INFORMATION REGARDING CARBON DISULFIDE AND BROMINE
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~Q0VHU4:1
Source: Occupational Diseases A Guide to Their Recognition, W. M. Gafafer,
Editor, U.S. Department of Health, Education and Welfare, Washington, D. C.,
pages 107-108, 3 references, 19641964
Abstract:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~Jf5B89:2
CARBON DISULFIDE
CASRN: 75-15-0
Probable Routes of Human Exposure :
Occupations with potential exposure to carbon
disulfide: Acetylene workers, ammonium salt makers, bromine
processors, carbonilide makers, carbon disulfide workers,
carbon tetrachloride makers, cellophane makers, rubbershoe cementers, coal tar
distillers, degreasers, drycleaners, dyestuff makers, electroplaters, enamelers,
enamel makers, explosive workers, fat processors, floatation-agent makers,
fumigant workers, glassmakers, glue workers, iodine processors, chemical
laboratory workers, lacquer makers, matchmakers, oil processors, optical
glassmakers, painters, paintmakers, paint-remover makers, paraffin workers,
pesticide makers, phospherus processors, preservative makers, putty makers,
rayon makers, resin makers, rocket-fuel makers, rubber- cement makers, rubber
dryers, rubber makers, rubber reclaimers, sclenium processor, tallowmakers,
textile makers, vacuum-tube makers, varnish-remover makers, veterinarians,
vulcanizers, and wax processors.
Artificial Pollution Sources :
Carbon disulfide's production
and use in the manufacture of rayon, carbon tetrachloride, xanthogenates, soil
disinfectants, electronic vacuum tubes, and as a solvent for phosphorus, sulfur,
selenium, bromine, iodine, fats,
resins, and rubbers(1) may result in its release to the environment through
various waste streams(SRC).
Synonyms :
KOHLENDISULFID (SCHWEFELKOHLENSTOFF)
(GERMAN)
**PEER REVIEWED**
Synonyms :
SCHWEFELKOHLENSTOFF
(GERMAN)
**PEER REVIEWED**
Major Uses :
MFR OF RAYON, CARBON TETRACHLORIDE,
XANTHOGENATES, SOIL DISINFECTANTS, ELECTRONIC VACUUM TUBES; SOLVENT FOR
PHOSPHORUS, SULFUR, SELENIUM, BROMINE,
IODINE, FATS, RESINS, & RUBBERS.
Environmental Fate/Exposure Summary :
Carbon disulfide's production
and use as a solvent and a chemical intermediate may result in its release to
the environment through various waste streams. If released to air, a vapor
pressure of 359 mm Hg at 25 deg C indicates carbon
disulfide will exist solely as a vapor in the ambient
atmosphere. Vapor-phase carbon disulfide will
be degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals; the half-life for this reaction in air is estimated to be 5.5 days. Carbon
disulfide has a weak UV adsorption band at 317 nm, suggesting a
potential for direct photolysis. If released to soil, carbon
disulfide is expected to have moderate mobility based upon an
estimated Koc of 270. Volatilization from moist soil surfaces is expected to
occur based upon a Henry's Law constant of 1.44X10-2 atm-cu m/mole at 24 deg C. Carbon
disulfide may potentially volatilize from dry soil surfaces
given its vapor pressure. If released into water, some adsorption of carbon
disulfide to suspended solids and sediment in the water column
is expected based upon the estimated Koc. Volatilization from water surfaces is
expected to be an important fate process based upon carbon
disulfide's Henry's Law constant. Estimated volatilization
half-lives for a model river and model lake are 2.6 hours and 3.5 days,
respectively. BCFs of <6.1 and <60 in carp suggest bioconcentration in
aquatic organisms is low to moderate. Occupational exposure to carbon
disulfide may occur through inhalation and dermal contact with
this compound at workplaces where carbon disulfide is
produced or used. As carbon disulfide occurs
ubiquitously in the environment, the general population is exposed to this
compound. Primary routes of exposure to carbon
disulfide are through inhalation of ambient air or ingestion of
fruits, vegetables, and other food products containing this compound. (SRC)
Food Survey Values :
Seven samples of lima beans, five of common
beans, two of lentils and one sample of mung beans, soybeans, and split peas
that were analyzed contained a mean carbon disulfide concn
of 2.3 ppb; range was 1.8 to 3.1 ppb(1). Some of these samples were obtained
from health stores and one was from a home garden where it was grown without the
use of herbicides or insecticides(1). Stored grain has been fumigated with carbon
disulfide in the past. The carbon
disulfide concn in 9 samples of wheat, range from 64 to 7500 ppb
although none was found in samples of corn, oats, corn meal, and corn grits(2).
While one sample of bleached flour contained 23 ppb, other samples tested,
including corn muffin mix, cake mixes, dried lima beans, noodles and rice, were
free of the fumigant(2). With the exception of granola, which contained 11 ppb
of carbon disulfide, none of the 18
samples of table-ready food items tested contained carbon
disulfide(3). The items tested contained representative samples
of most classes of food(3). In addition, samples of butter and margarine,
cheese, peanut butter, and highly processed foods from the US FDA's market
basket survey contained no carbon disulfide(3).
However some ready-to-eat food products, specifically two samples of corn chips,
and oat ring cereal contained 80, 230, and 95 ppb of carbon
disulfide, respectively(3). In an FDA Survey of 549 food items
for fumigant residues, 7 were found to contain carbon
disulfide(4). The avg concn of carbon
disulfide residues was 738 ppb(4). Carbon
disulfide has been identified as a volatile component in chicken
and beef flavor(5).
Natural Pollution Sources :
The ocean appears to be a major global source
of carbon disulfide(1-3). Current data
suggest that coastal areas and other areas of high biological productivity have
greater fluxes of carbon disulfide than
the open ocean(2). Emissions from the oceans have been estimated to be 6X10+11
g/yr(2). The microbial reduction of sulfates in soil produces fluxes of carbon
disulfide. The annual global emission from this source has been
estimated to be 9X10+11 g(2). Other natural sources include volcanic emissions,
estimated to be 2X10+10 g/yr, and marshlands, estimated emissions 1X10+11
g/yr(2). Fluxes of carbon disulfide from
a salt marsh was measured as 0.2 and 1.13 g Sulfur/sq m-yr and inland soil 0.001
g Sulfur/sq m-yr(5). However, the overall contribution of inland soil is much
higher(5). Some higher plants are known to emit carbon
disulfide(7,9). The principle source is the tree roots(9).
Emissions from tidal marshes is greatest when the soil moisture is at field
capacity(4). Diurnal variation in emissions rates correlate loosely with soil
temperature and solar irradiation(6). Carbon disulfide
emissions rates were highest in the early- to mid-afternoon and
lowest during the early morning. Carbon disulfide emissions
from a temperate pine forest increased nine-fold when nitrogen fertilizers were
added(8). However, similar increases were not observed in a temperate hardwood
forest. Carbon disulfide was only
emitted briefly from a normally aerobic loam soil and only in the saturated
static forest silty loam soil did not emit any carbon
disulfide(4).
Preventive Measures :
... Clothing wet with liquid carbon
disulfide should be placed in closed containers for storage
until it can be discarded or until provision is made for the removal of carbon
disulfide from the clothing. If the clothing is to be laundered
or otherwise cleaned to remove the carbon disulfide, the
person performing the operation should be informed of carbon
disulfide's hazardous properties. Any clothing which becomes wet
with liquid carbon disulfide should be
removed immediately and not reworn until the carbon
disulfide is removed from the clothing. Skin that becomes
contaminated with carbon disulfide should
be promptly washed or showered with soap or mild detergent and water to remove
any carbon disulfide.
Medical Surveillance :
Whole Blood: Reference Ranges: Normal - None
detected; Exposed - Not established; Toxic - Not established. The assessment of carbon
disulfide exposure can be accomplished through measurement of carbon
disulfide. However, data obtained from measurement of carbon
disulfide in blood have not shown a consistent correlation with
exposure. One reason that carbon disulfide in
blood is a poor indicator of exposure is due to its rapid clearance from this
tissue. A compounding factor in blood measurement is that there are two species
of carbon disulfide in the blood:
"Free" which is unbound carbon disulfide that
is dissolved in the plasma; and "bound" or "acid-labile" carbon
disulfide, which is dissolved in plasma lipids or bound
proteins. The equilibrium of these forms differs from individual to individual,
rendering blood tests less reliable. However, a new headspace gas chromatography
method that is being developed for acid labile carbon
disulfide may prove to be more reliable.
National Toxicology Program Studies :
Carbon disulfide (CS),
a widely used industrial chemical, was evaluated for toxic and teratogenic
effects in artificially inseminated New Zealand White (NZW) rabbits. Carbon
disulfide (0, 25, 75 and 150 mg/kg/day, po) in corn oil was
administered in a volume of 1 ml/kg body weight on gestational days (gd) 6
through 19. Females were weighed and observed during daily treatment and at 4
hours post-dosing for clinical signs of toxicity. At sacrifice on gd 30, a total
of 23-28 confirmed-pregnant females per treatment group were evaluated. The
gravid uterus for each dam was weighed and the number of implantation sites, and
live, dead, or resorbed fetuses were recorded. All live fetuses were weighed and
examined for external, visceral and skeletal malformations. The mortality rate
for treated females was 3.5% (1/29), 0% (0/26), 3.3% (1/30), and 7.1% (2/28) for
the vehicle control through high dose, respectively. Maternal body weight on gd
0, gd 6 (i .e., prior to the initiation of treatment), gd 12 (i.e., midway
through the treatment period) and gd 30 (i.e., immediately prior to sacrifice)
did not differ significantly among treatment groups. On gd 19 (i.e., the final
day of treatment) maternal body weight was decreased across treatment groups in
a dose-related manner with 150 mg/kg/day CS dams exhibiting body weights
significantly below vehicle controls. Maternal weight gain during treatment,
maternal weight gain during gestation and gravid uterine weight were each
decreased in a dose-related manner. Maternal weight gain during the treatment
period was significantly below controls for dams treated with 75 or 150
mg/kg/day carbon disulfide. Gestational
weight gain was below controls only for the high-dose group. Absolute weight
gain (i.e. maternal gestational weight gain minus gravid uterine weight) did not
differ significantly among treatment groups. Both absolute and relative maternal
liver weight were increased in a dose-related manner with statistically
significant increases above vehicle control observed in the 75 and 150 mg/kg/day
carbon disulfide groups. Since
maternal body weight at sacrifice did not differ among treatment groups, the
increase in absolute and relative maternal liver weight appears to reflect a
treatment related hepatic response, but the data collected did not allow further
characterization of this response. The percentage per litter of resorbed,
nonlive (i.e., dead plus resorbed) or affected (i.e., nonlive plus malformed)
fetuses was increased in a dose-related manner, and all carbon
disulfide-treated groups were significantly above vehicle
controls on these measures. The proportion of litters with one or more resorbed,
nonlive or affected fetuses also increased in a dose-related manner, but only
the high-dose group (150 mg/kg/day, carbon disulfide) was
significantly above vehicle controls on these measures. No statistically
significant differences among treatment groups were observed in the percentage
of dead fetuses (i.e., fetuses weighing approx 10 g with discernible digits, but
showing no vital signs at uterine dissection) per litter or in the proportion of
litters with one or more dead fetuses. Among those litters containing live
fetuses, there were no differences among dose groups in the proportion of males
per live litter. The number of live fetuses per litter, as well as average fetal
body weight per live litter, were reduced in a dose-related manner, with carbon
disulfide 150 litters significantly smaller than controls on
both measures. The percentage of fetuses malformed per litter, but not the
proportion of litters with one or more malformed fetuses, differed significantly
among treatment groups and a clear dose-effect relationship was observed. In
conclusion, carbon disulfide (25, 75
or 150 mg/kg/day, po) administered on gd 6 through 19, produced dose-related
maternal and fetal toxicity, and increased the incidence of malformed fetuses in
New Zealand White rabbits relative to the vehicle control group. The incidence
of resorptions was significantly increased at all doses tested (i.e., 12.30%,
32.47%, 41.60% and 61.16% resorbed in the vehicle through high-dose,
respectively), but the incidence of malformations in the control group (5.72%)
was significantly exceeded only in the high dose group (19.51% malformed fetuses
per litter).
Absorption, Distribution & Excretion :
Six human volunteers were exposed to 10 and 20
ppm carbon disulfide at rest and to 3
and 10 ppm carbon disulfide under a 50
W level of physical exercise during four consecutive periods of 50 min. Every 5
min a sample was taken from the mixed exhaled air in which the concentration of carbon
disulfide was determined. It was established that only an
apparent steady state was reached during this exposure period. The retention
values were established as 0.374 (SD= 0.106; n= 239) for exposure to 10 ppm carbon
disulfide at rest and as 0.410 (SD= 0.103; n= 239) for exposure
to 20 ppm carbon disulfide at rest.
During exposure to 10 ppm and 3 ppm carbon disulfide, combined
with a 50 W level of physical exercise, the retention values decreased to 0.286
(SD= 0.083; n= 239) and 0.277 (SD= 0.049; n= 239) respectively. The respiratory
uptake of carbon disulfide (mg carbon
disulfide) proved significantly influenced by the amount of body
fat estimated from skinfold thickness measurements.
Metabolism/Metabolites :
Carbon disulfide is
metabolized by two distinctly different pathways: ability of carbon
disulfide to spontaneously react with free amine and sulfhydryl
groups of amino acids and polypeptides, and microsomal metabolism of carbon
disulfide to reactive intermediates capable of covalently
binding to tissue macromolecules. Dithiocarbamates are formed during in vitro
incubations of carbon disulfide with
blood; treatment of the dithiocarbamate products with acid and heat liberates carbon
disulfide. Tissue concentrations of acid labile metabolites
exceed those of free carbon disulfide at
the end of an 8 hour, 2 mg/l carbon disulfide inhalation
exposure. Acid labile metabolites may also accumulate in the body after repeated
carbon disulfide exposure.
Metabolism/Metabolites :
In an attempt to further define the mechanisms
involved in carbon disulfide metabolism,
the relationship between carbon disulfide and
carbonyl sulfide metabolism was explored in male Sprague-Dawley rat hepatocytes
and liver microsomes. Pretreatment of animals with cobaltous chloride or
phenobarbital decreased or increased, respectively, the extent of carbon
disulfide metabolism by hepatic microsomes, as determined by the
formation of carbonyl sulfide and nonvolatile sulfur compounds. Carbon
disulfide metabolism in microsomes was biphasic in that there
was an initial period of rapid metabolite formation followed by a period of
slower metabolism. Carbon disulfide metabolism
in hepatocytes was biphasic as well. SKF-525A significantly inhibited carbon
disulfide metabolism in hepatocytes and microsomes from
phenobarbital treated rats. Acetazolamide did not significantly inhibit carbon
disulfide metabolism regardless of the metabolite studied.
Atmospheric Concentrations :
SOURCE DOMINATED: Carbon
disulfide was detected in air samples from municipal solid waste
composting facilities at a maximum concn of 150 ug/cu m; average concns of 5, 9,
8, and 6 ug/cu m were detected in air samples collected near newly formed
compost, from one-fifth to four-fifths through the active composting region, at
the end of the composting region, and outside the active composting region,
respectively(1). Carbon disulfide concns
in the air of the spinning department of a viscose rayon fiber factory ranged
from 0.1 to 8.5 ppm, mean 3 ppm; in the pause cabin, carbon
disulfide levels ranged from 0.01 to 1 ppm, mean 0.04 ppm(3).
Personal air samples collected from the breathing zone, shoulder area, ranged
from 2 to 39 ppm (TWA); corresponding samples drawn from the mask ranged from 1
to 14 ppm(2). Carbon disulfide levels
in ambient air samples from a factory producing viscose sheeting ranged from 0.2
to 9 ppm, mean 4 ppm; concns in personal air samples ranged from 3 to 7 ppm (TWA)(2).
Air samples collected from personal sampling tubes of workers during the
production of viscose rayon fibers ranged from 1.0 to 148 mg/cu m(3). Mean carbon
disulfide concns for workers in the viscose industry measured by
passive personal air monitoring were (department): 3.42 (spool spinning), 6.57
(spinning of technical rayon), 12.07 (washing), 3.63 (post-treatment), and 1.94
(second aging) ppm(4). Mean carbon disulfide concns
for workers in the viscose industry measured by active personal air monitoring
were (department): 4.18 (spool spinning), 6.05 (spinning of technical rayon),
9.54 (washing), and 2.00 (second aging) ppm(4). Mean carbon
disulfide concns for workers in the viscose industry measured by
stationary air monitoring were (department): 0.91 (spool spinning), 7.51
(spinning of technical rayon), 28.07 (washing), 1.63 (post-treatment), and 2.30
(second aging) ppm(4).
Environmental Abiotic Degradation :
The rate constant for the vapor-phase reaction
of carbon disulfide with
photochemically-produced hydroxyl radicals is 2.9X10-12 cu cm/molecule-sec at 24
deg C(1). This corresponds to an atmospheric half-life of about 5.5 days at an
atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1,SRC). Observed
temporal variability and vertical gradients suggest that the tropospheric
lifetime of carbon disulfide is quite
short(2). If the atmospheric concn of carbon disulfide
at 6.1 km altitude is typical for marine boundary layer levels,
the sharp decrease in concn at higher altitudes supports the concept of a
photochemical lifetime of a month or less in the troposphere(2). The
tropospheric half-life determined from estimates of sources and global burdens
of the chemical is 8.9 days(4). Carbon disulfide has
a weak UV adsorption band at 317 nm(3); however, photolysis is not considered to
be a significant loss mechanism for the chemical(4). The rate constant for the
vapor-phase reaction of carbon disulfide with
atomic oxygen is 3.6X10-12 cu cm/molecule- sec at 25 deg C(5). This corresponds
to an atmospheric half-life of about 8.9 days(SRC) assuming an atmospheric concn
of atomic oxygen is 2.5X10+5 radicals/cu cm(5,6). The rate constant for the
reaction of carbon disulfide with
hydroxyl radicals in aqueous solution is 8.0X10+9 L/mol sec at pH 7.6(7). This
corresponds to a half-life of about 100 days(SRC) at an avg aqueous hydroxyl
radical concn of 1X10-17 mol/l(8).
Medical Surveillance :
A complete history and physical examination:
The purpose is to detect existing conditions that might place the exposed
employee at increased risk, and to establish a baseline for future health
monitoring. Examination of the central and peripheral nervous systems, eyes,
cardiovascular system, kidneys, and liver should be stressed. The skin should be
examined for evidence of chronic disorder. Since kidney damage has been observed
in humans exposed to carbon disulfide, a
urinalysis should be obtained to determine, at a minimum, specific gravity,
albumin and glucose content, along with a microscopic /examination of/
centrifuged sediment. Since liver damage has been observed in humans exposed to carbon
disulfide, a profile of liver function should be obtained by
using a medically acceptable array of biochemical tests. An electrocardiogram: carbon
disulfide has caused arrhythmias and electrocardiographic
changes in humans. Periodic surveillance is indicated. Carbon
disulfide has caused ocular changes in humans. An ophthalmic
examination should be performed, including visual acuity. Workers should be
informed of potential undesirable effects of exposure to carbon
disulfide on reproduction (such as spermatic deficiences,
menstrual disorders, and spontaneous abortions).
Absorption, Distribution & Excretion :
/A study was conducted to determine the/
biochemical changes due to carbon disulfide in
11 male New Zealand white rabbits. The rabbits were exposed to carbon
disulfide by inhalation for 6 hours/day, 5 days/week, for up to
38 weeks. Concentrations of carbon disulfide were
250 ppm (775 mg/cu m) during the first 16 weeks, 500 ppm (1,555 mg/cu m) for the
next 5 weeks, and 750 ppm (2,330 mg/cu m) for the final 17 weeks. ... Carbon
disulfide in the exhaled breath averaged 1.4 ppm (4.3 mg/cu m)
when the exposure concn was 500 ppm (1,555 mg/cu m) and rose to 3.1 ppm (9.6
mg/cu m) when the exposure concentration was 750 ppm (2,330 mg/cu m). No carbon
disulfide was detected in the exhaled breath of rabbits exposed
at 250 ppm (775 mg/cu m).
Absorption, Distribution & Excretion :
The relationship between carbon
disulfide disposition and development of carbon
disulfide neurotoxicity is reviewed. Animal studies have
indicated that approximately 8 to 30% of the carbon
disulfide retained after inhalation exposure is excreted by the
lung; amounts less than 0.5% of retained carbon
disulfide are excreted by the kidney. Free carbon
disulfide reaches steady state concentrations in various tissues
within 4 to 5 hours after initiation of exposure.
Absorption, Distribution & Excretion :
Despite considerable variation between
individuals, absorption seems to be proportional to the concentration of carbon
disulfide in the inhaled air, and equilibrium between the carbon
disulfide content of inhaled and exhaled air is reached in 1-2
hours. At this point, the percentage retained is about 40-50%, and carbon
disulfide is distributed in the organism by the bloodstream,
where twice as much is taken up by the erythrocytes as by the plasma. As carbon
disulfide is readily soluble in fats and lipids, and binds to
amino acids and proteins, it disappears rapidly from the bloodstream and has a
high affinity for all tissues and organs. The order of affinity for different
organs has not been established in man. Between 10 and 30% of absorbed carbon
disulfide is exhaled, less than 1% is excreted in the urine ...
.
Environmental Water Concentrations :
SURFACE WATER: The mean concn of carbon
disulfide in the open waters of the Atlantic Ocean and the
Atlantic Ocean of Ireland are 0.52 and 0.78 parts per trillion, respectively(1).
The mean concn in stagnant bay water was 5.4 parts per trillion(1). Water
samples from 82 stations in Lake Ontario and 17 in the lower Niagara River were
analyzed for volatile organics(2). Two river samples contained 25 parts per
trillion of carbon disulfide while the
other station contained <20 parts per trillion, the detection limit(2).
Eleven lake samples contained quantifiable amounts of carbon
disulfide whose median and max concn was 400 and 3900 parts per
trillion, respectively(2). Half of the other samples contained trace quantities
of the chemical and the other stations contained <80 parts per trillion, the
detection limit(2). Carbon disulfide was
prominent in Toronto Harbor, with lower levels in Hamilton Harbor and Oak
Orchard Creek(2). In another study, carbon disulfide was
detected, but not quantified, in the central basin of Lake Erie, the Niagara
River, and open waters of Lake Ontario; it was absent from the western basin of
Lake Ontario(3).
Effluent Concentrations :
In a comprehensive survey of wastewater from
4000 industrial and publicly owned treatment works (POTWs) sponsored by the
Effluent Guidelines Division of the US EPA, carbon
disulfide was identified in discharges from the following
industrial category (frequency of occurrence; median concn in ppb): leather
tanning (1; 7.5), paint and ink (4; 1078.6), organics and plastics (30; 1654.3),
plastics and synthetics (4; 7075.4), pulp and paper (2; 215.6), pesticides
manufacture (1; 88.8), publicly owned treatment works (11; 45.8)(1). The highest
effluent concn was 18,943 ppb in the plastics and synthetics industry(1). In a
survey of 63 industrial waste water effluents, carbon
disulfide was identified in 8 samples, 6 of which were <10
ppb and 2 between 10 and 100 ppb(2). The concn of carbon
disulfide in offgas from two oil shale retorting processes were
24 ppm and 13 ppm(3). Carbon disulfide was
found in both the influent and effluent of a large community septic tank(4). The
combined concn of carbon disulfide and
dichloromethane in the effluent, which was 10 ppb, was much higher than that in
the influent and reflected the presence of anaerobic processes in the sewer line
or septic tank(4).
Non-Human Toxicity Excerpts :
/A study was conducted to determine the/
biochemical changes due to carbon disulfide in
11 male New Zealand white rabbits. The rabbits were exposed to carbon
disulfide by inhalation for 6 hours/day, 5 days/week, for up to
38 weeks. Concentrations of carbon disulfide were
250 ppm (775 mg/cu m) during the first 16 weeks, 500 ppm (1,555 mg/cu m) for the
next 5 weeks, and 750 ppm (2,330 mg/cu m) for the final 17 weeks. ... Total
serum cholesterol increased in exposed rabbits when the carbon
disulfide concentration was increased to 750 ppm (2,330 mg/cu m)
and returned to normal after cessation of exposure. ... Increased urinary and
fecal excretion of zinc by the exposed rabbits and a gradual decrease in the
mean concentration of zinc in the blood serum /was noted/ during the study.
Absorption, Distribution & Excretion :
Skin absorption of carbon
disulfide vapor in male albino rabbits was studied. ... After 3
hours of dermal exposure to carbon disulfide at
1,550 ppm (4820 mg/cu m), the exhaled air of the rabbit contained 2.5 ppm (7.8
mg/cu m) of the cmpd; 0.25 ppm (0.78 mg/cu m) could still be detected 1.5 hours
after cessation of the 3-hour exposure. Exposure of one rabbit to carbon
disulfide at 1,500 ppm (4665 mg/cu m), 3 hours/day for 8
consecutive days revealed that the concn of carbon
disulfide in the exhaled breath increased with the length of
exposure. ...
Interactions :
The effects of isopropyl alcohol on
hepatotoxicity of carbon disulfide was
examined in rat. Metabolism of carbon disulfide was
previously reported to involve two forms of cytochrome p450, a high affinity/low
capacity isoenzyme and a low affinity/high capacity isoenzyme. An 18 hr
pretreatment with isopropyl alcohol, resulted in a significantly greater decr in
cytochrome p450-dependent aniline hydroxylase activity than without
pretreatment. In addition, plasma transaminase activity (another hepatotoxic
parameter of carbon disulfide) incr.
Shorter pretreatment periods (from 2 hr to simultaneous admin) with the alcohol
had no effect on the CS2 induced damage to p450 while markedly reducing the
damage assessed by plasma transaminases of isopropyl alcohol. The results
support the hypothesis that the hepatotoxic effect of carbon
disulfide results from its metabolism, which is induced after an
18 hr exposure to isopropyl alcohol but which is inhibited when the liver is
exposed to both the alcohol and CS2 at the same time.
Volatilization from Water/Soil :
The Henry's Law constant for carbon
disulfide is 1.44X10-2 atm-cu m/mole at 24 deg C(1). This
Henry's Law constant indicates that carbon disulfide is
expected to volatilize rapidly from water surfaces(2,SRC). Based on this Henry's
Law constant, the estimated volatilization half-life from a model river (1 m
deep, flowing 1 m/sec, wind velocity of 3 m/sec) is approximately 2.6
hours(2,SRC). The estimated volatilization half-life from a model lake (1 m
deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec) is approximately 3.5
days(2,SRC). Carbon disulfide's Henry's
Law constant(1) indicates that volatilization from moist soil surfaces is
expected to occur(SRC). The Henry's Law constant in seawater at 24 deg C is
1.61X10-2 atm-cu m/mole(1). The Henry's Law constant increases by a factor of
four between 0.5 deg C and 32 deg C(1). The potential for volatilization of carbon
disulfide from dry soil surfaces may exist(SRC) based upon the
vapor pressure of 359 mm Hg(3).
Atmospheric Concentrations :
RURAL/REMOTE: Levels of carbon
disulfide in 61 air samples taken over the course of 2 days at
Wallops Island, VA ranged from 29 to 84 parts per trillion; median 41 parts per
trillion(1). At Harwell, England concns ranged from 70 to 370 parts per
trillion; avg 190 parts per trillion(3). Concns of carbon
disulfide varied with altitude, measuring: 115 parts per
trillion mean at 6.1 km altitude, 23 parts per trillion mean at 7.3 km altitude,
and 26 parts per trillion at 7.3 to 7.9 km altitude(1). The variation with
altitude has been ascribed to the updrafting of boundary layer air by cumulus
and cumulonimbus activity to the upper troposphere(1). URBAN/SUBURBAN: Mean,
minimum, and maximum carbon disulfide concns
in Philadelphia measured over a 40 day period (88 samples) were 65, 25, and 340
parts per trillion(2). It was detected, but not quantified, in air in
Leningrad(4). Carbon disulfide was
detected in air from three U.S. urban/suburban locations between 1979 to 1982 at
a mean concn of 0.3 ug/cu m; range 0.05 to 1.07 ug/cu m(5).
Probable Routes of Human Exposure :
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 44,441 workers, including 4,882 females, are
exposed to carbon disulfide in the
USA(1). Since the NOES survey excludes exposure to trade name chemicals which
may contain the chemical, occupational exposure may be considerably higher(SRC).
Occupational exposure to carbon disulfide may
occur through inhalation and dermal contact with this compound at workplaces
where carbon disulfide is produced or
used(SRC). The general population may be exposed to carbon
disulfide via inhalation of ambient air or ingestion of fruits,
vegetables, and other food products containing this compound(SRC).
Clinical Laboratory Methods :
The use of blood, exhaled air and urine as
biological monitors of exposure to carbon disulfide was
studied in England. A metabolite of carbon disulfide, 2-thiothiazolidine-4-carboxylic
acid was identified in urine through high performance liquid chromatography. The
head space analysis used was a sulfur specific detector to determine acid labile
carbon-disulfide in blood. End expired
breath samples were obtained through forced exhalation and carbon
disulfide was determined by a quadrupole mass spectrometer. A
general trend suggested increased uptake with increasing exposure.
Reproducibility was difficult to achieve.
Methods of Manufacturing :
... Acetylene and sulfur vapor. Carbon
disulfide and benzene are obtained from sulfur and ... ethylene,
above 1000 deg C. ... For reaction of hydrogen sulfide and carbon at 900 deg C,
a 70% conversion to carbon disulfide has
been claimed. Methane and sulfur dioxide form carbon
disulfide at elevated temp in the presence of suitable
catalysts, such as lead sulfide on pumice activated with hydrogen chloride,
giving an 84% yield at 850 deg C. ... /Using/ anthracite ... instead of methane,
a nearly quantitative conversion was obtained at 900-1000 deg C.
Human Toxicity Excerpts :
350 artificial-fiber plant workers were
examined to determine if there were changes in the oral cavity associated with
exposure to carbon disulfide. The
workers had been exposed to carbon disulfide at
concentrations of 0.02-0.065 mg/liter (6-21 ppm) and to hydrogen sulfide at
0.002-0.006 mg/liter (1-4 ppm) during the preceding 6 years ... . The group
exposed to carbon disulfide for less
than 5 years had significantly lower pH values for both the mucous membrane and
the saliva than did the controls (5.28 versus 6.09 and 5.30 versus 6.29,
respectively). Workers exposed for longer periods did not show this difference.
Based on an index of periodontic disturbances, the frequency of pathologic
changes in the periodontium of the exposed workers was significantly higher than
that of the controls. The intensity of these changes increased with length of
exposure, although the levels of significance did not. ...
Human Toxicity Excerpts :
/An investigation was conducted to determine
the effects of carbon disulfide exposure
on/ female viscose rayon workers in three different departments for possible
effects of /the compound/ on ovarian function and menstruation. The study
included 500 workers in the spinning shop, where carbon
disulfide concentrations sometimes exceeded 20 mg/cu m (6 ppm)
and hydrogen sulfide concentrations reportedly never exceeded 10 mg/cu m (7 ppm);
209 workers in the trimming department, where the concentration of neither carbon
disulfide nor hydrogen sulfide exceeded 10 mg/cu m (3 ppm); and
429 workers in the rewinding-sorting department (controls), not exposed to
either substance. Durations of menstrual flow of more than 5 days occurred in
17.8% of the spinners, 10.5% of the trimmers, and 5.1% of the controls (p<
0.0001). Workers in the spinning shop experienced irregular menstruation
significantly more frequently than the controls (7.6% and 1.6%, respectively;
p< 0.0001). The frequency of irregular menses increased with longer
occupational exposure. Heavy menstrual flow occurred in 12.5% of the spinners,
11% of the trimmers, and 2.3% of the controls (p< 0.001); painful
menstruation was also significantly more common in exposed workers (36% and 38%)
than controls (17%).
Human Toxicity Excerpts :
Cases of carbon
disulfide poisoning were reported. A 24 year old male, employed
in the curing room of an India rubber factory, was exposed to carbon
disulfide vapors for 8 months. He was admitted to the hospital
complaining of loss of sensation in the limbs, weakness, restlessness, insomnia,
memory loss, weight loss, and atrophy of arm and leg muscles. The subject had a
high stepping gait, and had difficulty standing erect. He had no ability to
produce dorsal flexion of the ankle, extension of the big toe, or inversion of
the foot. After 2.5 months, some traces of paralysis were still seen,
particularly in the dorsal flexions of the foot. Another subject, a 36 year old
male, had been exposed to carbon disulfide fumes
for 9 months in the curing room of an India rubber factory. He complained of
weakness, visual effects, deafness in one ear, pains and cramping in the lower
extremities, headache, insomnia, apathy, and memory loss. His paralysis was very
similar to that described for the other subject. After 1 month in the hospital,
the subject was much improved, although the muscles that produced dorsal flexion
of the feet were still comparatively paralyzed.
Non-Human Toxicity Excerpts :
Effects of carbon
disulfide on testicular tissues of rats were studied. Three
experiments were conducted using 85 mongrel rats, 2-5 months old and weighing
200-260 g. In the first experiment, 12 rats were injected ip every second day
for 60 days with 12.5 mg/kg of distilled carbon
disulfide dissolved in peanut oil; 5 were given pure peanut oil;
and 5 were untreated. In the second experiment, 15 animals were given ip doses
of 25.0 mg/kg every other day for 60 days; 10 rats were given pure peanut oil;
and 9 were untreated. In the third experiment, 10 were given 25.0 mg/kg ip every
other day for 120 days; 10 were injected with peanut oil; and 9 were untreated.
... The testicles of rats from exposed and control groups had similar histologic
and histochemical patterns. However, exposed rats had thickened vascular walls,
blood-cell-engorged vessels, disorganized seminiferous epithelium, and decreased
numbers of spermatozoa. Rats injected with carbon
disulfide for a 120-day period, however, showed marked
testicular damage. Advanced regressive lesions involving all parts of the
testicles of the usually round and smooth tubular basement membrane.
Spermatogonia were few and sometimes nonexistent in the seminiferous tubules,
and spermatogenesis was absent. Leydig cells showed degeneration and atrophy.
Absorption, Distribution & Excretion :
LARGE CONCN OF BOTH FREE & BOUND CARBON
DISULFIDE ARE FOUND IN BRAIN (GUINEA PIG STUDIES) &
PERIPHERAL NERVES (RAT STUDIES) OF EXPOSED ANIMALS. RATIO OF BOUND TO FREE CARBON
DISULFIDE IN BRAIN IS 3:1. BLOOD & FATTY TISSUES CONTAIN
MAINLY BOUND CARBON DISULFIDE, WHILE
LIVER CONTAINS MAINLY FREE.
Interactions :
Inhibition of drug metabolism in 19 healthy
men experimentally exposed to carbon disulfide was
studied. The men, 21-40 years old, were exposed for 6 consecutive hours in an
inhalation chamber to carbon disulfide at
10, 20, 40, or 80 ppm (31, 62, 124, or 248 mg/cu m) ... . In the first of three
experiments, each subject received 7 mg/kg of amidopyrine orally just prior to
chamber exposure ... . Urine samples collected 3, 6, 9, 12, 16, 24, and 33 hours
after the beginning of exposure were analyzed for metabolites of amidopyrine,
4-aminoantipyrine, and acetyl-4-aminoantipyrine. ... In the single 6 hour
exposures, concentrations of 10 ppm (31 mg/cu m) caused no appreciable reduction
in urinary excretion of acetyl-4-aminoantipyrine but caused significant
reductions in free 4-aminoantipyrine and total 4-aminoantipyrine. At carbon
disulfide concentrations of 20, 40, and 80 ppm (31, 124, 248
mg/cu m), reductions in free 4-aminoantipyrine, acetyl-4-aminoantipyrine, and
total 4-aminoantipyrine were statistically significant. ...
Environmental Fate :
TERRESTRIAL FATE: Based on a classification
scheme(1), an estimated Koc value of 270(SRC), determined from a log Kow of
1.94(2) and a regression-derived equation(3), indicates that carbon
disulfide is expected to have moderate mobility in soil(SRC).
Volatilization of carbon disulfide from
moist soil surfaces is expected to occur(SRC) given a Henry's Law constant of
1.44X10-2 atm-cu m/mole at 24 deg C(4). The potential for volatilization of carbon
disulfide from dry soil surfaces may exist(SRC) based upon a
vapor pressure of 359 mm Hg(5). Biodegradation data are insufficient to predict
the importance of biodegradation in the environment(SRC).
Soil Adsorption/Mobility :
The Koc of carbon
disulfide is estimated as approximately 270(SRC), using a log
Kow of 1.94(1) and a regression-derived equation(2,SRC). According to a
classification scheme(3), this estimated Koc value suggests that carbon
disulfide is expected to have moderate mobility in soil(SRC).
The avg adsorption of carbon disulfide after
10 minutes by 4 air-dried soils was 46% but only 12% by the same soils at 50%
water-holding capacity(4). However, after 8 hr the rate of adsorption was
greater by moist soil, but only when the soil was unsterilized(4). Further
experiments suggest that this "adsorption" in moist soils is the
result of microbial action(4).
Atmospheric Concentrations :
SOURCE DOMINATED: Workplace concn of carbon
disulfide in the viscose rayon industry ranged from <3 ppm to
peaks exceeding 2,000 ppm(1). 12 of 36 air samples of carbon
disulfide in the breathing zone of workers in the spinning and
cutting rooms of a viscose rayon plant contained >20 ppm 8 hr TWA, the OSHA
standard and 7 samples exceeded 100 ppm, the acceptable max peak concn(1). In a
further study, 10-20 min breathing zone concn of 8 cutters ranged from <20 to
>2,000 ppm and exceeded 100 ppm in more than half of the 196 samples
taken(1). The concns for 6 workers in the spinning area were far lower. The
overall TWA concn was 11.2 ppm with a range of 0.9 to 127 ppm(1). Shift TWA
concns for the cutters ranged from 9.5 to 129 ppm for the cutters and 4.3 to
11.1 ppm for the spinners(1). Seven of the eight cutters were exposed to concn
higher than the OSHA standard for an 8 hr day(1). Half of the general room
samples exceed the 30 ppm ceiling limit(1). Extensive long term monitoring in a
Finnish viscose rayon plant showed that concn levels of carbon
disulfide that generally exceeded 40 ppm before 1950 have been
dropping and had fallen below 5 ppm by 1972(1). Environmental concn in a US
viscose rayon plant were reported to be between 10 to 15 ppm(1).
Body Burden :
All 8 samples of mother's milk from 4 urban
areas of the U.S. contained carbon disulfide(1).
Carbon disulfide was qualitatively
detected in samples of mother's milk from Bayonne, NJ, Jersey City, NJ,
Pittsburgh, PA, and Baton Rouge, LA(2). Diurnal 2-thiothiazolidine-4-carboxylic
acid, an indicator of exposure to carbon disulfide, excretion
in urine samples collected from viscose production workers ranged from 3.4 to
41.5 mmol(3). Urinary concn of 2-thiothiazolidine-4-carboxylic acid (TTCA) of
workers during the production of viscose rayon fibers ranged from not detected
to 2.3 mg TTCA/g creatinine(4). Mean TTCA concns in urine of workers in the
viscose industry were, mg/l (department): 1.96 (spool spinning), 5.06 (spinning
of technical rayon), 6.55 (washing), 2.27 (post-treatment), and 1.14 (second
aging)(5).
Corrosivity :
Carbon disulfide is
normally stored and handled in mild steel equipment. Copper and copper alloys
are attacked by carbon disulfide and
must be avoided.
Hazardous Reactivities & Incompatibilities :
Carbon disulfide vapor,
alone or mixed with nitrogen, did not decompose explosively in the range 0.4-2.1
bar/88-142 deg C when initialized with high energy sparks or a hot wire at
700-900 deg C. The endothermic sulfide will ... decompose explosively to its
elements with mercury fulminate initiation. A screening jacket filled with carbon
disulfide was used to surround the reaction tube used in flash
photolysis experiments. When the quartz lamp was discharged, some vapor of the
disulfide which had leaked out, ignited in the radiation flash and exploded.
Disposal Methods :
Carbon disulfide is
a waste chemical stream constituent which may be subjected to ultimate disposal
by controlled incineration. A sulfur dioxide scrubber is necessary when
combusting significant quantities of carbon disulfide.
Disposal Methods :
Adsorption: The CS2 /carbon
disulfide/ adsorption employs activated coal which adsorbs it
from the mixture with hydrogen sulfide in the absence of free oxygen. An
industrial installation with the capacity to regenerate as much as 80-90% of carbon
disulfide contained in the gas-air mixture has been developed.
Medical Surveillance :
Other Tissues: The assessment of carbon
disulfide exposure can also be accomplished through measurement
of carbon disulfide in breath and milk
samples. Air levels may yield some information about recent, short term
exposure, but correlation with actual exposure levels has been poor. Milk
analysis may be useful as a qualitative indicator of exposure only.
Human Toxicity Excerpts :
Five hundred synthetic fiber workers who had
been exposed to carbon disulfide at
concentrations reportedly not exceeding 0.01 mg/liter (3 ppm) were studied.
Workers were 18-60 years old and had been exposed for periods of 0.5-30 years.
Those exposed for short periods of time (usually less than 5 years) generally
had mild visual disturbances such as conjuntival inflammations, temporary
corneal opacities, and disturbed color vision. Prolonged exposure to carbon
disulfide was reported to have caused irreversible vascular
effects and inflammatory degenerative changes in the retina.
Human Toxicity Excerpts :
Male viscose rayon workers, diagnosed as
chronically poisoned by carbon disulfide were
studied. ... Concentrations at which the viscose rayon workers were exposed were
10-30 ppm (31-93 mg/cu m) in the 1960's, 20-40 ppm (62-124 mg/cu m) in the
1950's, and higher than 40 ppm (124 mg/cu m) prior to 1950. The most significant
differences between the poisoned and control groups were the prevalence of
general fatigue, insomnia, paresthesia, and headaches in the exposed workers
(p< 0.001 for all four symptoms). Psychologic testing revealed mild
intellectual impairment, reduction of sensorimotor speed, and impaired
psychomotor ability. The psychologic disturbances were said to correlate well
with duration of exposure, ie, patients with shorter carbon
disulfide histories generally had milder disturbances.
Human Toxicity Excerpts :
Pregnancy data for 380 women employed in the
viscose industry /were analyzed/ to determine the effects of carbon
disulfide on pregnancy. The exposed group included 189 women
who, before and during pregnancy, were exposed to carbon
disulfide at concentrations reported to be 2.7 times the Soviet
permissible limit of 10 mg/cu m (3 ppm). ... Several pregnancy complications
were recorded, and comparisons were made between exposed and control women. The
rate of threatened pregnancy terminations in the exposed group was 25.9/100
pregnant women versus 13.1/100 pregnant women in the controls (p< 0.05). The
difference was still significant after adjustment for the differences in age and
job longevity. Threatened pregnancy terminations occurred more frequently in the
exposed women than in the controls, 12.5% versus 9.4% in the 20- to 24-year-old
age group and 35.4% versus 13.6% in the 25- to 29-year-old age group.
Spontaneous abortions occurred in 14.3% of the exposed women and 6.8% of the
controls (p< 0.05).
Human Toxicity Excerpts :
Thirty workers of a viscose rayon industry had
a complete eye examination in 1979 including visual acuity, perimetry, color
vision testing, fluorescein angiography, ERG and EOG, for possible signs of
chronic carbon disulfide poisoning.
Fundus anomalies and abnormal electrooculogram's and electroretinogram's were
found. Twenty-nine of these thirty workers were reexamined in 1983. A number of
them were no longer exposed to carbon disulfide for
a period varying between 1 and 43 months. The fundus signs (pigmentary changes
and vascular lesions) increased in frequency, even if the patient was no longer
exposed.
Human Toxicity Excerpts :
Carbon disulfide is
a potent nerve toxin; it also may accelerate coronary artery disease. Peripheral
neuropathies, cranial nerve dysfunction, and neuropsychiatric changes are
present in over 70% of chronic carbon sulfide victims. Impaired psychomotor
function ... and higher cortical function ... as well as neurasthenic symptoms
... characterize the neurologic illness associated with excessive carbon
disulfide exposures. These neuropsychiatric symptoms may be
irreversible. Chronic long-term exposures (eg, in rayon workers) may result in
elevated blood cholesterol, retinopathy ... peripheral neuropathy, decreased
glucose tolerance, reduced serum thyroxine levels, and parkinsonism. Increases
in atherosclerosis, coronary artery disease, deaths, suicide rates, personality
changes, and hypertensive disease have been suggested, but not confirmed, by
epidemiological studies.
Non-Human Toxicity Excerpts :
Female albino rats were exposed to carbon
disulfide vapor to study its effects on the course and duration
of pregnancy. The animals, in groups of 12-20, were exposed to carbon
disulfide at a concentration of 2,000 mg/cu m (642 ppm) for 2
hours/day during the entire pregnancy. Two identical series of tests were
performed on rats. In the first experiment, 16.8% pre-implantation embryonic
mortality occurred in the 12 exposed animals and 3.3% in the 12 controls (P<
0.05). In the second experiment, the pre-implantation mortality rate was 22.6%
in 12 exposed rats and 6.5% in 14 controls (p< 0.05). The reproductive
success of each exposed group was lower than that of its control group in both
experiments (6.8 versus 9.7 fetuses per rat, p< 0.05, and 8.0 versus 9.3
fetuses per rat). There were seven post-implantation deaths in the fetuses of
exposed rats and none in those of the controls. There were no significant
differences between experimental and control rats in the mean corpus luteum
counts or in mean fetal weights.
Non-Human Toxicity Excerpts :
Female Wistar rats were exposed to 100 or 600
ppm of carbon disulfide for 6 hr/day,
5 days/wk, for 12 wk to determine the effects on tissue Vitamin B6
concentrations. Liver, kidney, and brain tissue were assayed at the end of 12 wk
(12 rats/group and 12 controls exposed to fresh air) for five forms of B6:
pyridoxine, pyroxidal, pyridoxamine, pyridoxal phosphate, and pyridoxamine
phosphate. During the experiment, urine was assayed for 4-pyridoxic acid on day
5 of wk 2, 4, 6, 10, and 12. By wk eight there were significant differences
(p< 0.01) in the body weights of the 3 groups; 600 ppm, 208 + or - 7.5 g; 100
ppm, 216 + or - 9.2 g; and control, 221 + or - 5.2 g. Excretion of 4-pyridoxic
acid throughout the experiment after exposure to 100 ppm was essentially the
same as the control, but excretion of 4-pyridoxic acid after exposure to 600 ppm
was significantly decreased (p< 0.01) during the first 4 wk of exposure and
was continuous (p< 0.05) for the 12 wk. Pyridoxine was not detected in liver,
kidney, or brain tissue and pyridoxamine was detected only in liver tissue. Even
exposure to 600 ppm, carbon disulfide had
no significant effect on the content of the forms of vitamin B6 in any of the
tissues examined.
Non-Human Toxicity Excerpts :
... CARBON DISULFIDE
IS ... RECOGNIZED AS INHIBITOR OF BRAIN MONOAMINE OXIDASE ...
MONOAMINE OXIDASE ALSO CONTAINS COPPER AND UTILIZES PYRODOXYLPHOSPHATE (A FORM
OF VITAMIN B6) AS A COENZYME. SINCE CARBON DISULFIDE CAN
REACT WITH PYRIDOXAMINE TO FORM PYRIDOXAMINEDITHIOCARBAMIC ACID (WHICH IN TURN
CAN BE OXIDIZED BY IODINE IN VITRO TO AN ANALOGUE OF DISULFIRAM), TWO POSSIBLE
MECHANISMS EXIST FOR INHIBITION OF MONOAMINE OXIDASE.
Absorption, Distribution & Excretion :
ABSORPTION OCCURS THROUGH ALL PORTALS
INCLUDING THE INTACT SKIN. ... CARBON DISULFIDE VAPOR
IS RAPIDLY ABSORBED WHEN INHALED; AN APPROXIMATE EQUILIBRIUM BETWEEN BLOOD AND
INHALED VAPOR IS REACHED IN 1-2 HOURS. ... SOME ABSORBED CARBON
DISULFIDE IS EXCRETED IN EXPIRED AIR ... TRACES HAVE BEEN FOUND
IN THE BLOOD 80 HR AFTER TERMINATION OF EXPOSURE, ABOUT 70% OF AN INHALED DOSE
IS EXCRETED OR METABOLIZED WITHIN A FEW HOURS. THE REMAINING 30% IS SLOWLY
EXCRETED IN THE URINE AS SUCH OR AS METABOLITES.
Mechanism of Action :
Chelation of copper-containing enzyme by the
reaction products of carbon disulfide and
biological amines has been observed and has been proposed as one of the
mechanisms by which carbon disulfide induces
neurotoxicity.
Environmental Fate :
AQUATIC FATE: Based on a classification
scheme(1), an estimated Koc value of 270(SRC), determined from a log Kow of
1.94(2) and a regression-derived equation(3), indicates that some adsorption of carbon
disulfide to suspended solids and sediment in the water column
is expected(SRC). Carbon disulfide is
expected to volatilize from water surfaces(3,SRC) based on a Henry's Law
constant of 1.44X10-2 atm-cu m/mole at 24 deg C(4). Estimated volatilization
half-lives for a model river and model lake are 2.6 hours and 3.5 days,
respectively(3,SRC). According to a classification scheme(5), BCFs of <6.1
and <60 in carp at 50 and 5 ug/l, respectively(6) suggest bioconcentration in
aquatic organisms is low to moderate(SRC). Biodegradation data are insufficient
to predict the importance of biodegradation in the environment(SRC).
Environmental Fate :
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), carbon disulfide, which
has a vapor pressure of 359 mm Hg at 25 deg C(2), is expected to exist solely as
a vapor in the ambient atmosphere. Vapor-phase carbon
disulfide is degraded in the atmosphere by reaction with
photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction
in air is estimated to be 5.5 days(3,SRC).
Environmental Biodegradation :
It has been demonstrated that the adsorption
of carbon disulfide by moist
unsterilized soil increases sharply after approximately 3 hr and the time for
complete sorption of the gas decreases with repeated dosing(1). This behavior
does not occur with air-dried or sterilized soil and has been ascribed to
microbial utilization of the chemical(1). Carbon
disulfide is oxidized by some heterotrophs(2).
Environmental Water Concentrations :
DRINKING WATER: Drinking water samples from
nine cities in the US and one rural well contained no carbon
disulfide (no detection limit stated)(1). It was detected, but
not quantified, in New Orleans(2), Miami, and Cincinnati drinking water(3).
Water samples obtained from collapsible fabric tanks used for potable water
storage for U.S. Army field exercises in 1982 and 1987 contained a maximum carbon
disulfide concn of 33 ug/l(4).
Effluent Concentrations :
Carbon disulfide was
detected in air samples collected from blower exhausts, from an active
composting operation, at a concn of 224 ug/cu m(1). Carbon
disulfide was detected at a concn of 10 ppb in water collected
from a monitoring well at the Ionia City Landfill, MI(2). It has been detected
in leachate liquid from the Lipari Landfill, NJ at concns ranging from 5 to 42
ug/l(3).
Sediment/Soil Concentrations :
The mean concn of carbon
disulfide in 5 samples of mud from the sea bottom was 29.5 parts
per trillion(1). Concns in salt marshes ranged from 76 to 228 ng/l(2). Soil
samples from the Lipari Landfill, NJ contained carbon
disulfide at an avg concn of 220 ug/kg; maximum concn 1,300 ug/kg(3).
It was also detected in soils from Chestnut Branch Marsh, located adjacent to
the landfill, at concns ranging from 11 to 33 ug/kg(3).
Milk Concentrations :
All 8 samples of mother's milk from 4 urban
areas of the U.S. contained carbon disulfide(1).
Carbon disulfide was qualitatively
detected in samples of mother's milk from Bayonne, NJ, Jersey City, NJ,
Pittsburgh, PA, and Baton Rouge, LA(2).
Probable Routes of Human Exposure :
Exposure to carbon
disulfide is mostly occupational via inhalation and dermal
contact with the vapor or dermal contact with the liquid. Inhalation is the
principal route of absorption(1). While workers engaged in any process using carbon
disulfide may be exposed to some degree, in practice, only
workers in the viscose rayon industry are exposed to high concn(1).
Clinical Laboratory Methods :
Carbon disulfide in
urine (treated with a solution of sodium azide, iodine and potassium iodide)
using Iodine-Azide Test; concentrations of less than 20 ppm carbon
disulfide in air were not detectable.
Methods of Manufacturing :
(1) Reaction of natural gas or petroleum
fractions with sulfur. (2) From natural gas and hydrogen sulfide at very high
temperature (plasma process). (3) By heating sulfur and charcoal and condensing
the carbon disulfide vapors.
Formulations/Preparations :
Modern plants generally produce carbon
disulfide of about 99.99% purity.
Major Uses :
For Carbon disulfide
(USEPA/OPP Pesticide Code: 016401) there are 0 labels match. /SRP:
Not registered for current use in the U.S., but approved pesticide uses may
change periodically and so federal, state and local authorities must be
consulted for currently approved uses./
Major Uses :
Miscellaneous application include direct uses
of carbon disulfide for the cold
vulcanization of rubber, as a flame lubricant in cutting glass, and for
generating petroleum catalysts ... .
Consumption Patterns :
CHEMICAL PROFILE: Carbon
disulfide. Carbon tetrachloride, 38%; rayon, 34%; rubber
chemicals, 7%; cellophane and other regenerated cellulosics, 6%; agricultural
chemicals, 5%; miscellaneous, 10%.
Consumption Patterns :
CHEMICAL PROFILE: Carbon
disulfide. Demand: 1988: 400 million lb; 1989: 390 million lb;
1993 /projected/: 325 million lb. (Includes imports, which totaled 2.8 million
lb in 1987; exports are negligible.)
Odor :
When pure, carbon
disulfide has sweetish aromatic odor similar to that of
chloroform.
Corrosivity :
Liquid carbon
disulfide will attack some forms of plastics, rubber, and
coatings.
Solubilities :
Solubility of water in carbon
disulfide: 86 ppm at 10 deg C; 142 ppm at 25 deg C
Other Chemical/Physical Properties :
DIPOLE MOMENT 0.0; HEAT OF FUSION 1.049
KCAL/MOLE; HEAT CAPACITY @ 24.3 DEG C: 18.17 CAL/MOLE/DEG; EBULLIOSCOPIC
CONSTANT 2.35 DEG; DIELECTRIC CONSTANT 2.641 AT LOW FREQUENCIES; BURNS WITH BLUE
FLAME TO CARBON DIOXIDE AND SULFUR DIOXIDE; AZEOTROPE WITH WATER BP 42.6 DEG C,
CONTAINS 97.2% CARBON DISULFIDE
Fire Potential :
Carbon disulfide vapor
is explosive, igniting spontaneously on contact with sparks or at temperatures
above 147 degrees C.
Toxic Combustion Products :
Toxic gases and vapors (such as sulfur dioxide
and carbon monoxide) may be released in a fire involving carbon
disulfide.
Hazardous Reactivities & Incompatibilities :
Disposal of 2 liters of the solvent into a
rusted iron sewer caused an explosion. Initiation of the solvent-air mixture by
rust was suspected. A hot gauze falling from a tripod into a lab sink containing
some carbon disulfide initiated two
explosions. ... The vapor or liquid has been known to ignite on contact with
steam pipes, particularly if rusted. When a winchester of the solvent fell off a
high shelf and broke behind a rusted steel cupboard, ignition occurred.
Hazardous Reactivities & Incompatibilities :
The bis- or tris-complexes of phenylcopper
with triphenylphosphine react violently and exothermically with carbon
disulfide, even at 0 deg C.
Hazardous Reactivities & Incompatibilities :
Carbon disulfide plus
any of the azides produces violently explosive, extremely sensitive salts.
Hazardous Reactivities & Incompatibilities :
Mixing carbon
disulfide and ethylenediamine in a closed container caused the
temperature and pressure to increase.
Protective Equipment & Clothing :
If the use of respirators is necessary, the
only respirators permitted are those that have been approved by the Mine Safety
and Health Administration (formerly Mining Enforcement and Safety
Administration) or by the National Institute for Occupational Safety and Health.
... Employees should be provided with and required to use impervious clothing,
gloves, face shields (eight-inch minimum), and other appropriate protective
clothing necessary to prevent skin contact. ... Employees should be provided
with and required to use splash-proof safety goggles where liquid carbon
disulfide may contact the eyes.
Preventive Measures :
Areas suspected of high concn of carbon
disulfide vapor should not be entered because of the explosion
hazard.
Preventive Measures :
CARBON DISULFIDE SHOULD
NOT BE ALLOWED TO ENTER A CONFINED SPACE, SUCH AS A SEWER, BECAUSE OF THE
POSSIBILITY OF AN EXPLOSION.
Storage Conditions :
Protect containers against physical damage.
Store in well detached and isolated places from other buildings, other materials
and possible sources of ignition, preferably in a building of noncombustible, or
better, constructed with floor level ventilation. Avoid direct sunlight. Tanks
should be submerged in water or located over concrete basins containing water of
sufficient compacity to hold all of the tank contents in addition to the water.
Water or inert gas should be provided over the carbon
disulfide in all tanks. No electrical installations or heating
facilities should be permitted in or near storage area.
Cleanup Methods :
1. REMOVE ALL IGNITION SOURCES. 2. VENTILATE
AREA OF SPILL OR LEAK. 3. FOR SMALL QUANTITIES, ABSORB ON PAPER TOWELS.
EVAPORATE IN A SAFE PLACE (SUCH AS A FUME HOOD). ALLOW SUFFICIENT TIME FOR
EVAPORATING VAPORS TO COMPLETELY CLEAR THE HOOD DUCTWORK. BURN THE PAPER IN A
SUITABLE LOCATION AWAY FROM COMBUSTIBLE MATERIALS. LARGE QUANTITIES CAN BE
RECLAIMED OR COLLECTED AND ATOMIZED IN A SUITABLE COMBUSTION CHAMBER EQUIPPED
WITH AN APPROPRIATE EFFLUENT GAS CLEANING DEVICE. CARBON
DISULFIDE SHOULD NOT BE ALLOWED TO ENTER A CONFINED SPACE, SUCH
AS A SEWER, BECAUSE OF THE POSSIBILITY OF AN EXPLOSION.
Disposal Methods :
Reuse: This cmpd is a very flammable liquid
which evaporates readily. It burns ... to carbon dioxide (harmless) and sulfur
dioxide. ... The pure liquid presents an acute fire and explosion hazard. ... If
quantity is large, carbon disulfide may
be recovered by distillation and repackaged for use. Recommendable methods:
Evaporation, adsorption, & incineration. Not recommendable method: Landfill.
Peer-review: Care. Substance very easily ignited. Landfill is not recommendable
due to the high flammability. Evaporate small amt only. (Peer-review conclusions
of an IRPTC expert consultation (May 1985))
Antidote and Emergency Treatment :
For basic treatment: Establish a patent
airway. Suction if necessary. Watch for signs of respiratory insufficiency and
assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10
to 15 L/min. Anticipate seizures and treat if necessary ... . Monitor for shock
and treat if necessary ... . For eye contamination, flush eyes immediately with
water. Irrigate each eye continuously with normal saline during transport ... .
Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200
mL water for dilution if the patient can swallow, has a strong gag reflex, and
does not drool. Administer activated charcoal ... . Cover skin burns with
sterile dressings after decontamination ... . /Carbon
disulfide and related compounds/
Antidote and Emergency Treatment :
For advanced treatment: Consider orotracheal
or nasotracheal intubation for airway control in the patient who is unconscious.
Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with
lactated Ringer's TKO /SRP: To keep open, "minimal flow rate"/. Treat
seizures with diazepam (Valium) ... . For hypotension with signs of hypovolemia,
administer fluid cautiously. Watch for signs of fluid overload ... . Use
proparacaine hydrochloride to assist eye irrigation ... . /Carbon
disulfide and related compounds/
Human Toxicity Excerpts :
WOMEN APPEAR TO BE MORE SENSITIVE THAN MEN TO
THE NEUROTOXIC EFFECTS OF CARBON DISULFIDE. ... ABNORMALLY
HIGH SERUM LEVELS OF CHOLESTEROL AND BETA-LIPOPROTEIN ... IN CHRONICALLY EXPOSED
WORKERS ... WITH HIGH INCIDENCE OF HYPERTENSION AND ATHEROSCLEROSIS AND ...
REDUCTION IN FIBRINOLYSIS ACTIVITY OF BLOOD SERUM. ... CHRONIC GASTRITIS WITH
DYSPEPSIA ... .
Human Toxicity Excerpts :
IN A SURVEY OF RAYON FACTORIES WHERE CARBON
DISULFIDE IN AIR WAS 37-56 MG/CU M, FEMALE SPINNERS SHOWED HIGH
INCIDENCE OF MENSTRUAL DISTURBANCES & PREGNANCY TOXEMIA.
Human Toxicity Excerpts :
AT 10.2 UG/CU M MEDIUM, CARBON
DISULFIDE INCREASED FREQUENCY OF SISTER CHROMATID EXCHANGES IN
CULTURED HUMAN PERIPHERAL BLOOD LYMPHOCYTES BY APPROX 50%. LOWER CONCN HAD NO
EFFECT.
Human Toxicity Excerpts :
/A study was conducted to compare/ 118 male
viscose rayon workers who had been exposed /to carbon
disulfide/ for a mean of 15 years with 100 papermill workers
(controls) for possible neurophysiologic differences. ... The greatest
difference between exposed and control workers was found in the conduction
velocities of the slower motor fibers in the ulnar nerve (39.8 versus 44.1
m/second, p< 0.0005) and the deep peroneal nerve (35.5 versus 38.2 m/second,
p< 0.0005). Significant differences from normal were also found in the
maximum motor conduction velocities of the posterior tibial nerve (40.5 versus
42.4 m/second, p< 0.0005) and deep peroneal nerve (45.9 versus 47.3 m/second,
p< 0025). A conduction velocity was determined for each nerve tested such
that 5% of the controls showed a conduction velocity below this value; each
subject was then assigned a total conduction velocity score by counting one
point for each nerve whose conduction velocity was below the limit for that
nerve. The distribution of scores showed significantly slower conduction
velocities in exposed workers. The lower conduction velocity scores /were
regarded/ as an indication of increased polyneuropathy. The exposed group also
had a larger number of abnormal EEG's (21 of 54) than did the controls (6 of
50); was significant at the 1% level.
Human Toxicity Excerpts :
138 artificial silk workers whose exposure to carbon
disulfide, averaging more than 10 years, had been at
concentrations averaging between 20 and 42 mg/cu m (6-13 ppm) during the past 8
years, with peaks of 120-180 mg/cu m (39-58 ppm) /were examined/; earlier
levels, believed to have been higher, were not documented. Atherosclerotic
changes, as indicated by clinical, electrocardiographic, oscillometric, and
optic fundi examination and by estimation of cholesterolemia, triglyceridemia,
were found in 30.4% of the subjects and arterial hypertension in 23.2%; 14.5% of
the workers showed both conditions. ...
Human Toxicity Excerpts :
... Employees were often exposed to carbon
disulfide 10-12 hours/day at concentrations of up to 2.50
mg/liter (800 ppm), although the mean concentrations ranged from 0.45 to 1.0
mg/liter (144-321 ppm). In the 100 workers examined, polyneuritic symptoms were
observed in 88% of the patients. ...
Human Toxicity Excerpts :
WOMEN EMPLOYED IN RAYON TEXTILE JOBS &
PAPER PRODUCTS JOBS HAD INCREASED RATE (P< 0.10) OF SPONTANEOUS ABORTIONS;
THE WIVES OF MEN EMPLOYED IN TRANSPORT & COMMUNICATION, IN RAYON TEXTILE
JOBS & IN CHEMICAL PROCESS JOBS ALSO HAD INCREASED RATE OF SPONTANEOUS
ABORTIONS. NO EVIDENCE WAS FOUND THAT LEVEL OF CARBON
DISULFIDE COULD BE ASSOC WITH RISK OF SPONTANEOUS ABORTIONS.
Human Toxicity Excerpts :
The spinners, the workers most heavily exposed
to carbon disulfide, have a
significantly higher mortality from all causes than the least exposed group. The
excess mortality is largely accounted for by ischemic heart disease for which
the spinners have a standard mortality ratio of 172. When mortality is related
to an exposure score in the same group, both all cause (p< 0.01) and ischemic
heart disease (p< 0.001) mortality increase with increasing exposure level.
When this analysis is repeated covering all ages these trends become much less
strong and only that for ischemic heart disease remains significant (p<
0.05). Over the age of 65 there is a tendency for mortality to decline with
increasing exposure.
Human Toxicity Excerpts :
Effects of carbon
disulfide in air: slight or none (160-230 ppm); slight symptoms
after several hr (320-390 ppm); symptoms after 30 min (420-510 ppm); serious
symptoms after 30 min (1150 ppm); dangerous to life after 30 min (3210-3850 ppm);
fatal in 30 min (4815 ppm) /From table/
Human Toxicity Excerpts :
Retinopathy seen in /workers exposed to carbon
disulfide/ in Japan, ... consists of microaneurysns and small
hemmorhages ... . In Finland positive findings were delayed peripapillary
filling on fluoresein angiography, widening of retinal arterioles, and lower
peak to ocular pulse wave.
Human Toxicity Excerpts :
Local contact results in erythema and pain
since carbon disulfide is one of the
most potent fat solvents. Prolonged contact produces vesiculation and chemical
burns. Severe chemical burns of the cornea result from direct contact with the
eyes.
Human Toxicity Excerpts :
Adverse effects of carbon
disulfide exposure on reproductive function...have been reported
in exposed workers, with significantly lower sperm counts and more abnormal
spermatozoa than in unexposed control subjects.
Human Toxicity Excerpts :
Of 27 patients that were acutely exposed to
airborne carbon disulfide, 59% had a
headache, 52% experienced nausea, 4% experienced vomiting, 40% felt a burning of
the throat, lips, or skin, 59% experienced dizziness, 15% had shortness of
breath or chest pain, and 7% experienced impotence.
Non-Human Toxicity Excerpts :
CARBON DISULFIDE WAS
NOT MUTAGENIC TO SALMONELLA TYPHIMURIUM STRAINS TA98 & TA100 AT 300-1000
UMOL NOR TO ESCHERICHIA COLI STRAIN WP2 UVRA AT 20-600 UMOL WITH OR WITHOUT
METABOLIC ACTIVATION, NOR IN DROSOPHILA MELANOGASTER AT 200-800 PPM.
Non-Human Toxicity Excerpts :
PRENATAL EXPOSURE OF ALBINO RATS TO CARBON
DISULFIDE AT 10 & 0.03 MG/CU M LED TO INHIBITION &
RETARDATION OF DEVELOPMENT OF MIXED FUNCTION OXIDASE SYSTEM.
Non-Human Toxicity Excerpts :
Carbon disulfide exposure
can induce kynureninase and lead to disorders of tryptophan metabolism.
Non-Human Toxicity Excerpts :
...eight dogs were exposed to 400 ppm carbon
disulfide in air 8 hr per day, 5 days per week, for 10-15 weeks.
When removed from the chamber, the dogs were drowsy and staggered and stumbled
as if drunk. They were very thirsty but did not eat for hours after leaving the
chamber. Although they slept most of the time they were in the chamber, they
were excited and noisy at night in their kennels. The dogs also developed many
clinical and pathological signs analogous to those in workers: marked behavioral
changes and toxic disease of nerve cells of the cortex of the brain were
observed in all of them. Rigidity and tremor (parkinsonism) and choreatic
movements were seen frequently, as was disease of the nerve cells of the basal
ganglia. Motor weakness, flaccid paralysis, and nerve tenderness were the most
frequent signs observed; the peripheral nerves showed axonal degeneration while
the myelin sheath was well preserved. Cardiovascular changes included
electrocardiographic abnormalitities, especially inversion of the T wave,
retinal angiospasms, and artherosclerosis of the veins of the cortex of the
brain.
Non-Human Toxicity Excerpts :
In rats, carbon
disulfide causes progressive testicular atrophy after repeated
parenteral administration. The testes from these animals exhibit vasodilation,
hemorrhage, and fluid exudation into the testicular parenchyma, suggesting a
possible vascular origin for the atrophy. Testicular damage is not observed
after inhalation exposure.
Human Toxicity Values :
Most acute carbon
disulfide fatalities result from an ingestion of which 15 ml may
be fatal to an adult.
National Toxicology Program Studies :
Carbon disulfide (CS),
... was evaluated for toxic and teratogenic effects in timed-pregnant CD rats.
CS (0, 100, 200, 400 and 600 mg/kg/day, po) in corn oil was administered in a
volume of 5 ml per kilogram of body weight on gestational days (gd) 6 through
15. Females were weighed and observed during daily treatment and at 1 and 4
hours post-dosing for clinical signs of toxicity. At sacrifice on gestational
days 20, a total of 22-27 confirmed-pregnant females per treatment group were
evaluated. The gravid uterus for each dam was weighed and the number of
implantation sites, and live, dead or resorbed fetuses were recorded. ... During
CS treatment, dams exhibited clinical signs including rough or erect coat,
lethargy, postural abnormalities, hind limb paralysis and weight loss; clinical
signs were most frequent and severe in the 400 and 600 mg/kg/day groups. The
maternal mortality rate was 4% (1/25) for the 400 mg/kg/day group and 0% for all
other dose groups. On gestational days 11, 15 and 20 maternal body weight was
decreased across treatment groups in a dose-related manner with 400 mg/kg/day CS
dams exhibiting body weights significantly below vehicle controls on gestational
days 15 and 20, and 600 mg/kg/day CS dams exhibiting body weights significantly
below controls on gestational days 11, 15 and 20. ... Maternal weight gain
during the treatment period was significantly below controls for dams treated
with 200, 400 or 600 mg/kg/day CS. Absolute weight gain was significantly below
controls for the 400 and 600 mg/kg/day CS groups. Gestational weight gain was
below controls for all CS-treated groups. Relative maternal liver weight was
increased in a dose-related manner with statistically significant increases
above vehicle control observed in the 400 and 600 mg/kg/day CS groups; absolute
maternal liver weight did not differ among treatment groups. The percentage per
litter of resorbed, dead, nonlive (i.e., dead plus resorbed) or affected (i.e.,
nonlive plus malformed) fetuses did not differ among dose groups. Among those
litters containing live fetuses, there were no differences among dose groups in
the number of live fetuses per live litter or in the proportion of males per
live litter. Average fetal body weight per live litter was reduced in a
dose-related manner, with CS 200, 400 and 600 mg/kg/day litters significantly
below controls; males and females were equally affected on this measure. The
percentage of fetuses malformed per litter, but not the proportion of litters
with one or more malformed fetuses, differed significantly among treatment
groups, but no clear dose-effect relationship was observed. In conclusion, CS
(0, 100, 200, 400 or 600 mg/kg/day, po) administered on gd 6 through 15,
produced dose-related maternal and fetal toxicity, but failed to increase the
incidence of malformations in CD rats relative to vehicle control subjects.
Absorption, Distribution & Excretion :
CARBON DISULFIDE CAN
REACH FETUSES THROUGH PLACENTA OR BABIES BY WAY OF MOTHER MILK WHEN PREGNANT OR
BREAST-FEEDING DURING OR FOLLOWING EXPOSURE.
Absorption, Distribution & Excretion :
Carbon disulfide blood
concentrations reached maximum levels after 2 hours of exposure to about 30 ppm
of vapor in air and ranged from 0.15-0.28 mg/l.
Absorption, Distribution & Excretion :
People not previously exposed absorb about 80%
of inhaled vapor during the first 15 minutes, but proportion falls to about 40%
after 45 minutes and remains at that level for some time. If workers are
previously exposed, about 55% of the inhaled vapor is absorbed during the first
15 minutes. Excretion through the lungs and the urine is small, with about 92%
of carbon disulfide retained in the
tissues and metabolized.
Metabolism/Metabolites :
A SMALL AMT OF CARBON
DISULFIDE IS APPARENTLY CONVERTED TO HYDROGEN SULFIDE, WHICH IS
RAPIDLY OXIDIZED TO SULFATE AND EXCRETED IN THE URINE.
Metabolism/Metabolites :
CARBON DISULFIDE REACTS
WITH A VARIETY OF NUCLEOPHILIC FUNCTIONAL GROUPS ... AMINO, TO FORM
DITHIOCARBAMIC ACIDS ... MERCAPTO, TO FORM TRITHIOCARBAMIC ACIDS ... HYDROXYL,
TO FORM XANTHOGENIC ACIDS ... CMPD WITH TWO SUCH GROUPS TO FORM HETEROCYCLES.
Metabolism/Metabolites :
CARBON DISULFIDE ADMIN
IP TO RATS WAS OXIDIZED TO (14)CO2 TO AN EXTENT PROPORTIONAL TO THE AMOUNT OF
CYTOCHROME P450 PRESENT IN THE LIVER AT THE TIME OF ADMIN.
Metabolism/Metabolites :
Between 10 and 30% of absorbed carbon
disulfide is exhaled, less than 1% is excreted in the urine, and
the remaining 70-90% undergoes biotransformation before excretion in the urine
in the form of sulfur-containing metabolites, only some of which have been
identified (eg, thiourea and mercaptothiazolinone).
Biological Half-Life :
Half-life for disappearance of /carbon
disulfide/ from blood is estimated at less than 1 hour.
Mechanism of Action :
MICROSOMAL METAB OF CARBON-CENTERED THIONON-SULFUR
CONTAINING CMPD IS DISCUSSED USING CARBON DISULFIDE, THIOACETAMINE,
METHIMAZOLE & ALPHA-NAPHTHYLTHIOUREA AS EXAMPLES. IT IS SUGGESTED THAT
COVALENT BINDING OF ATOMIC SULFUR RELEASED IN CYTOCHROME P450 MONOOXYGENASE-CATALYZED
METABOLISM OF THIONON-SULFUR COMPOUNDS IS RESPONSIBLE FOR MONOOXYGENASE
INHIBITION.
Interactions :
... SIGNS OF CARBON
DISULFIDE POISONING IN ANIMALS ARE INTENSIFIED BY RESERPINE,
IPRONIAZID, AND AMPHETAMINE. ...
Interactions :
... TRYPTOPHAN-ENRICHED DIET INCREASES
TOXICITY OF CARBON DISULFIDE. ...
Interactions :
IT IS NOW RECOGNIZED THAT THE NEURAL RESPONSES
TO CARBON DISULFIDE ARE GREATLY
INFLUENCED BY THE MINERAL CONTENT OF THE DIET, AT LEAST IN ANIMALS. A HIGHLY
MINERALIZED DIET OFFERING SUBSTANTIAL PROTECTION FROM NEUROLOGIC EFFECTS.
Interactions :
INCLUSION OF EQUIMOLAR MIXT OF CARBON
DISULFIDE IN ORAL DOSE OF APPROX 4 LD50'S OF CARBON
TETRACHLORIDE (5 MMOL/KG) TO PHENOBARBITONE-PRETREATED RATS REDUCED THE AMT OF
LIVER INJURY DUE TO CARBON TETRACHLORIDE & PREVENTED DEATHS.
Interactions :
In cholesterol fed rabbits carbon
disulfide greatly accelerated formation of atheroma.
Interactions :
Pregnant rats were exposed to 0, 100, 200, 400
or 800 ppm of carbon disulfide (CS2),
100 ppm hydrogen sulfide (H2S) alone or in combination with 400 or 800 ppm CS2,
6 hr/day during days 6-20 gestation. Maternal reproduction and fetal parameters
were evaluated on gestational day 21. Treatment with 100 or 200 ppm CS2 or with
100 ppm H2S caused no maternal toxicity or adverse effects on the developing
embryo or fetus. Exposure to 400 or 800 ppm CS2 resulted in a low incidence of
club foot and in a significant reduction of maternal weight gain. Significant
incr in unossified sternebrae occurred at 800 ppm CS2 and reduction of fetal
body weight at 400 and 800 ppm CS2. The latter effect was enhanced by
combination with 100 ppm H2S. ... At levels of exposure associated with maternal
toxicity, CS2 leads to an incr in incidence of club foot and to fetal toxicity
which is enhanced by simultaneous exposure to H2S.
Environmental Abiotic Degradation :
Carbon disulfide hydrolyzes
to carbon dioxide and hydrogen disulfide in alkaline solutions(1). The half-life
for hydrolysis at pH 9 extrapolated from measurements at higher pH is 1.1 yr
(1). It is stable in oxygenated seawater for >10 days(2).
Environmental Bioconcentration :
BCFs of <6.1 and <60 were measured in
carp for carbon disulfide at
concentrations of 50 and 5 ug/l, respectively(1). According to a classification
scheme(2), these BCFs suggest bioconcentration in aquatic organisms is low to
moderate(SRC).
Environmental Water Concentrations :
GROUNDWATER: Groundwater samples collected
from the Lipari Landfill, NJ in 1984, contained carbon
disulfide at <50 ppb(1).
Food Survey Values :
Carbon disulfide was
detected in the following fruits and vegetables sampled from a major wholesale
market in Sydney, Australia between 1993 and 1995, ug/g (n,% positive): apples,
0.06 to 1.74 (40,82.5%); avocado, <0.02 to 0.12 (16,6.3%); banana, <0.02
(13,0%); beans, 0.07 to 0.68 (25,44.0%); brocol, 0.08 to 1.09 (21,100%);
cabbage, 0.04 to 1.37(25,80.0%); bok choy, <0.02 to 0.12 (7,14.3%); capsicum,
0.04 to 0.59 (24,37.5%); carrots, 0.07 to 1.17 (56,21.4%); cauliflower, 0.07 to
1.11 (22,45.5%); celery, 0.06 to 1.70 (22,27.3%); cherries, 0.02 to 0.91
(21,38.1%); chinese cabbage, 0.25 to 2.19 (6,50.0%); citrus, 0.08 to 0.33
(45,6.7%); cucumber, 0.03 to 3.05 (14,71.4%); grapes, 0.08 to 4.11 (45,80.0%);
lettuce, 0.07 to 0.77 (39,38.5%); mango, 0.08 to 0.40 (16,37.5%); mushroom,
<0.02 to 0.12 (17,5.9%); nectarines, <0.02 to 8.9 (38,47.4%); onion, 0.04
to 4.20 (46,28.3%); peach, 0.07 to 3.31 (36,63.0%); pears, 0.07 to 1.35
(27,63.0%); potato, 0.01 to 0.93 (51,37.3%); rockmelon, 0.02 to 0.1 (24,16.7%);
silver beet, 0.03 to 4.68 (20,55.0%); strawberries, 0.004 to 2.50 (24,29.2%);
tomato, 0.51 to 1.19 (60,38.3%); zucchini, 0.04 to 0.21 (22,27.3%)(1).
Other Environmental Concentrations :
Carbon disulfide was
identified as a volatile compound released from textile floor coverings(1). It
was identified in headspace emissions from new carpeting (75% olefin, 25% nylon,
polypropylene backing) at approx. 100 ug/cu m(2).
Atmospheric Standards :
This action promulgates standards of
performance for equipment leaks of Volatile Organic Compounds (VOC) in the
Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect
of these standards is to require all newly constructed, modified, and
reconstructed SOCMI process units to use the best demonstrated system of
continuous emission reduction for equipment leaks of VOC, considering costs, non
air quality health and environmental impact and energy requirements. Carbon
disulfide is produced, as an intermediate or a final product, by
process units covered under this subpart.
Atmospheric Standards :
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Carbon
disulfide is included on this list.
CERCLA Reportable Quantities :
Releases of CERCLA hazardous substances are
subject to the release reporting requirement of CERCLA section 103, codified at
40 CFR part 302, in addition to the requirements of 40 CFR part 355. Carbon
Disulfide is an extremely hazardous substance (EHS) subject to
reporting requirements when stored in amounts in excess of its threshold
planning quantity (TPQ) of 10,000 lbs.
TSCA Requirements :
Pursuant to section 8(d) of TSCA, EPA
promulgated a model Health and Safety Data Reporting Rule. The section 8(d)
model rule requires manufacturers, importers, and processors of listed chemical
substances and mixtures to submit to EPA copies and lists of unpublished health
and safety studies. Carbon disulfide is
included on this list.
RCRA Requirements :
P022; As stipulated in 40 CFR 261.33, when carbon
disulfide, as a commercial chemical product or manufacturing
chemical intermediate or an off-specification commercial chemical product or a
manufacturing chemical intermediate, becomes a waste, it must be managed
according to federal and/or state hazardous waste regulations. Also defined as a
hazardous waste is any container or inner liner used to hold this waste or any
residue, contaminated soil, water, or other debris resulting from the cleanup of
a spill, into water or on dry land, of this waste. Generators of small
quantities of this waste may qualify for partial exclusion from hazardous waste
regulations (40 CFR 261.5(e)).
RCRA Requirements :
F005; When carbon
disulfide is a spent solvent, it is classified as a hazardous
waste from a nonspecific source (F005), as stated in 40 CFR 261.31, and must be
managed according to State and/or Federal hazardous waste regulations.
Sampling Procedures :
NIOSH Method 1600. Analyte: Carbon
disulfide. Matrix: Air. Sampler: Solid sorbent plus drying tube
(coconut shell charcoal, 100 mg/50 mg, and sodium sulfate, 270 mg). Flow Rate:
0.01 to 0.2 l/min. Sample Size: 5 liters. Shipment: Dryer attached to charcoal.
Sample Stability: 1 week @ 25 deg C; 6 weeks @ 0 deg C.
Analytic Laboratory Methods :
Carbon disulfide in
biological liquids is analyzed using headspace GC with a GC detector. Retention
time 0.40 relative to ethanel, whose absolute retention time is 1.9 + or - 0.1
minutes on a 6'x1/4" od column packed with 5% Carbowax K-600 and 3%
Halcomid 18 on 60 to 80 mesh Teflon 6HC.
Analytic Laboratory Methods :
NIOSH Method 1600. Determination of Carbon
Disulfide by Gas Chromatography with Flame Photometric Detection
(GC/FID). Detection limit= 2 mg/cu m.
Analytic Laboratory Methods :
EPA Method 8015. Direct Injection or
Purge-and-Trap Gas Chromatography for the determination of nonhalogenated
volatile organics in solid waste. Under the prescribed conditions carbon
disulfide can be detected using this method. No statistical
analysis was determined; specific method performance information will be
provided as it becomes available.
Analytic Laboratory Methods :
EPA Method 8240. Gas Chromatography/Mass
Spectrometry for the determination of volatile Organics. This method can be used
to quantify most volatile organic compounds including carbon
disulfide that have boiling points below 200 deg C and are
insoluble or slightly soluble in water. The detection limit is not given.
Precision and method accuracy were found to be directly related to the
concentration of the analyte and essentially independent of the sample matrix.
Special Reports :
COPPOCK RW ET AL; VET HUM TOXICOL 23 (5): 331
(1981). A REVIEW ON TOXICOLOGY OF CARBON DISULFIDE.
Special Reports :
NIOSH; Criteria Document: Carbon
Disulfide (1977) DHEW Pub NIOSH 77-156
Special Reports :
DHHS/ATSDR; Toxicological Profile for Carbon
Disulfide TP-91/09 (1992)
Special Reports :
Santodonato J; Monograph on Human Exposure to
Chemicals in the Workplace: Carbon Disulfide 7
(1986).
GLCC
RELATED TOXIC SUBSTANCES FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND
2004