are classified as human carcinogens
(IARC, 1997), are formed during EDC/VC production. Concentrations in
VC distillation residues (PU4043) (probably "heavy ends") for two
production factories were 3192 and 5602 ng ITEQ (international toxic
equivalent)/kg, which was estimated to be 12 to 30 g of dioxin/year at
a production level of 200 000 tonnes VC/year in heavy ends (Stringer
et al., 1995). However, the VC/PVC industry argues that, although
dioxins may be found in production wastes, these are incinerated and
are not ultimately emitted to the environment (Fairley, 1997), at
least in those countries where waste streams are regulated (not all
countries possess such high standards of waste incineration). Some
companies do not incinerate their waste products but dispose of them
in other ways, e.g., deep-well injection (Stringer et al., 1995).

Wastewater from VC production can also be contaminated with
PCDDs/PCDFs, in particular if they contain suspended solids.
Installation of filtration devices should lower solid levels and
subsequently PCDD/PCDF emissions (Stringer et al., 1995). Using such
filtration devices, PCDD/PCDF concentrations in wastewater from
EDC/VC/PVC facilities in the USA ranged from not detectable to 6.7
pg/litre TEQ (Carroll et al., 1996).

Annual global emission of dioxins into the environment from
EDC/VC manufacture has been estimated to be 0.002-0.09 kg TEQ by the
European PVC industry but 1.8 kg by Greenpeace (Miller, 1993).

Virgin suspension PVC resin from 11 major production sites in
Europe was found not to contain any process-generated PCDDs/PCDFs at
concentrations above the limits of quantification (2 ppt) (Wagenaar et
al., 1998).

3.2.3 Accidental releases of VC

3.2.3.1 PVC plant and transport accidents

An explosion occurred at a VC recovery plant in 1978 in Germany,
which was set off by vinyl chloride peroxides (Terwiesch, 1982; see
also section 2.2).

A freight train with 12 tank cars of VC was derailed in McGregor,
Manitoba, Canada in March, 1980 under near-blizzard conditions and
-20°C and two of the tanks released VC (Charlton et al., 1983). One
car lost 47 500 litres in the first hour and the other car lost
23 100 litres at an initial rate of 1400 litres/hour, decreasing to
45 litres/hour after 31 h. In the first 15 min, 5680 litres of VC
vapourized by free surface evaporation; thereafter only 2.5% of the
discharging liquid evaporated rapidly. The remaining liquid in the
snow bank was assumed to have evaporated at a rate of 15% per hour,
leaving about 900 litres of VC in the snow bank after 36 h. Although
there was an explosion hazard, no fire occurred.

Two incidences, in 1988 and 1996, occurred in Germany involving
accidental release of VC due to derailment of trains transporting the
liquid substance (Neuhoff, 1988; Anon, 1996). Both accidents were
followed by explosion and fire. Derailment of a goods train occurred
1 km from Schönebeck (near Magdeburg in Germany) and the subsequent
explosion and fire produced a 600- to 800-m black column of smoke. In
all, 1044 tonnes of VC were involved of which 261 tonnes burnt and
350 tonnes could be reclaimed after the fire; 153 tonnes of HCl were
released. Median measurements of the numerous air samples taken at the
place of accident or surroundings did not exceed the German technical
guidance level of 5 vol ppm, although these were not taken until 14 h
after the fire. Maximum concentrations of VC measured were 78 mg/m³
(30 ppm) near the train and 26 mg/m³ (10 ppm) at a distance of 200 m
from the centre of the fire (Hahn et al., 1998). Levels in nearby
industrial sewage pipes were up to 1250 ppm (Anon, 1996). A cytogenic
analysis was carried out on some of the general population exposed to
VC from this accident (Hüttner & Nikolova, 1998; see section 8.1 and
Table 42).

3.2.3.2 Leakage and discharge from VC/PVC plants

Leakage from a waste liquor basin of a VC/PVC plant in Finland
caused high concentrations of VC and dichloroethene in groundwater in
1974. Concentrations of up to 484 mg/litre of the chlorocarbons were
measured in groundwater in the mid-1980s (Nystén, 1988).

It should be noted that in the 1960s and before, when the
toxicity of VC was not known, large amounts of PVC production sludges
containing VC were dumped onto landfills (and possibly still are in
countries where there are no adequate restrictions).

3.2.4 VC residues in virgin PVC resin and products

3.2.4.1 VC residues in different PVC samples

VC is not soluble in PVC nor is it absorbed or adsorbed in the
resin particle. It is entrapped and can escape to the ambient air
(Wheeler, 1981). PVC in a bulk-container loses its residual monomer at
a rate of 25 to 50% per month. Heating tends to accelerate this step,
but when the residual monomer has disappeared PVC is not a significant
source of VC.

Since the 1970s when VC was confirmed as a human carcinogen, it
has been mandatory in many countries to "degas" PVC after
polymerization (see section 3.3.1) and before further processing.
There are limit values for VC content in PVC (see Annex I). For
example, in 1974 raw PVC usually contained more than 1000 ppm of
residual VC. This was subsequently reduced to 10 ppm by regulation
(German Environmental Office, 1978). In a survey of 45 samples of raw
PVC from various countries carried out in 1976-1977, over a third had
VC residues of > 1 ppm, but a third had residues of over 50 ppm, with
4 samples over 200 ppm. The samples with the highest residue level
came from Hungary, Rumania, Italy and the USA (German Environmental
Office, 1978).

3.2.4.2 VC residues in PVC products

In a survey of PVC products carried out in 1976-1977, the
following indoor artic