March 31, 1987
820D87001
VINYL CHLORIDE
Health Advisory Draft
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
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This Health Advisory (HA) is based on information presented in the
Office of Drinking Water's Health Effects Criteria Document (CD) for vinyl
chloride (U.S. EPA, 1985a). The HA and CD formats are similar for easy
reference. Individuals desiring further information on the toxicological
data base or rationale for risk characterization should consult the CD. The
CD is available for review at each EPA Regional Office of Drinking Water
counterpart (e.g., Water Supply Branch or Drinking Water Branch), or for a
fee from the National Technical Information Service, U.S. Department of
Commerce, 5285 Port Royal Rd., Springfield, VA 22161, PB t 86-118320/AS. The
toll-free number is (800) 336-4700; in the Washington, D.C. area: (703) 487-4650,
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 75-01-4
Structural Formula
H-C=C-C1
i I
H H
Synonyms
Uses
Monochloroethylene, chloroethene
Vinyl chloride and polyvinyl chloride (PVC) are used as raw materials
in the plastics, rubber, paper, glass and automotive industries.
In addition, vinyl chloride and PVC are used in the manufacture of
electrical wire insulation and cables, piping, industrial and household
equipment, medical supplies, food packaging materials and building
and construction products. Vinyl chloride copolymers and PVC are
distributed and processed in a variety of forms, including dry resins,
plastisol (dispersions in plasticizers), organosol (aispersions in
plasticizers plus volatile solvent), and latex (a colloidal dispersion
in water used to coat paper, fabric or leather) (U.S. EPA, 1985a).
Properties (U.S. EPA (1985a)
Chemical Formula
Molecular Weight
Physical State
Boiling Point
Melting Point
Density
Vapor Pressure
Specific Gravity
Water Solubility
Taste Threshold (water)
Odor Threshold (water)
Conversion Factor (air)
*Amoore and Hautala (1983)
H2C=CHC1
62.5
Gas
-13.3°C
2,530 mmHg at 20°C
0.91
1.1 g/L water at 28°C
not available
3.4 mg/L*
1 ppm = 2.6
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Vinyl Chloride March 31, 1987
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Occurrence
Vinyl chloride is a synthetic chemical with no natural sources.
Since 1979, yearly production of vinyl chloride has been approximately
7 billion Ibs (U.S. ITC, 1983). Vinyl chloride is polymerized, and
little is released to the environment. Environmental releases will
be limited to the areas where vinyl chloride is produced and used.
Vinyl chloride released to the air is degraded in a matter of a few
hours (U.S.EPA, 1980a). Vinyl chloride released to surface waters
migrates to the atmosphere in a few hours or days where it undergoes
photochemical oxidation. Vinyl chloride which is released to the
ground does not adsorb onto soil and migrates readily to ground
water. Evidence from laboratory studies suggests that vinyl chloride
in ground water may degrade to C02 and Cl~ (Vogel and McCarty, 1985).
Vinyl chloride is expected to remain in ground water for months to
years. Vinyl chloride has been reported to be a degradation product
of trichloroethylene and tetrachloroethylene in ground water (Parsons,
1984). Vinyl chloride does not bioaccumulate in individual animals
or food chains.
Vinyl chloride does not occur widely in the environment because of
its rapid degradation and limited release. Vinyl chloride is a
relatively rare contaminant in ground and surface waters with higher
levels found in ground water. The Ground Water Supply Survey of
drinking water supplies have found that less than 2% of all ground
water derived public water systems contain vinyl chloride at levels
of 1 ug/L or higher. Vinyl chloride almost always co-occurs with
trichloroethylene. Public systems derived from surface water also
have been found to contain vinyl chloride but at lower levels. No
information on the levels of vinyl chloride in food have been identi-
fied. Based upon the limited uses of vinyl chloride and its physical
chemical properties, little or no exposure is expected from food.
Vinyl chloride occurs in air in urban areas and near the sites of its
production and use. Atmospheric concentrations are in the ppt
range (U.S. EPA, 1979).
The major source of exposure to vinyl chloride is from contaminated
water.
III. PHARMACOKINETICS
Absorption
Vinyl chloride is absorbed rapidly in rats following ingestion and
inhalation (Withey, 1976; Duprat et al., 1977).
Using statistical modeling, Withey and Collins (1976) concluded that,
for rats, a total liquid intake containing 20 ppm (wt/wt) vinyl
chloride would be equivalent to an inhalation exposure of about 2 ppm
(vol/vol) for 24 hours.
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Distribution
0 Upon either inhalation or ingestion of 14C-vinyl chloride in rats, the
greatest amount of 1 4C activity was found 72 hours after treatment
in liver followed by kidney, muscle, lung and fat (Watanabe et al.,
1976a,b). Another study of inhalation exposure of rats to 14c-vinyl
chloride showed the highest 14C activity immediately after treatment
in liver and kidney, followed by spleen and brain (Bolt et al., 1976).
Metabolism
0 Bartsch and Montesano (1975) reported two possible metabolic pathways
for vinyl chloride, one involving alcohol dehydrogenase, the other
involving mixed function oxidase. Hefner et al, (1975) concluded
that the dominant pathway at lower exposure levels probably involves
alcohol dehydrogenase.
0 Vinyl chloride metabolism is saturable (Hefner et al., 1975; Watanabe
et al., 1976a; Bolt et-al., 1977).
0 Chloroethylene oxide, presumably through mixed-function oxidase, may
be the main metabolite capable of alkylating intracellular macro-
molecules (Laib and Bolt, 1977).
Excretion
0 Rats administered vinyl chloride by ingestion or inhalation exhale
greater amounts of unmetabolized vinyl chloride as the dose is
increased (Watanabe et al., 1976a, b).
0 Vinyl chloride metabolites are excreted mainly in the urine. In
rats, urinary metabolites include N-acetyl-S-(2-hydroxyethylcysteine)
and thiodiglycolic acid (Watanabe et al., 1976a).
HEALTH EFFECTS
Humans
0 Cancer findings in humans are described under Carcinogenicity.
0 Mutagenic effects in humans are described under Mutagenicity.
0 Developmental studies in humans are described under Developmental
Effects.
0 At high inhalation exposure levels, e.g., 40—900 ppm (104-2,344 mg/m3),
workers have experienced dizziness, headaches, euphoria and narcosis
(U.S. EPA, 1985a).
0 Symptoms of chronic inhalation exposure of workers to the vinyl
chloride-polyvinyl chloride industry include hepatotoxicity (Marstellar^
et al. 1975), acro-osteolysis (Lilis et al., 1975), central nervous
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Vinyl Chloride March 31, 1987
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system disturbances, pulmonary insufficiency, cardiovascular toxicity,
and gastrointestinal toxicity (Miller et al., 1975; Selikoff and
Hammond, 1975; Suciu et al., 1975). Data on dose-responses in humans
are scarce because few measurements of ambient vinyl chloride levels
in the workplace were made before 1975 (Mancuso, 1975).
Animals
Short-term Exposure
0 Inhalation exposure to high levels (ca. 100,000 ppm or 260,417
of vinyl chloride can induce narcosis and death, and, to lower doses,
ataxia, narcosis, congestion and edema in lungs and hyperemia in
liver in several species (U.S. EPA, 1985a).
Long-term Exposure
0 Administration of vinyl chloride monomer to rats by gavage for 13
weeks resulted in hematologic, biochemical and organ weight effects
at doses above 30 mg/kg (Feron et al., 1975).
0 Inhalation exposure of rats, guinea pigs, rabbits and dogs to 50 ppm
(130 mg/m3) vinyl chloride, 7 hours/day, 130 exposures in 139 days,
did not induce toxicity as judged by appearance, mortality, growth,
hematology, liver weight and pathology. Rats exposed to 100 ppm
(260 mg/m3) 2 hours/day for six months, had increased liver weights
(Torkelson et al., 1961).
Reproductive Effects
0 Potential effects on reproductive capacity have not been studied.
Developmental Effects
0 Infante et al. (1975a,b) reported an association between human
exposure to vinyl chloride and birth defects and fetal loss, but this
association was contradicted by Edmonds et al. (1975) and Hatch et
al. (1981).
0 Inhalation exposure of rats and rabbits to vinyl chloride concentrations
as high as 2,500 ppm (6,500 mg/m3) on days 5 to 15 (rats) and 6 to
18 (rabbits) of gestation and mice to vinyl chloride levels as high as
500 ppm (1,300 mg/m3) on days 5 to 15 of gestation did not induce
teratogenic effects but did increase skeletal variants in high dose nice
(John et al., 1977) .
0 A developmental effects study with vinyl chloride in rats exposed by
inhalation to 600 or 6,000 ppm (2,160 or 21,160 mg/m3) 4 hours daily
on gestation days 9 through 21 was negative for teratogenicity and
inconclusive for fetotoxicity (Radike et al., 1977).
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Mutagenicity
0 Chromosomal effects of vinyl chloride exposure in workers is conflicting
in that positive (Ducatmann et al., 1975; Purchase et al., 1975) and
negative (Killian et al., 1975; Picciano et al., 1977) results have
been reported. Picciano et al. (1977) reported exposures of 0.13 to
15.2 ppm (0.34 to 40 rng/rn^, time-weighted averages) for 1 to 332
months.
0 Vinyl chloride is mutagenic, presumably through active metabolites in
various systems including metabolically activated systems witn S_. typhi-
murium (Bartsch et al., 1975); _E. coli (Greim et al., 1975); yeast
(Loprieno et al., 1977); germ cells of Drosophija (Verburgt and
Vogel, 1977); and Chinese hamster V79 cells (Hubermann et al., 1975).
0 Dominant lethal studies with vinyl chloride in CD-1 mice were negative
(Anderson et al., 1976).
Carcinogenicity
0 Increases in the occurrence of liver angiosarcomas as well as in tumors
of the brain, lung, and hematopoietic and lymphopoietic tissues have
been associated with occupational exposure to the vinyl chloride-
polyvinyl chloride industry in humans (IARC, 1979). The initial
report of a link between vinyl chloride exposure and cancer in humans
by Creech and Johnson (1974), as well as subsequent reports by others,
indicates the high risk and specificity of association with liver
angiosarcoma, a very rare tumor in humans.
0 Ingestion of vinyl chloride monomer in the diet by rats at feeding
levels as low as 1.7 and 5 mg/kg/day over their lifespan induced
hepatocellular carcinomas and liver angiosarcomas, respectively, as
well as other adverse hepatic effects (Feron et al., 1981). Til
et al. (1983) extended the Feron et al. (1981) work to include lower
doses and did not find a significant (P<0.05) increase in carcinogenic
effects at feeding levels as high as 0.13 mg/kg/day. Administration
of vinyl chloride monomer by gastric intubation for at least 52 weeks
resulted in carcinogenic effects in liver and other tissue sites in
rats (Feron et al., 1981; Maltoni et al., 1981).
0 Chronic inhalation of vinyl chloride has induced cancer in liver and
other tissue sites in rats and mice (Lee et al., 1977, 1978; Maltoni
et al., 1981).
V. QUANTIFICATION OF TQXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
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Vinyl Chloride March 31, 1987
HA = (NOAEL or LOAEL) x (BW) = _ mg/L ( _ Ug/L)
(UF) x ( _ L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Ef fact-Level
in mg/kg bw/day .
BW = assumed body weight of a child (10 kg) or
an adult (70 kg) .
UF = uncertainty factor (10, 1 00 or 1,000), in
accordance with NAS/ODW guidelines.
_ L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
There are insufficient data for calculation of a One-day Health Advisory.
The Ten-day HA of 2.6 mg/L is proposed as a conservative estimate for a
One-day HA.
Ten-day Health Advisory
Inhalation data by Torkelson et al. (1961) were not selected for the
Ten-day HA calculation because of preference for studies with oral exposure.
Feron et al. (1975) reported a subchronic toxicity study in which vinyl
chloride monomer (VCM) dissolved in soybean oil was administered by gavage to
male and female Wistar rats, initially weighing 44 g, at doses of 30, 100 or
300 mg/kg once daily, 6 days per week for 13 weeks. Several hematological,
biochemical and organ weight values were significantly (P<0.05 or less)
different in both mid- and high-dose animals compared to controls. The NOAEL
in this study was identified as 30 mg/kg.
The Ten-day HA, as well as the One-day HA, for a 1 0-kg child is calculated
as follows:
Ten-day HA = (30 mg/kg/day (6/7) (10 kg) = 2i6 /L (2,500 ug/L)
(100) (1 L/day)
where:
30 mg/kg/day = NOAEL based on absence of biochemical and organ weight
effects in rats exposed orally to vinyl chloride.
6/7 = expansion of 6 days/week treatment in the Feron et al.
(1975) study to 7 days/week to represent daily exposure.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
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Longer-term Health Advisory
The Longer-term HA can be calculated from the -lifetime feeding study in
rats by Til et al. (1983). Til et al. (1983) have extended the earlier work
by Feron et al. (1981) to include lower doses with basically the same protocol
used in the latter study. Carcinogenic and noncarcinogenic effects were evi-
dent with a vinyl chloride dietary level of 1.3 mg/kg/day. At dietary levels
of 0.014 and 0.13 mg/kg/day, increased incidences of basophilic foci of cellu-
lar alteration in the liver of female rats were evident. However, basophilic
foci by themselves are concluded not to represent an adverse effect on the
liver in the absence of additional effects indicative of liver lesions such
as those found in the 1.3 mg/kg/day group; and a dose-related increase in
basophilic foci was not evident. Therefore, the dose of 0.13 mg/kg/day is
identified as the NOAEL for noncarcinogenic effects for the Longer-term HA
calculation.
Using the 0.13 mg/kg/day NOAEL from the Til et al. (1983) study, the
Longer-term HA for a 10-kg child is calculated as follows:
Longer-term HA = (0.13 mg/kg/day) (10 kg) = 0>013 /L (13 /L)
(100) (1 L/day)
where:
0.13 mg/kg/day = NOAEL based on absence of adverse liver effects
in rats.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
The Longer-term HA for a 70-kg adult is calculated as follows:
Longer-term HA = (0'13 mg/kg/day) (70 kg) = 0.046 mg/L (46 ug/L)
(100) (2 L/day)
where:
0.13 mg/kg/day = NOAEL based on absence of adverse liver effects
in rats.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2 L/day = assumed daily water consumption of an adult.
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Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking-
water) lifetime exposure- level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
Because vinyl chloride is classified as a human carcinogen (IARC Group 1
and EPA Group A), a Lifetime Health Advisory is not recommended.
Evaluation of Carcinogenic Potential
0 Applying the criteria described in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986), vinyl chloride may be classified
in Group A: Human carcinogen. This category is for agents for which
there is sufficient evidence to support the causal association between
exposure to the agents and cancer.
0 The IARC (1979) has concluded that there is sufficient evidence to
classify vinyl chloride as a human carcinogen in its Category 1.
0 EPA's Carcinogen Assessment Group (CAG) recently has recalculated its
excess carcinogenic risk estimates resulting from lifetime exposure
to vinyl chloride through the drinking water (U.S. EPA, 19S5a). CAG
based its preliminary revised estimates on the Feron et al. (1981)
study. The total number of tumors, considering tumors of the lung
and liver, in rats exposed through the diet was used to calculate the
excess cancer risk. Using the 95% upper limit Cq-j* = 2.3 (mg/kg/day)-1 j
with the linearized multistage model, they calculated that consuming
2 liters of water per day with vinyl chloride concentration of 1.5 ug/L,
0.15 ug/L and 0.015 ug/L would increase the risk of one excess cancer
per 10,000 (10-4), 100,000 (10-5) Or 1,000,000 (10-6) people exposed,
respectively, per lifetime. The CAG is presently reassessing the
cancer risk estimate based on the Feron et al. (1981) study by taking
into account the more recent data by Til et al. (1983) which, as
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Vinyl Chloride March 31, 1987
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described previously, is an extension of the earlier Feron et al.
(1981) work to include lower doses.
0 Maximum likelihood estimates as well as 95% upper limits of cancer
risks by the multistage model are presented. Expressing risk as
cases/lifetime/person, examples would be 0.01 mg/kg/day or 0.35 mg/L
exposure associated with risks of 1 .6 x 1 0"2 (MLE) and 1.9 x 10-2
(UL) and 0.001 mg/kg/day exposure associated with risks of 1.6 x 10-3
(MLE) and 1.9 x 10-3 (UL).
0 Cancer risk estimates (95% upper limit) with other models are presented
for comparison with that derived with the multistage. For example,
one excess cancer per 1,000,000 (10"6) is associated with exposure
to vinyl chloride in drinking water at levels of 50 ug/L (probit),
0.5 ug/L (logit), and 0.02 ug/L (Weibull). While recognized as
statistically alternative approaches, the range of risks described by
using any of these modeling approaches has little biological signifi-
cance unless data can be used to support the selection of one model
over another. In the interest of consistency of approach and in
providing an upper bound on the potential cancer risk, the EPA has
recommended use of the linearized multistage approach.
VI. OTHER CRITERIA, GUIDANCE, AND STANDARDS
0 The National Academy of Sciences (NAS, 1977) estimated a 10-6 risk
(95% upper bound estimate) from lifetime exposure to 1 ug vinyl
chloride/L drinking water with the multistage model and the lifetime
ingestion study in rats by Maltoni et al. (1981).
0 The final RMCL by the U.S. EPA Office of Drinking Water is zero, the
proposed MCL is 1 ug/L, and the practical quantitation level is 1 ug/L
(U.S. EPA, 1985b).
0 Ambient water quality critera (U.S. EPA, 1980b) are 20, 2 and 0.2 ug/L
for risks of 10"^, 10"^, and 10"^, respectively, assuming consumption
of 2 liters of water and 6.5 grams of contaminated fish per day by a
70 kg adult.
0 A workplace standard of 1 ppm (time-weighted average) was set by OSHA
in 1974 based on the demonstration of angiosarcoma of the liver in
vinyl chloride workers (Federal Register. 39:35890).
0 The ACGIH (1982) has recommended a TLV of 5 ppm (10 mg/m3).
VII. ANALYTICAL METHODS
Analysis of vinyl chloride is by a purge and trap gas chromatographic
procedure used for the determination of volatile organohalides in
drinking water (U.S. EPA, 1985c). This method calls for the bubbling
of an inert gas through a sample of water and trapping the purged
vinyl chloride on an adsorbent material. The adsorbent material is
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Vinyl Chloride
March 31, 1987
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heated to drive off the vinyl chloride onto a gas chromatographic
column. This method is applicable to the measurement of vinyl chloride
over a concentration range of 0.06 to 1500 ug/L. Confirmatory analysis
for vinyl chloride is by mass spectrometry (U.S. EPA, 1985d). The
detection limit for confirmation by mass spectrometry is 0.3 ug/L.
VIII. TREATMENT TECHNOLOGIES
0 The value of the Henry's Law Constant for vinyl chloride (6.4
atm-m3/mole) suggests aeration as a potential removal technique
for vinyl chloride in water (ESE,1984). Removals of up to 99.27%
were achieved at 9°C using a pilot packed tower aerator. In similar
studies, vinyl chloride was removed from ground water using a
spray aeration system with total VOC concentration was 100 to
200 ug/L (ESE, 1984). Greater than 99.9% VOC removal was obtained
using a four-stage aeration system; each stage employed 20 shower
heads with a pressure drop of approximately 10 pounds per square
inch. In-well aeration has also demonstrated up to 97% removal of
vinyl chloride using an air-lift pump. However, practical considera-
tions are likely to limit the application of this (Miltner, 1984).
0 The concentration of vinyl chloride in southern Florida ground water
declined by 25% to 52% following passage through lime softening basins
and filters (Wood and DeMarco, 1980). Since vinyl chloride is a
highly volatile compound, it is probably volatilized during treatment
(ESE, 1984).
0 Adsorption techniques have been less successful than aeration in
removing vinyl chloride from water. In a pilot study, water from a
ground water treatment plant was passed through a series of four
30-inch granular activated carbon (Filtrasorb 400) columns (Wood and
DeMarco, 1980; Symons, 1978); the empty bed contact time was approxi-
mately six minutes per column. Influent vinyl chloride concentrations
ranged from below detection to 19 ug/1; erratic removal was reported.
To maintain effluent concentrations below 0.5 ug/1, the estimated
column capacity to breakthrough was 810, 1,250, 2,760 and 2,050 bed
volumes for empty bed contact times of 6, 12, 19 and 25 minutes,
respectively. In addition, the estimated service life of the acti-
vated carbon was low. Similarly, poor removal of vinyl chloride was
achieved using an experimental synthetic resin, Ambersorb XE-340,
(Symons, 1978).
0 Treatment technologies for the removal of vinyl chloride from water
have not been extensively evaluated except on an experimental level.
Available information suggests aeration merits further investigation.
Selection of individual or combinations of technologies to achieve
vinyl chloride removal must be based on a case-by-case technical
evaluation, and an assessment of the economics involved.
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Vinyl Chloride March 31, 1987
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IX. REFERENCES
ACGIH. 1982. American Conference of Governmental Industrial Hygienists.
Threshold limit values for chemical substances and physical agents in
the workroom environment. Cincinnati, OH.
Amoore, J.E., and E. Hautala. 1983. Odor as an aid to chemical safety:
Odor thresholds compared with threshold limit values and volatilities
for 214 industrial chemicals in air and water dilution. J. Appl. Toxicol.
3:272-290.
Anderson, D., M.C.E. Hodge and I.F.H. Purchase. 1976. Vinyl chloride:
Dominant lethal studies in male CD-1 mice. Mutat. Res. 40:359-370.
Bartsch, H., C. Malaveille and R. Montesano. 1975. Human, rat and mouse
liver-mediated mutagencity of vinyl chloride in S_. typhimurium strains.
Int. J. Cancer. 15:429-437.
Bartsch, H., and R. Montesano. 1975. Mutagenic and carcinogenic effects of
vinyl chloride. Mutat. Res. 32:93-114.
Bolt, H.M., H. Kappus, A. Buchter and W. Bolt. 1976. Disposition of
(1,2-140 vinyl chloride in the rat. Arch. Toxicol. 35:153-162.
Bolt, H.M., R.J. Laib, H. Kappus and A. Buchter. 1977. Pharmacokinetics of
vinyl chloride in the rat. Toxicol. 7:179-188.
Creech, J.L., and M.N. Johnson. 1974. Angiosarcoma of the liver in the
manufacture of polyvinyl chloride. J. Occup. Med. 20:338-340.
Ducatman, A., K. Hirschhorn and I.J. Selikoff. 1975. Vinyl chloride expo-
sure and human chromosome aberrations. Mutat. Res. 31:163-168.
Duprat, P., J.P. Fabry, D. Gradiski and J.L. Magadur. 1977. Metabolic
approach to industrial poisoning: blood kinetics and distribution of
14c-vinyl chloride monomer (V.C.M.). Acta. Pharmacol. Toxicol. Suppl.
(Kbh) 41(1):142-143.
Edmonds, L.D., H. Falk and J.E. Nissim. 1975. Congenital malformations and
vinyl chloride. Lancet. 2:1098.
ESE, 1984. Environmental Science and Engineering. Technologies and costs for
the removal of volatile organic chemicals from potable water supplies.
(Draft) ESE No. 84-912-0300. Prepared for U.S. EPA, Science and Technology
Branch, CSD, ODW, Washington, DC.
Federal Register. 39:35890.
Feron, V.J., A.J. Speek, M.I. Williams, D. van Battum and A.F. de Groot.
1975. Observations on the oral administration and toxicity of vinyl
chloride in rats. Fd. Cosmet. Toxicol. 13:633-638.
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Feron, V.J., C.F.M. Hendrikson, A.J. Speek, H.P. Til and B.J. Spit. 1981.
Lifespan oral toxicity study of vinyl chloride in rats. Fd. Cosmet.
Toxicol. 19:317-331.
Greim, H., G. Bonse, Z. Radwan, D. Reichert and D. Henschler. 1975.
Mutagenicity In vitro and potential carcinogenicity of chlorinated
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