IPCS INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
Health and Safety Guide No. 109
VINYL CHLORIDE
UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION
IPCS
Health and Safety Guide No. 109
VINYL CHLORIDE HEALTH AND SAFETY GUIDE
This is a companion volume to Environmental Health Criteria 215:
Vinyl chloride
Published by the World Health Organization for the International
Programme on Chemical Safety (a collaborative programme 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
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.
WHO Library Cataloguing in Publication Data
Vinyl chloride: health and safety guide.
(Health and safety guide ; no. 109)
1.Vinyl chloride - toxicity 2.Environmental exposure
3.Occupational exposure 4.Guidelines
I.International Programme on Chemical Safety II.Series
ISBN 92 4 151109 5 (NLM Classification: QV 633)
ISSN 0259-7268
The World Health Organization welcomes requests for permission to
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Applications and enquiries should be addressed to the Office of
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(c) World Health Organization 1999
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CONTENTS
INTRODUCTION
1. PRODUCT IDENTITY AND USES
1.1. Identity
1.2. Physical and chemical properties
1.3. Conversion factors
1.4. Analytical methods
1.5. Production and uses
2. SUMMARY AND EVALUATION
2.1. Exposure
2.1.1. General population
2.1.2. Occupational exposure
2.2. Uptake, metabolism and excretion
2.3. Effects on organisms in the environment
2.4. Effects on experimental animals and in vitro test systems
2.5. Effects on humans
3. RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH
3.1. Public health
3.2. Occupational health
4. HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY ACTION
4.1. Human health hazards, prevention and
protection, first aid
4.1.1. Information for physicians
4.1.1.1 Signs and symptoms of exposure
4.1.1.2 First aid
4.1.1.3 Medical treatment
4.1.1.4 Effects of chronic exposure
4.1.2. Health surveillance advice
4.1.2.1 Initial medical screening
4.1.2.2 Periodic medical examination
4.1.3. Prevention and protection
4.2. Explosion and fire hazards
4.2.1. Explosion hazards
4.2.2. Fire hazards
4.3. Handling and storage
4.4. Spillage
5. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION
6. SUMMARY OF CHEMICAL SAFETY INFORMATION
7. CURRENT REGULATIONS, GUIDELINES AND
STANDARDS
7.1. Previous evaluations by international bodies
7.2. Occupational exposure limit values
7.3. Labelling, packaging and transport
7.4. Waste disposal
BIBLIOGRAPHY
INTRODUCTION
The Environmental Health Criteria (EHC) monographs produced by the
International Programme on Chemical Safety include an assessment of
the effects on the environment and on human health of exposure to a
chemical or combination of chemicals, or physical or biological
agents. They also provide guidelines for setting exposure limits.
The purpose of a Health and Safety Guide is to facilitate the
application of these guidelines in national chemical safety
programmes. The first three sections of a Health and Safety Guide
highlight the relevant technical information in the corresponding EHC.
Section 4 includes advice on preventive and protective measures and
emergency action; health workers should be thoroughly familiar with
the medical information to ensure that they can act efficiently in an
emergency. Within the Guide is a Summary of Chemical Safety
Information which should be readily available, and should be clearly
explained, to all who could come into contact with the chemical. The
section on regulatory information has been extracted from the legal
file of the International Register of Potentially Toxic Chemicals
(IRPTC) and from other United Nations sources.
The target readership includes occupational health services, those in
ministries, governmental agencies, industry, and trade unions who are
involved in the safe use of chemicals and the avoidance of
environmental health hazards, and those wanting more information on
this topic. An attempt has been made to use only terms that will be
familiar to the intended user. However, sections 1 and 2 inevitably
contain some technical terms. A bibliography has been included for
readers who require further background information.
Revision of the information in this Guide will take place in due
course, and the eventual aim is to use standardized terminology.
Comments on any difficulties encountered in using the Guide would be
very helpful and should be addressed to:
The Director
International Programme on Chemical Safety
World Health Organization
1211 Geneva 27
Switzerland
THE INFORMATION IN THIS GUIDE SHOULD BE CONSIDERED AS A STARTING
POINT TO A COMPREHENSIVE HEALTH AND SAFETY PROGRAMME
1. PRODUCT IDENTITY AND USES
1.1 Identity
CAS/IUPAC name Chloroethene
Chemical formula: C2H3Cl
Chemical structure: H2C=CHCl
Common synonyms: Vinyl chloride, VC, VCM, 1-chloroethylene
CAS registry number: 75-01-4
EC number: 602-023-007
EINECS number: 2008310
RTECS registry number: KU9625000
UN transport number 1086 (inhibited)
1.2 Physical and chemical properties
At ambient temperature, vinyl chloride (VC) is a colourless,
compress liquefied flammable gas. It has a slightly sweet odour but
the odour threshold value is very subjective and is far above the
present accepted occupational safety threshold values. VC is heavier
than air. It has relatively low solubility in water but is soluble in
almost all organic solvents. With air, very explosive peroxides can be
formed. Combustion of VC in air produces hydrogen chloride. At ambient
temperatures in the absence of air, dry purified VC is highly stable
and non-corrosive.
Other physical and chemical properties of vinyl chloride are
given in the Summary of Chemical Safety Information (section 6).
1.3 Conversion factors
1 ppm = 2.59 mg/m3 at 20°C and 101.3 kPa
1 mg/m3 = 0.386 ppm
1.4 Analytical methods
The concentration of VC in air can be monitored by trapping it on
adsorbents and, after liquid or thermal desorption, analysis by gas
chromatography (GC). 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, flame
ionization detection (FID) or photo-ionization detection (PID). For
continuous monitoring, infrared and GC/FID analysers combined with
data logging and processing have been used, whereas, for 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 mass spectrometry detectors.
1.5 Production and uses
VC is produced industrially by two main reactions: 1) the
hydrochlorination of acetylene; 2) the thermal cracking (at about
500°C) of 1,2-dichloroethane produced by direct chlorination (ethylene
and chlorine) or oxychlorination (ethylene, HCl and air/O2) of
ethylene in the "balanced process". The latter process is most
commonly used nowadays.
About 95% of the world production of VC is used for the
production of polyvinyl chloride (PVC, where n = 700-1500) and the
manufacture of co-polymers with monomers such as vinyl acetate or
vinylidene chloride. The remainder goes into the production of
chlorinated solvents, primarily 1,1,1-trichloroethane (10 000
tonnes/year). The world production of PVC (and therefore VC) in 1998
was about 27 million tonnes. PVC accounts for 20% of plastic material
usage and is used in most industrial sectors.
2. SUMMARY AND EVALUATION
2.1 Exposure
2.1.1 General population
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.
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.
In the majority of drinking-water samples analysed in the past,
VC was not present at detectable concentrations. The maximum VC
concentration reported in finished drinking-water was 10 µg/litre.
Although there is a lack of recent data on VC concentrations in
drinking-water, 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
body weight per day was estimated for the late 1970s and early 1980s.
An early study identified VC in tobacco smoke at the ng/cigarette
range.
The few data available show that VC can be present in the tissues
of small aquatic invertebrates and fish.
2.1.2 Occupational exposure
The main route of occupational exposure is via inhalation and
occurs primarily in VC/PVC plants. Occupational exposure to VC
amounted to several thousands of mg/m3 in the 1940s and 1950s and
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.
2.2 Uptake, metabolism and excretion
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.
The main route of metabolism of VC involves oxidation by
cytochrome P-450 (CYP2E1) to form chloroethylene oxide (CEO), a highly
reactive epoxide which rapidly rearranges to form chloroacetaldehyde
(CAA). The primary detoxification reaction of these two reactive
metabolites is conjugation with glutathione catalysed by glutathione
S-transferase. The conjugation products are further modified to
substituted cysteine derivatives and excreted via urine, and the CO2
generated is exhaled.
After exposure to low doses, VC is metabolically eliminated and
nonvolatile metabolites are excreted mainly in the urine. After
exposure by inhalation, the metabolic elimination velocity is lower in
humans than in laboratory animals on a body weight basis. However, on
a body surface area basis, the metabolic clearance of VC in humans is
comparable to that of other mammalian species. With increasing oral or
inhalation exposure, the major route of excretion in animals is
exhalation of unchanged VC, indicating the saturation of metabolic
pathways. Independently of applied dose, the excretion of metabolites
via faeces is only a minor route.
With regard to carcinogenicity, CEO is thought to be the most
important metabolite of VC. CEO reacts with DNA to produce
promutagenic exocyclic etheno adducts.
2.3 Effects on organisms in the environment
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.
2.4 Effects on experimental animals and in vitro test systems
VC appears to be of low acute toxicity when administered to
various species by inhalation. The 2-h LC50 values for rat, mouse,
guinea-pig and rabbit were reported to be 390 000, 293 000, 595 000
and 295 000 mg/m3, respectively. VC has a narcotic effect after
inhalative administration. In rats, mice and hamsters, death by
respiratory failure was preceded by increased motor activity, ataxia
and convulsions. In dogs, severe cardiac arrythmias occurred after
inhalative exposure to 260 000 mg/m3. After acute inhalative 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.
In various species, the main target organ for short-term (up to 6
months) inhalation toxicity of VC is 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 inhalation exposure to VC resulted in increased
mortality in some strains of rats at a dose as low as 260 mg/m3, in
mice at 130 mg/m3 and in hamsters at 520 mg/m3. 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.
Long-term feeding studies showed increased mortality, increased
liver weights and morphological alteration of the liver. In rats,
liver cell polymorphism (variation in size and shape of hepatocytes
and their nuclei) could be seen at levels as low as 1.3 mg/kg body
weight, and the NOAEL was 0.13 mg/kg body weight.
Long-term feeding studies in rats with VC in PVC granules yielded
significantly increased incidences of angiosarcoma of the liver (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 was
similar to that observed in rats, but an increase in lung tumours was
only observed in mice. In hamsters, increased incidences of ASL,
mammary gland and acoustic duct tumours, melanomas, stomach and skin
epithelial tumours were 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 Salmonella
typhimurium strains TA100, TA1530 and TA1535 but not in TA98, TA1537
or TA1538, indicating mutations as a result of base-pair substitution
rather than frameshift mutations.
Other gene mutation assays in bacteria, yeast cells, plant
(Tradescantia) cuttings and mammalian cells have revealed positive
results in the presence of metabolic activation. VC induced gene
conversion in Saccharomyces cerevisiae, unscheduled DNA synthesis in
rat hepatocytes and sister-chromatid exchanges (SCE) in human
lymphocytes in the presence of a metabolic activation system. Cell
transformation assays revealed positive results with and without
metabolic activation.
VC exposure induced gene mutation and mitotic recombination in
Drosophila melanogaster but not gene mutations in mammalian germ
cells in vivo. VC showed clastogenic effects in rodents, increased
SCE in hamsters and induced DNA breaks in mice. VC also induced gene
conversion and forward mutations in yeast in host-mediated assays in
rats.
2.5 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 sister-chromatid
exchanges (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
liver angiosarcoma from highly exposed autoclave workers and in
hepatocellular carcinoma from another exposed worker.
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.
Children living near landfill sites and other point sources may
be at increased risk based on suggestive evidence of early
life-sensitivity in animal studies. However, there is no direct
evidence in humans.
In epidemiological studies, a clear dose-response relationship 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.
3. RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH
3.1 Public health
The following measures should be taken:
* worldwide application of production technologies leading to low
residual VC levels in PVC;
* implementation and enforcement worldwide of steps that guarantee
minimal emissions of VC at production sites;
* identification, surveillance and emission and exposure control of
contaminated areas such as landfill sites.
3.2 Occupational health
Since VC is a genotoxic carcinogen, exposures should be kept as
low as possible, using the best available technology worldwide.
More information, education and training of workers potentially
exposed to VC regarding the risks involved and safe working procedures
and habits is required.
Monitoring and record-keeping of exposure and record-keeping of
exposed workers are needed.
4. HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY
ACTION
4.1 Human health hazards, prevention and protection, first aid
4.1.1 Information for physicians
4.1.1.1 Signs and symptoms of exposure
Exposure to levels of VC above 25 900 mg/m3 (10 000 ppm) causes
acute effects on the central nervous system, e.g., dizziness,
disorientation and narcosis, and higher concentrations in air may
prove fatal.
4.1.1.2 First aid
a) Eye contact
Immediately flush with large amounts of water for at least 15
min, occasionally lifting upper and lower lids. Seek medical attention
immediately. VC is stored under pressure; exposure to escaping gas may
cause frostbite.
b) Skin contact
Quickly remove victim from source of contamination and
flush/immerse affected part in warm water. Seek medical attention.
Exposure to escaping compress liquefied gas may cause frostbite.
c) Breathing
Remove the person from exposure.
Begin artificial respiration if breathing has stopped and
cardio-pulmonary resuscitation if heart action has stopped.
Transfer immediately to a medical facility.
4.1.1.3 Medical treatment
In case of intoxication the treatment is supportive. Death may
result from central nervous system depression and/or cardiac
arrhythmia.
4.1.1.4 Effects of chronic exposure
Chronic health effects observed after exposure to high levels of
VC monomer gas are angiosarcoma of the liver and obstructive disease
of peripheral arteries, which may appear as Raynaud's phenomenon,
scleroderma-like disease or acro-osteolysis.
Possible other effects at similar levels of exposure include
tumours of the brain and hepatocellular carcinoma.
VC may also cause liver toxicity.
4.1.2 Health surveillance advice
4.1.2.1 Initial medical screening
Liver function tests form the basis of initial medical screening.
4.1.2.2 Periodic medical examination
The primary method of prevention is by monitoring of exposure.
When low levels of exposure cannot be guaranteed, medical screening
may be useful. It should be directed towards assessment of the
peripheral vascular system and the function of the liver.
Ad hoc cytogenetic studies can be performed.
4.1.3 Prevention and protection
VC is a human carcinogen. There may be no safe level of exposure,
so all contact should be reduced to the lowest possible level. Odour
is an inadequate warning of excessive exposure.
Engineering controls are the most effective way of reducing
exposure. The best protection is to enclose operations and provide
local exhaust ventilation at the site of chemical release.
Protective clothing and, where necessary, an approved
air-purifying respirator should be used. When the level of exposure is
not known or the airborne exposure guidelines may be exceeded, an
approved positive-pressure breathing apparatus should be used. Safety
glasses should be worn.
A pit or tank must never be entered without adhering to the
following safety procedures: never alone, always with a lifeline, and
always with a positive pressure supply of fresh air.
Continuous exposure monitoring and record keeping is necessary.
4.2 Explosion and fire hazards
4.2.1 Explosion hazards
VC forms explosive mixtures with air. It can also form
shock-sensitive peroxides on exposure to air.
Heat and contact with oxidizing agents, oxygen, air, sunlight and
other polymerization catalysts must be avoided.
VC vapour polymerizes in the presence of air and may block
ventilation systems, leading to a risk of explosion and/or fire
hazard.
4.2.2 Fire hazards
VC is a highly flammable liquid or gas and a dangerous fire
hazard. Hazardous decomposition products (hydrogen chloride, phosgene
and others) are formed on complete or incomplete combustion.
A fire involving VC should be controlled with alcohol foam, dry
chemical or carbon dioxide. Water must not be used.
Containers may explode in case of fire. Water spray should be
used to keep fire-exposed containers cool.
4.3 Handling and storage
VC should be stored in cool well-ventilated areas, out of direct
sunlight. It is usually stored under pressure and handled as a liquid.
It must be kept away from sparks, flames and other ignition sources.
VC vapour is heavier than air and will tend to collect in low
areas. It should not be used in confined spaces.
4.4 Spillage
Leaks should be stopped as soon as possible. All sources of
ignition must be eliminated. VC vapour can travel to an ignition
source and flash back causing a flash fire. Because of the explosive
hazard, fire at a leak must not be extinguished unless the leak is
simultaneously closed.
In the event of a spillage, liquid should be contained and
discharges to streams or sewer system prevented. People performing the
clean-up should have full protective equipment and positive-pressure
breathing apparatus.
5. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION
There is very limited information on the environmental effects of
VC. Laboratory tests indicate that it has low toxicity for aquatic
organisms. If released to soil or surface water, volatilization is
likely to take place. Biodegradation is possible but very slow in
anaerobic environments. VC is not expected to hydrolyse, adsorb to
organic fractions of soils or sediments, or to biomagnify. VC has been
found to leach into groundwater and has been found there as a
degradation product of trichloroethylene and related solvents, where
it may remain under certain conditions.
6. SUMMARY OF CHEMICAL SAFETY INFORMATION
This summary should be easily available to all health workers
concerned with, and users of, vinyl chloride. It should be displayed
at, or near, entrances to areas where there is potential exposure to
vinyl chloride, and on processing equipment with containers. The
summary should be translated into the appropriate language(s). All
persons potentially exposed to the chemical should also have the
instructions in the summary clearly explained.
SUMMARY OF CHEMICAL SAFETY INFORMATION
Vinyl chloride
CAS Registry No. 75-01-4
C2H3Cl
PHYSICAL PROPERTIES OTHER CHARACTERISTICS
Relative molecular mass 62.5 Colourless flammable gas with a slightly sweet odour. It is
Boiling point (°C) -13 heavier than air and may travel along the ground. It can
Melting point (°C) -154 under specific circumstances form peroxides, initiating
Relative density (water = 1) 0.9 explosive polymerization. It will polymerize readily due to
Solubility in water none heating, under the influence of air, light, and on contact
Relative vapour density (air = 1) 2.2 with a catalyst, strong oxidizing agents and metals such as
Flash point (closed cup) (°C) -78 copper and aluminium, with fire or explosion hazard. It
Auto-ignition temperature (°C) 472 decomposes on burning producing toxic and corrosive fumes
Explosive limits, vol % in air 3.6-33 (hydrogen chloride and phosgene).
HAZARDS/SYMPTOMS PREVENTION AND PROTECTION FIRST AID
EYES: irritation, redness, Wear safety goggles. Rinse with plenty of water for at least 15 min (remove contact
pain lenses) obtain medical attention immediately.
SKIN: contact with compressed Avoid skin contact. Wear In the event of frostbite, rinse with plenty of water.
liquid causes frostbite protective clothing and Do not remove clothes.
protective
(cold-insulating) gloves.
INHALATION: can cause dizziness, Apply ventilation local Remove victim to fresh air and place in half-sitting
drowsiness, headache, exhaust or breathing position; obtain medical attention immediately.
unconsciousness protection; avoid
inhalation of vapour.
SUMMARY OF CHEMICAL SAFETY INFORMATION (continued)
INGESTION: Do not eat, drink or smoke
during work. Wash hands
before eating.
SPILLAGE STORAGE FIRE AND EXPLOSION
Evacuate the danger area. Wear Store in a cool and Extremely flammable; gives off irritating or
complete protective clothing, fireproofed area, separated toxic fumes in a fire; gas/air mixtures are
including self-contained breathing from incompatible materials explosive. In case of fire, extinguish with
apparatus to clean up the spill. (see under "Other powder, carbon dioxide; keep cylinders cool
characteristics"). by spraying with water.
WASTE DISPOSAL PACKAGING & LABELLING
Incinerate at high temperatures; EU Classification
complete combustion necessary to Symbol: F+, T
avoid formation of phosgene; acid R: 45-12
scrubber needed to remove halo S: 53-45
acids formed. Note: D
UN Classification
UN TDG Hazard Class: 2.1
7. CURRENT REGULATIONS, GUIDELINES AND STANDARDS
7.1 Previous evaluations by international bodies
Vinyl chloride was evaluated by the International Agency for
Research on Cancer (IARC, 1979) and updated in Supplement 7 (IARC,
1987). There was sufficient evidence for carcinogenicity of vinyl
chloride in humans and sufficient evidence for carcinogenicity in
animals. The overall evaluation was that vinyl chloride is
carcinogenic to humans (Group 1).
Using results from the rat bioassay of Til et al. (1983) and
applying the linearized multistage model, the human lifetime exposure
for a 10-5 excess risk of ASL was calculated to be 20 µg per day in
the Guidelines for Drinking-water Quality (WHO, 1996). It was assumed
that, in humans, the number of cancers at other sites may equal that
of ASL, so that a correction (factor of 2) for cancers other than ASL
was justified. A concentration in drinking-water of 5 µg/litre was
calculated as being associated with an excess risk of 10-5.
7.2 Occupational exposure limit values
Some examples of present exposure limit values are given in the
table on the next page.
7.3 Labelling, packaging and transport
EU labelling
Symbol: F+, T
R: 45-12 45 = may cause cancer
12 = extremely flammable
S: 53-45 53 = avoid exposure - obtain special instruction before
use
45 = in case of accident or if you feel unwell,
seek medical advice immediately (show the
label where possible)
Note: D
UNTDG hazard class 2.1
7.4 Waste disposal
Waste material containing vinyl chloride should be disposed of by
incineration.
CURRENT REGULATIONS, GUIDELINES AND STANDARDS
Exposure limit values
Country/organization Exposure limit descriptiona Value Value Referenceb
(ppm) (mg/m3)
Europe personal (8-h TWA) 7 18.2 CEC (1978)
United Kingdom HSC (1995)
Germany BIA (1997)
Finland 5 12.8 Gov. Res. (1992)
Europe working-area (annual) 3 8 CEC (1978)
United Kingdom HSC (1995)
Germany BIA (1997)
Finland Gov. Res. (1992)
Czech Republic MACK 10 Bencko & Ungváry (1994)
Slovakia
Hungary
Poland
USA 15 min 5 12.8 OSHA (1998)
8 h 1 2.6 OSHA (1998)
0 NIOSH (1997)
(no detectable
exposure levels)
TLV TWA (8 h) 2.6 ACGIH (1999)
a TWA = time-weighted average; TLV = threshold limit value; MAKK = maximal allowable concentration (k indicates the
carcinogenic properties of VC).
b OSHA = US Occupational Safety and Health Administration; ACGIH = US American Conference of Governmental and Industrial
Hygienists Inc.; HSC = UK Health and Safety Commission; BIA = German Professional Associations' Institute for Occupational
Safety; Gov. Res. = Finnish Government Resolution
BIBLIOGRAPHY
ACGIH (1999) Threshold limit values for chemical substances and
physical agents and biological exposure indices. Cincinnati, American
Conference of Governmental and Industrial Hygienists.
BIA (1997) List of hazardous substances. German Professional
Associations' Institute for Occupational Safety, Sankt Augustin,
Germany, 592-593 (in German).
CEC (1978) Council directive of 29 June 1978 on the approximation of
the laws, regulations and administrative provisions of the Member
States on the protection of the health of workers exposed to vinyl
chloride monomer. Official Journal of the European Communities L197,
22 July 1978, 12-18.
CEC (1987) Legislation on dangerous substances. Classification and
labelling in the European Communities, Vol.2. Brussels, Commission of
the European Communities.
CEC/IPCS (1991) International Chemical Safety Card 0082: Vinyl
chloride. Luxembourg, Commission of the European Communities.
Gov. Res. (1992) Finnish Government Resolution 919, 4 pp (in Finnish).
HSG (1995) Control of vinyl chloride at work: Approved code of
practice. UK Health and Safety Commission, Sudbury, Suffolk, UK Health
and Safety Executive, 10 pp.
IARC (1979) Vinyl chloride, polyvinyl chloride and vinyl
chloride-vinyl acetate copolymers. Lyon, International Agency for
Research on Cancer, pp 377-438 (IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans, Volume 19).
IARC (1987) Overall evaluations of carcinogenicity: An updating of
IARC monographs, Volumes 1 to 42. Lyon, International Agency for
Research on Cancer, pp 373-376 (IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans, Supplement 7).
IPCS (1993) Poisons Information Monograph No. 558 Vinyl chloride.
Geneva, World Health Organization. 22 pp.
IPCS (1999) Environmental Health Criteria 215: Vinyl chloride. Geneva,
World Health Organization.
NIOSH (1997) Pocket guide to chemical hazards. Cincinnati, Ohio,
National Institute for Occupational Safety and Health (US Department
of Health and Human Services) p 330-331
OSHA (1990) US Department of Labour, Occupational Safety and Health
Administration: Title 29, Code of Federal Regulations, Part 1910,
1910.1017 to end, pp.138-143.
Til HP, Immel HP & Feron FJ (1983) Lifespan oral carcinogenicity study
of vinyl chloride in rats. In: TNO (Netherlands organization for
applied scientific research) ed. TNO Report V83.285/291099. Zeist, TNO
pp 1-29.
United Nations (1997) Recommendations on the transport of dangerous
goods. Model regulations, 10th rev. ed. New York and Geneva, United
Nations, 573 pp.
WHO (1996) Guidelines for drinking-water quality. Geneva, World Health
Organization.