CARBON DISULFIDE
CARBON DISULFIDEHuman Health Effects:
Human Toxicity Excerpts:
/AFTER INGESTION/ VICTIMS EXHIBITED SPASMODIC
TREMORS, PROSTRATION, DYSPNEA, CYANOSIS, PERIPHERAL VASCULAR COLLAPSE,
HYPOTHERMIA, MYDRIASIS, CONVULSIONS, COMA AND DEATH IN FEW HR FROM RESPIRATORY
PARALYSIS. ONLY MILD GASTROINTESTINAL IRRITATION AND VISCERAL CONGESTION WERE
NOTED AT AUTOPSY.
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 ... .
INDUSTRIALLY EXPOSED WORKERS HAVE EXHIBITED
... NEUROPSYCHIATRIC DISORDERS RANGING FROM IRRITABILITY TO MANIC-DEPRESSIVE
PSYCHOSIS ... CLINICAL MANIFESTATIONS OF NERVE DAMAGE ARE ... BLINDNESS, AND
SIGNS OF PARKINSONISM ...
IT DISSOLVES FATTY LAYER OF EPIDERMIS, &
WORKMEN WHO PUT THEIR HANDS IN LIQ SUFFER FROM DRY, CRACKED SKIN, ON WHICH
ECZEMATOUS LESIONS & EVEN ULCERS APPEAR.
... IN ... 343 VISCOUS RAYON WORKERS & 343
NON EXPOSED MEN, TESTED FOR CORONARY HEART DISEASE THE TOTAL MORTALITY WAS 48
(14%) IN THE EXPOSED GROUP AND 31 (9%) IN THE NON-EXPOSED GROUP.
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.
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.
SYMPTOMATOLOGY: Acute: 1. Mild to moderate
irritation of skin, eyes and mucous membranes from liquid or concentrated
vapors. If its evaporation is prevented, the liquid acts as a skin vesicant.
Percutaneous absorption occurs. 2. Headache. 3. Garlicky breath, nausea,
vomiting, diarrhea (even after vapor exposures), and occasionally abdominal
pain. 4. Weak pulse, palpitations. 5. Fatigue, weakness in the legs, unsteady
gait, vertigo. 6. Hyperesthesia, agitation, mania, hallucinations of sight,
hearing, taste, and smell in acute, massive vapor exposures and sometimes in
ingestion episodes. 7. Central nervous depression with respiratory paralysis. 8.
Death may occur during coma or after a convulsion.
SYMPTOMATOLOGY: Chronic: 1. Headache, fatigue,
inability to concentrate, insomnia, dyspepsia, tremor, giddiness or vertigo. 2.
Peripheral polyneuritis is often encountered: formication, pain, weakness,
paralysis. The absence of a corneal reflex is highly characteristic ... 3.
Emotional instability of all grades ranging from mild neurasthenia and
depression to frank psychosis with psychomotor excitement, delirium and
hallucinations. 4. Chronic, low-grade exposures of many years duration are
associated with a high incidence of hypertension, atherosclerosis, renal and
other parenchymal lesions (for example, stomach and perhaps liver). 5. Recovery
may occur within a few months or perhaps a few years, but paralyses may be
permanent.
Type of exposure: occupational; group exposed:
male workers; type of study: semen analysis, reproductive history; effects:
impotence, loss of libido /From table/
Effects on eye-sight have been observed before
other symptoms became evident. Studies indicated a gradual and slow incr in the
sensitivity of the eyes to light. Alterations in dark adaptation also occurred,
in most cases after 4 yr of exposure. ...
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.
...
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.
/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.
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.
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).
/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%).
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. ...
... 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. ...
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.
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.
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.
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.
SEVERE INTOXICATIONS HAVE RESULTED FROM
PROLONGED VAPOR EXPOSURES TO CONCN AS LOW AS 30 PPM.
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/
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.
Exposed workers showed very little increased
morbidity, but exposure dependent increases in pathological changes such as
increased frequency of angina and myocardial infarction, systolic and diastolic
blood velocity, increased symptoms of muscular weakness, increased low density
lipoproteins, increased fasting blood sugar, increased proportion of abnormal
sperm forms, and increased incidence of retinal abnormalities.
WORKERS EXPOSED TO AN AVG CONCN OF 9 PPM UP TO
2 YEARS SHOWED BIOCHEMICAL AND NERVOUS CHANGES. ... THE INCIDENCE AND DEGREE OF
THESE CHANGES WERE PROPORTIONAL TO THE EXPOSURE.
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.
Acute inhalation produces rapid onset of both
local irritation and CNS symptoms ranging from pharyngitis, nausea, vomiting,
dizziness, fatigue, headache, mood changes, lethargy, and blurred vision to
agitation, delirium, hallucinations, convulsions, coma, and death.
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.
Long-term exposure to levels in excess of 20
ppm may result in atherogenic and diabetogenic changes.
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.
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.
...a two- to threefold increase in coronary
heart disease has been reported.
Human Toxicity Values:
Most acute carbon disulfide fatalities
result from an ingestion of which 15 ml may be fatal to an adult.
Skin, Eye and Respiratory Irritations:
Severely irritating to eyes, skin and mucous
membranes. ... Skin sensitization may occur.
Drug Warnings:
VET: WITHHOLD FOOD & WATER FOR @ LEAST 4
HR AFTER TREATMENT. FATS & OILS ENHANCE ABSORPTION. AVOID USE OF HIGH DOSAGE
IN DEBILITATED OR SICK HORSES, OR THOSE IN LAST MONTH OR TWO OF PREGNANCY.
ADMIN ... IN ... GELATIN CAPSULES ...
RUPTURING CAPSULES CAN LEAD TO BLISTERING OF MUCOUS MEMBRANES, RESPIRATORY
DISTRESS, ANESTHESIA, & EVEN DEATH.
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).
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.
Urine: Reference Ranges: Normal - None
detected (2-thio-4-thiazolidine carboxylic acid); Exposed - BEI (sampling time
is end of shift, measured as the metabolite, 2-thio-4-thiazolidine carboxylic
acid, TTCA): 5 mg/g creatinine. Biological Tolerance Value for a Working
Material, BAT (sampling time is end of exposure or end of shift, measured as the
metabolite, 2-thio-4-thiazolidine carboxylic acid, TTCA): 8 mg/L; Toxic - Not
established.
Serum or Plasma: Reference Ranges: Normal -
None detected; Exposed - Not established; Toxic - Not established.
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.
Respiratory Symptom Questionnaires:
Questionnaires have been published by the American Thoracic Society and the
British Medical Research Council. These questionnaires have been found to be
useful in identification of people with chronic bronchitis, however certain
pulmonary function tests such as FEV 1 have been found to be better predictors
of chronic airflow obstruction.
Chest Radiography: This test is widely used
for assessing pulmonary disease. Chest radiographs have been found to be useful
for detection of early lung cancer in asymptomatic people, especially for
detection of peripheral tumors such as adenocarcinomas. However, even though
OSHA mandates this test for exposure to some toxicants such as asbestos, there
are conflicting views on its efficacy in detection of pulmonary disease.
Pulmonary Function Tests: The tests that have
been found to be practical for population monitoring include: Spirometry and
expiratory flow-volume curves; Determination of lung volumes; Diffusing capacity
for carbon monoxide; Single-breath nitrogen washout; Inhalation challenge tests;
Serial measurements of peak expiratory flow; Exercise testing.
Sputum Cytology: Sputum cytology along with
chest radiographs have been the standard procedures for detecting early lung
cancer in asymptomatic patients. Sputum cytology has been found to be useful for
detection of central tumors, especially squamous carcinomas. For this test to be
effective, exfoliated respiratory mucosal cells must be present in the
expectorated specimen. Pooling of sputum collected over 2-3 days may enhance the
sensitivity of this test by increasing the yield of exfoliated cells in the
specimen.
Evaluation of Peripheral Neuropathy: Nerve
conduction study; Electromyography; Quantitative sensory testing; Thermography.
Evaluation of Central Nervous System Effects:
Evaluation of CNS effects can be performed through neuropsychological
assessment, which consists of a clinical interview and administration of
standardized personality and neuropsychological tests. The areas that the
neuropsychology test batteries focus on include the domains of memory and
attention; visuoperceptual, visual scanning, visuospatial, and visual memory;
and motor speed and reaction time. There is limited data on which components of
the test batteries are best indicators of early CNS effects.
Evaluation of Cranial Neuropathies: Evaluation
of cranial nerve damage, as evidenced by symptoms such as loss of balance,
visual function, smell, taste, or sensation on the face, can be accomplished
through a physical examination focusing on tests such as: Smell assessment -
standardized odor threshold and identification testing; Vision assessment -
standard acuity tests, visual field tests, contrast sensitivity, and color
vision measurements (vision assessment); Facial and Trigeminal Nerve assessment
- blink reflex (pontograrn); Vestibular assessment - pure tone audiometry for
bone- and air-conducted sounds, threshold decay at 4 kHz, speech discrimination
and speech reception thresholds, tympanograms and acoustic thresholds,
electronystagmograms; Hearing assessment - audiometry testing.
Populations at Special Risk:
Employees at increased risk: those with
problems concerning central and peripheral nervous systems, eyes, cardiovascular
system, kidneys, and liver, & /SRP: alcoholics/.
Probable Routes of Human Exposure:
Inhalation of vapor which may be compounded by
percutaneous absorption of liquid or vapor, ingestion, and skin and eye contact.
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.
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).
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).
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).
Average Daily Intake:
AIR INTAKE: (assume mean concn of 0.3 ug/cu
m(1)): 6 ug(SRC). FOOD INTAKE: (assume 0.02 to 3.05 ug/g(2)): 32 to 4,880 ug(SRC).
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
ADMIN ... IN ... GELATIN CAPSULES ...
RUPTURING CAPSULES CAN LEAD TO BLISTERING OF MUCOUS MEMBRANES, RESPIRATORY
DISTRESS, ANESTHESIA, & EVEN DEATH.
LARGE OR TOXIC DOSES RESULT IN EXCITEMENT
FOLLOWED BY MUSCULAR WEAKNESS & POSSIBLY COLLAPSE, COMA, & DEATH.
IT ... CAUSES VITAMIN B DEFICIENCY, WHICH IN
TURN UPSETS CARBOHYDRATE METABOLISM & MORE PARTICULARLY METABOLISM OF
CEREBRAL CARBOHYDRATES ...
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.
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.
INHALATION EXPOSURE OF PREGNANT ALBINO RATS TO
10 & 0.03 MG/CU M DID NOT PRODUCE CONGENITAL MALFORMATIONS OR FUNCTIONAL
BIOCHEMICAL CHANGES IN NEONATE, BUT IT AFFECTS POSTNATAL DEVELOPMENT AT 10 MG/CU
M CAUSING IMPAIRMENT OF VIABILITY, RETARDATION OF MORPHOLOGICAL & SENSORY
DEVELOPMENT & BEHAVIORAL DEVIATIONS.
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.
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.
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.
Carbon disulfide exposure
can induce kynureninase and lead to disorders of tryptophan metabolism.
/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.
...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.
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.
... 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.
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.
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).
Non-Human Toxicity Values:
LD50 Rat oral 3188 mg/kg
LC50 Rat inhalation 25 g/cu m/2 hr
LD50 Mouse oral 2780 mg/kg
LC50 Mouse inhalation 10 g/cu m/2 hr
LD50 Guinea pig oral 2125 mg/kg
Ecotoxicity Values:
TLm Mosquitofish 162-135 mg/l/24-96 hr
/Conditions of bioassay not specified/
Metabolism/Pharmacokinetics:
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.
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.
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.
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).
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.
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.
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.
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.
CARBON DISULFIDE CAN
REACH FETUSES THROUGH PLACENTA OR BABIES BY WAY OF MOTHER MILK WHEN PREGNANT OR
BREAST-FEEDING DURING OR FOLLOWING EXPOSURE.
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.
Blood concentrations of 0.10-0.70 mg/l were
observed during exposure to air concentrations on the order of 80 ppm.
/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).
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. ...
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.
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.
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 ... .
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.
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.
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.
Interactions:
... SIGNS OF CARBON
DISULFIDE POISONING IN ANIMALS ARE INTENSIFIED BY RESERPINE, IPRONIAZID,
AND AMPHETAMINE. ...
... TRYPTOPHAN-ENRICHED DIET INCREASES
TOXICITY OF CARBON DISULFIDE. ...
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.
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.
In cholesterol fed rabbits carbon
disulfide greatly accelerated formation of atheroma.
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. ...
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.
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.
Pharmacology:
Therapeutic Uses:
MEDICATION (VET):: PRIMARILY FOR REMOVAL OF
BOT /FLY/ INFESTATIONS FROM STOMACH OF HORSES. ... ADMIN BY STOMACH TUBE OR IN
SOFT "UNBREAKABLE" ... GELATIN CAPSULES AFTER 18 HR
MEDICATION (VET): ANTHELMINTIC
Drug Warnings:
VET: WITHHOLD FOOD & WATER FOR @ LEAST 4
HR AFTER TREATMENT. FATS & OILS ENHANCE ABSORPTION. AVOID USE OF HIGH DOSAGE
IN DEBILITATED OR SICK HORSES, OR THOSE IN LAST MONTH OR TWO OF PREGNANCY.
ADMIN ... IN ... GELATIN CAPSULES ...
RUPTURING CAPSULES CAN LEAD TO BLISTERING OF MUCOUS MEMBRANES, RESPIRATORY
DISTRESS, ANESTHESIA, & EVEN DEATH.
Interactions:
... SIGNS OF CARBON
DISULFIDE POISONING IN ANIMALS ARE INTENSIFIED BY RESERPINE, IPRONIAZID,
AND AMPHETAMINE. ...
... TRYPTOPHAN-ENRICHED DIET INCREASES
TOXICITY OF CARBON DISULFIDE. ...
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.
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.
In cholesterol fed rabbits carbon
disulfide greatly accelerated formation of atheroma.
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. ...
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.
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 Fate & Exposure:
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)
Probable Routes of Human Exposure:
Inhalation of vapor which may be compounded by
percutaneous absorption of liquid or vapor, ingestion, and skin and eye contact.
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.
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).
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).
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).
Average Daily Intake:
AIR INTAKE: (assume mean concn of 0.3 ug/cu
m(1)): 6 ug(SRC). FOOD INTAKE: (assume 0.02 to 3.05 ug/g(2)): 32 to 4,880 ug(SRC).
Natural Pollution Sources:
MINUTE AMT OCCUR IN COAL TAR & IN CRUDE
PETROLEUM.
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).
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).
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).
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).
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 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).
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).
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).
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).
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).
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).
GROUNDWATER: Groundwater samples collected
from the Lipari Landfill, NJ in 1984, contained carbon
disulfide at <50 ppb(1).
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).
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).
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).
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).
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).
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).
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).
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).
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).
Environmental Standards & Regulations:
TSCA Requirements:
Section 8(a) of TSCA requires manufacturers of
this chemical substance to report preliminary assessment information concerned
with production, use, and exposure to EPA as cited in the preamble in 51 FR
41329.
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.
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
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.
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)).
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.
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.
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.
Clean Water Act Requirements:
Designated as a hazardous substance under
section 311(b)(2)(A) of the Federal Water Pollution Control Act and further
regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations
apply to discharges of this substance.
State Drinking Water Guidelines:
(AZ) ARIZONA 830 ug/l
(FL) FLORIDA 700 ug/l
(MI) MICHIGAN 80 ug/l
(MN) MINNESOTA 700 ug/l
(NH) NEW HAMPSHIRE 7.0 ug/l
(WI) WISCONSIN 1000 ug/l
Chemical/Physical Properties:
Molecular Formula:
C-S2
Molecular Weight:
76.14
Color/Form:
MOBILE ... LIQUID
Clear, colorless or faintly yellow liquid
Odor:
PUREST DISTILLATES HAVE SWEET, PLEASING, &
ETHEREAL ODOR ... USUAL COMMERCIAL AND REAGENT GRADES ARE FOUL SMELLING
When pure, carbon disulfide has
sweetish aromatic odor similar to that of chloroform.
Boiling Point:
46 DEG C @ 760 MM HG
Melting Point:
-111.5 DEG C
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.
Liquid carbon disulfide will
attack some forms of plastics, rubber, and coatings.
Critical Temperature & Pressure:
CRITICAL TEMP: 280 DEG C; CRITICAL PRESSURE:
72.9 ATM
Density/Specific Gravity:
1.2632 @ 20 DEG C/4 DEG C
Heat of Combustion:
-5814 BTU/LB= -3230 CAL/G= -135.2X10+5
JOULES/KG
Heat of Vaporization:
84.1 CAL/G AT BP
Octanol/Water Partition Coefficient:
log Kow= 1.94
Solubilities:
Miscible with anhydrous methanol, ethanol,
ether, benzene, chloroform, carbon tetrachloride, and oils
Solubility of water in carbon
disulfide: 86 ppm at 10 deg C; 142 ppm at 25 deg C
In water, 2860 mg/l at 25 deg C.
Spectral Properties:
INDEX OF REFRACTION 1.6319 @ 20 DEG C
IR: 10977 (Sadtler Research Laboratories IR
Grating Collection)
UV: 596 (Sadtler Research Laboratories
Spectral Collection)
MASS: 89 (Atlas of Mass Spectral Data, John
Wiley & Sons, New York)
Surface Tension:
32.25 dynes/cm at 20 deg C
Vapor Density:
2.67 (AIR= 1)
Vapor Pressure:
359 mm Hg at 25 deg C
Relative Evaporation Rate:
22.6 (butyl acetate= 1)
Viscosity:
COEFFICIENT OF VISCOSITY 0.363 @ 20 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
CAN CHELATE TRACE METALS, ESPECIALLY COPPER
& ZINC
LIQ-WATER INTERFACIAL TENSION: 48.4 DYNES/CM=
0.484 N/M @ 20 DEG C; LATENT HEAT OF VAPORIZATION: 153 BTU/LB= 85 CAL/G=
3.559X10+5 JOULES/KG
Liquid heat capacity= 0.239 Btu/lb ft @ 70 deg
F
Saturated vapor pressure= 5.990 lb/sq in @ 70
deg C
Saturated vapor density= 0.08021 lb/cu ft @ 70
deg C
Ideal heat capacity= 0.115 Btu/lb @ 60 deg F
Latent heat of fusion: 57.7 kJ/kg
Solubility of sulfur: 17-47 wt% at 0-40 deg C
Crude technical product has disagreeable odor
of decaying radishes.
The Henry's Law constant= 1.44X10-2 atm-cu
m/mole at 24 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Toxic; may be fatal if inhaled,
ingested or absorbed through skin. Inhalation or contact with some of these
materials will irritate or burn skin and eyes. Fire will produce irritating,
corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff
from fire control or dilution water may cause pollution.
Fire or explosion: Highly flammable: Will be
easily ignited by heat, sparks or flames. Vapors may form explosive mixtures
with air. Vapors may travel to source of ignition and flash back. Most vapors
are heavier than air. They will spread along ground and collect in low or
confined areas (sewers, basements, tanks). Vapor explosion and poison hazard
indoors, outdoors or in sewers. Those substances designated with a "P"
may polymerize explosively when heated or involved in a fire. Runoff to sewer
may create fire or explosion hazard. Containers may explode when heated. Many
liquids are lighter than water.
Public safety: Call Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 100 to
200 meters (330 to 660 feet) in all directions. Keep unauthorized personnel
away. Stay upwind. Keep out of low areas. Ventilate closed spaces before
entering.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. It may provide little or
no thermal protection. Structural firefighters' protective clothing provides
limited protection in fire situations ONLY; it is not effective in spill
situations.
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: CAUTION: All these products have a very
low flash point. Use of water spray when fighting fire may be inefficient. Small
fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Large fires:
Water spray, fog or alcohol-resistant foam. Move containers from fire area if
you can do it without risk. Dike fire control water for later disposal; do not
scatter the material. Use water spray or fog; do not use straight streams. Fire
involving tanks or car/trailer loads: Fight fire from maximum distance or use
unmanned hose holders or monitor nozzles. Cool containers with flooding
quantities of water until well after fire is out. Withdraw immediately in case
of rising sound from venting safety devices or discoloration of tank. ALWAYS
stay away from tanks engulfed in fire. For massive fire use unmanned hose
holders or monitor nozzles; if this is impossible, withdraw from area and let
fire burn.
Spill or leak: Fully encapsulating, vapor
protective clothing should be worn for spills and leaks with no fire. ELIMINATE
all ignition sources (no smoking, flares, sparks or flames in immediate area).
All equipment used when handling the product must be grounded. Do not touch or
walk through spilled material. Stop leak if you can do it without risk. Prevent
entry into waterways, sewers, basements or confined areas. A vapor suppressing
foam may be used to reduce vapors. Small spills: Absorb with earth, sand or
other non-combustible material and transfer to containers for later disposal.
Use clean non-sparking tools to collect absorbed material. Large spills: Dike
far ahead of liquid spill for later disposal. Water spray may reduce vapor; but
may not prevent ignition in closed spaces.
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the
substance; induce artificial respiration with the aid of a pocket mask equipped
with a one-way valve or other proper respiratory medical device. Administer
oxygen if breathing is difficult. Remove and isolate contaminated clothing and
shoes. In case of contact with substance, immediately flush skin or eyes with
running water for at least 20 minutes. Wash skin with soap and water. Keep
victim warm and quiet. Effects of exposure (inhalation, ingestion or skin
contact) to substance may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves.
Odor Threshold:
0.1 TO 0.2 PPM
Detection, odor, in air; purity not specified:
2.60x10-3 mg/l (gas).
Recognition, odor, in air; purity not
specified: 2.10x10-1 ppm.
Odor Low: 0.0243 mg/m Odor High: 23.1 mg/m
Skin, Eye and Respiratory Irritations:
Severely irritating to eyes, skin and mucous
membranes. ... Skin sensitization may occur.
Fire Potential:
MAY ACCUMULATE STATIC ELECTRICITY.
Carbon disulfide vapor
is explosive, igniting spontaneously on contact with sparks or at temperatures
above 147 degrees C.
The vapor ignites on contact with fluorine.
DANGEROUS WHEN EXPOSED TO HEAT, FLAME, SPARKS,
FRICTION, OR OXIDIZING MATERIALS.
NFPA Hazard Classification:
Health: 3. 3= Materials that, on short
exposure, could cause serious temporary or residual injury, including those
requiring protection from all bodily contact. Fire fighters may enter the area
only if they are protected from all contact with the material. Full protective
clothing, including self-contained breathing apparatus, coat, pants, gloves,
boots, and bands around legs, arms, and waist, should be provided. No skin
surface should be exposed.
Flammability: 3. 3= This degree includes Class
IB and IC flammable liquids and materials that can be easily ignited under
almost all normal temperature conditions. Water may be ineffective in
controlling or extinguishing fires in such materials.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Flammable Limits:
Lower Flammable Limit: 1.3% by volume; Upper
Flammable Limit: 50.0% by volume
Flash Point:
30 deg C (Closed Cup)
Autoignition Temperature:
IGNITION TEMP DANGEROUSLY LOW; 194 DEG F (90
DEG C)
Fire Fighting Procedures:
To fight fire, use water, carbon dioxide, dry
chemical, fog, mist.
Water and foam may be ineffective on fire.
Do not extinguish the fire unless flow can be
stopped or safely confined. Use water in flooding quantities as fog. Cool all
affected containers with flooding quantities of water. Apply water from as far a
distance as possible.
Toxic Combustion Products:
Toxic gases and vapors (such as sulfur dioxide
and carbon monoxide) may be released in a fire involving carbon
disulfide.
Firefighting Hazards:
Flashback along vapor trail may occur. Vapor
may explode if ignited in an enclosed area.
Explosive Limits & Potential:
Ignition and potentially explosive reaction
when heated in contact with rust or iron. Mixtures with sodium or
potassium-sodium alloys are powerful, shock-sensitive explosives. Explodes on
contact with permanganic acid. Potentially explosive reaction with nitrogen
oxide; chlorine (catalyzed by iron). Mixtures with dinitrogen tetraoxide are
heat-, spark- and shock-sensitive explosives.
EXPLOSIVE RANGE 1 TO 50% (VOL/VOL) IN AIR
Hazardous Reactivities & Incompatibilities:
Can react vigorously with oxidizing materials
Incompatible with air, metals, and oxidants.
Strong oxidizers; chemically-active metals
such as sodium, potassium & zinc; azides; rust; halogens; amines [Note:
Vapors may be ignited by contact with ordinary light bulb].
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 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.
The bis- or tris-complexes of phenylcopper
with triphenylphosphine react violently and exothermically with carbon
disulfide, even at 0 deg C.
Carbon disulfide plus
any of the azides produces violently explosive, extremely sensitive salts.
Reacts violently with azides, CsN3, ClO,
ethylamine diamine, ethylene imine, Pb(N3)2, LiN3, (water + permanganates), KN3,
RbN3, NaN3, phenylcopper-triphenylphosphine complexes.
Mixing carbon disulfide and
ethylenediamine in a closed container caused the temperature and pressure to
increase.
Hazardous Decomposition:
Decomposes on standing for a long time.
When heated to decomp, emits highly toxic
fumes of /sulfur oxides/.
Other Hazardous Reaction:
May travel a considerable distance to a source
of ignition and flash back. Vapors may be ignited by contact with an ordinary
light bulb.
Immediately Dangerous to Life or Health:
500 ppm
Protective Equipment & Clothing:
POSSIBLE EXPOSURE TO FAIRLY HIGH CONCN OF
VAPOR (SPLASHING OF LIQUID IN WORKSHOP, CLEANING OR REPAIR OF TANKS) REQUIRES
USE OF SAFETY GOGGLES, GAS MASK, APRON, & RUBBER GLOVES.
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.
Wear appropriate personal protective clothing
to prevent skin contact.
Wear appropriate eye protection to prevent eye
contact.
Recommendations for respirator selection. Max
concn for use: 10 ppm. Respirator Class(es): Any chemical cartridge respirator
with organic vapor cartridge(s). Any supplied-air respirator.
Recommendations for respirator selection. Max
concn for use: 25 ppm. Respirator Class(es): Any supplied-air respirator
operated in a continuous flow mode. Any powered, air-purifying respirator with
organic vapor cartridge(s).
Recommendations for respirator selection. Max
concn for use: 50 ppm. Respirator Class(es): Any chemical cartridge respirator
with a full facepiece and organic vapor cartridge(s). Any air-purifying, full-facepiece
respirator (gas mask) with a chin-style, front- or back-mounted organic vapor
canister. Any powered, air-purifying respirator with a tight-fitting facepiece
and organic vapor cartridge(s). Any self-contained breathing apparatus with a
full facepiece. Any supplied-air respirator with a full facepiece.
Recommendations for respirator selection. Max
concn for use: 500 ppm. Respirator Class(es): Any supplied-air respirator
operated in a pressure-demand or other positive-pressure mode.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive-pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in a
pressure-demand or other positive-pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a
chin-style, front- or back-mounted organic vapor canister. Any appropriate
escape-type, self-contained breathing apparatus.
Preventive Measures:
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
SRP: Local exhaust ventilation should be
applied wherever there is an incidence of point source emissions or dispersion
of regulated contaminants in the work area. Ventilation control of the
contaminant as close to its point of generation is both the most economical and
safest method to minimize personnel exposure to airborne contaminants.
Areas suspected of high concn of carbon
disulfide vapor should not be entered because of the explosion hazard.
... 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.
Large spill from a tank or from many
containers or drums: First, isolate in all directions 70 feet, then evacuate in
a downwind direction 0.2 square miles.
CARBON DISULFIDE SHOULD
NOT BE ALLOWED TO ENTER A CONFINED SPACE, SUCH AS A SEWER, BECAUSE OF THE
POSSIBILITY OF AN EXPLOSION.
Respirators may be used when engineering and
work practice controls are not technically feasible, when such controls are in
the process of being installed, or when they fail and need to be supplemented.
Respirators may also be used for operations which require entry into tanks or
closed vessels, and in emergency situations. ...
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet should be
immediately removed due to its flammability hazard.
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers. Contaminated clothing should not be taken home at end of shift, but
should remain at employee's place of work for cleaning.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
Storage Conditions:
... MUST BE STORED IN AIRTIGHT DRUMS, HANDLED
WITH PRECAUTIONS, & IN SUMMER KEPT IN SHADE & SPRAYED WITH WATER TO
PREVENT PRESSURE DEVELOPING. LARGE QUANTITIES ... MUST BE STORED UNDER WATER.
Storage temp: ambient
... Should be kept away from heat, sparks, and
flames, and adequate ventilation should be provided. ... Storage and handling
equipment are generally of conventional carbon steel construction. All parts of
a system, incl piping, valves, and movable containers, must be earth-ground and
firmly bonded by good electrical conductors to eliminate the possibility of
static charge build-up and spark discharge.
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.
Land spill: Dig a pit, pond, lagoon, holding
area to contain liquid or solid material. Dike surface flow using soil, sand
bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash
or cement powder. Apply appropriate foam to diminish vapor and fire hazard.
Water spill: Neutralize with agricultural lime
(CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). If dissolved,
in region of 10 ppm or greater concentration, apply activated carbon at ten
times the spilled amount. Use mechanical dredges or lifts to remove immobilized
masses of pollutants and precipitates.
Air spill: Apply water spray or mist to knock
down vapors. Combustion products include corrosive or toxic vapors.
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste numbers P022, D003,
and F005 must conform with USEPA regulations in storage, transportation,
treatment and disposal of waste.
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.
A good candidate for liquid injection
incineration at a temperature range of 650 to 1,600 deg C and a residence time
of 0.1 to 2 seconds. A good candidate for rotary kiln incineration at a
temperature range of 820 to 1,600 deg C and residence times of seconds for
liquids and gases, and hours for solids. A good candidate for fluidized bed
incineration at a temperature range of 450 to 980 deg C and residence times of
seconds for liquids and gases, and longer for solids.
This compound should be susceptible to removal
from waste water by air stripping.
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))
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.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-2 8-hr
Time Weighted Avg 20 ppm.
Permissible Exposure Limit: Table Z-2
Acceptable Ceiling Concentration: 30 ppm.
Permissible Exposure Limit: Table Z-2
Acceptable maximum peak above the acceptable ceiling concentration for an 8-hour
shift. Concentration: 100 ppm. Maximum Duration: 30 minutes.
Vacated 1989 OSHA PEL TWA 4 ppm (12 mg/cu m);
STEL 12 ppm (36 mg/cu m), skin designation, is still enforced in some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 10 ppm, skin.
Excursion Limit Recommendation: Excursions in
worker exposure levels may exceed three times the TLV-TWA for no more than a
total of 30 min during a work day, and under no circumstances should they exceed
five times the TLV-TWA, provided that the TLV-TWA is not exceeded.
Biological Exposure Index (BEI): Determinant:
2-thiothiazolidine-4-carboxylic acid (TTCA) in urine; Sampling Time: end of
shift; BEI: 5 mg/g creatinine.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 1 ppm (3 mg/cu m). Skin.
Recommended Exposure Limit: 15 Min Short-Term
Exposure Limit: 10 ppm (30 mg/cu m). Skin.
Immediately Dangerous to Life or Health:
500 ppm
Other Occupational Permissible Levels:
Australia: 10ppm, skin; Federal Republic of
Germany: 10 ppm, short-term level 20 ppm, 30-minute average value, 4 times per
shift, skin, Pregnancy Group B, probably risk of damage to developing embryo or
fetus; Sweden: 5 ppm, short-term value 8ppm, 15 minutes, skin; United Kingdom:
10 ppm, skin
Emergency Response Planning Guidelines (ERPG):
ERPG(1) 1 ppm (no more than mild, transient effects) for up to 1 hr exposure;
ERPG(2) 50 ppm (without serious, adverse effects) for up to 1 hr exposure;
ERPG(3) 500 ppm (not life threatening) up to 1 hr exposure.
Manufacturing/Use Information:
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./
MFR OF RAYON, CARBON TETRACHLORIDE,
XANTHOGENATES, SOIL DISINFECTANTS, ELECTRONIC VACUUM TUBES; SOLVENT FOR
PHOSPHORUS, SULFUR, SELENIUM, BROMINE, IODINE, FATS, RESINS, & RUBBERS.
MEDICATION (VET):
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 ... .
Optical glass, paints, enamels, varnishes,
paint removers, tallow, explosives, rocket fuel, putty preservatives, rubber
cement, solvent for ... waxes, lacquers, camphor, resins, vulcanized rubber ...
and pesticide intermediates.
Food-related uses incl preservation of fresh
fruit, in adhesive compositions for food packaging, and as a solvent in the
extraction of growth inhibitors.
Insecticide used for fumigation of nursery
stock and for soil treatment against insects and nematodes. /Former use/
Used for fumigation in airtight storage
warehouses, airtight flat storages, bins, grain elevators, railroad boxcars,
shipholds, barges and cereal mills. /Former use/
Used as seed treatment on conifers.
... USED IN THE XANTHATION OF CELLULOSE IN THE
PREPARATION OF VISCOSE ...
... Cellophane; Manufacture of flotation
agents ...
Process solvent
Used as a chemical intermediate for the
synthesis of acetone-1,3-dicarboxylic acid; ammonium thiocyanate; antimony
diamyldithiocarbamate; astemizole; azathioprine; 2-benzoxazolethiol; bitoscanate;
cefotetan; N-cyanoimido-S,,S-dimethyldithiocarbamate; di-n-butylthiourea;
dicyclohexylcarbodiimide; diethylthiourea; 2,5-dimercapto-1,3,4-thiadiazole;
N,N'-dimethyldiphenylthiuram disulphide; dipentamethylenethiuram tetrasulphide;
dithianon; di-o-tolylguanidine; di-o-tolylthiourea; ethyidimuron;
ethylenethiourea; 5-(2-hydroxyethyl)-4-methylthiazole; lead
diamyldithiocarbamate; 2-mercaptobenzimidazole; 2-mercaptomethylbenzimidazole;
metam-sodium; 1-methylamino-1-methylthio-2-nitroethylene;
2-methyl-5-mercapto-1,3,4-thiadiazole; 4-methylthiazole; metiram; metribuzin;
nabam; nickel di-n-butyldithiocarbamate; N-oxydiethylenedithiocarbamyl-N'-oxydiethylenesulphenamide;
phenyl isothiocyanate; piperidinium pentamethylenedithiocarbamate; potassium
amyl xanthate; potassium ethyl xanthate; potassium isopropyl xanthate; propineb;
sodium cellulose xanthate; sodium diethyldithiocarbamate; sodium
dimethyldithiocarbamate; sodium isobutyl xanthate; sodium isopropyl xanthate;
starch, sodium xanthate; thiamine; thiocarbanilide; thiophosgene;
trichloromethanesulphenyl chloride; tricyclazole; zinc diamyldithiocarbamate;
zinc dibenzyldithiocarbamate; zinc di-n-butyldithiocarbamate; zinc
ethylphenyldithiocarbamate; zinc pentamethylenedithiocarbamate.
Manufacturers:
Akzo America, Inc, Akzo Chemicals Inc, Hq, 111
West 40th St, New York, NY 10018, (212) 382-5500; Akzo Chemical Division, 300
South Riverside Plaza, Chicago, IL 60606; Production sites: Delaware City, DE
19706; Le Moyne, AL 36505
Elf Atochem North America, Inc., 2000 Market
Street, 21st Floor, Philadelphia, PA 19103-3222, (215)419-7000; Organic
Chemicals Division, 2231 Haden Road, Houston, TX 77015 (713)455-1211; Production
Site: Houston, TX 77015.
PPG Industries, Inc, Hq, One PPG Place,
Pittsburgh, PA 15272, (412) 434-3131; Chemicals Group; Production site: Natrium,
WV 26155
Methods of Manufacturing:
Metallurgical coke and sulfur (reaction;
coproduced with hydrogen sulfide)
(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.
... 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.
Commercial production is from preheated
natural gas which is mixed with vaporized sulfur and passed over a catalyst.
General Manufacturing Information:
Not for fumigation of stored beans, cowpeas,
or peas.
Formulations/Preparations:
GENERALLY USED ALONE BUT, FOR SOIL TREATMENT,
EMULSIONS OR SOLN WITH ALKALI (THIOCARBONATES) HAVE BEEN MARKETED.
GRADE: 99.9%, SPECTROPHOTOMETRIC
Grades: technical; reagent
Liquid grade
Modern plants generally produce carbon
disulfide of about 99.99% purity.
Impurities:
Impurities: Sulfur compounds.
Consumption Patterns:
Rayon, 40%; cellophane (10% carbon
tetrachloride), 25%; rubber chemicals, 10%; miscellaneous (including pesticides
and paraffin solvent), 15% (1984) /Estimate/
CHEMICAL PROFILE: Carbon
disulfide. Carbon tetrachloride, 38%; rayon, 34%; rubber chemicals, 7%;
cellophane and other regenerated cellulosics, 6%; agricultural chemicals, 5%;
miscellaneous, 10%.
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.)
Rayon, 53%; agricultural and other chemicals,
25%; rubber chemicals, 13%; cellophane and other regenerated cellulosics, 7%;
miscellaneous, as an industrial solvent and for producing mercaptoethylamine, an
intermediate for anti-ulcer drugs, 2%.
U. S. Production:
(1977) 2.29X10+11 G
(1982) 1.18X10+11 G
(1984) 1.68X10+11 g
(1985) 1.43X10+11 g /estimate/
(1974) 780 million pounds (approx)
U. S. Imports:
(1985) 1.36X10+9 g
U. S. Exports:
(1978) 5.49X10+9 G
(1983) 4.32X10+8 G
(1985) 1.64X10+9 g
Laboratory Methods:
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.
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.
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.
NIOSH Method 1600. Determination of Carbon
Disulfide by Gas Chromatography with Flame Photometric Detection
(GC/FID). Detection limit= 2 mg/cu m.
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.
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.
EMSLC Method 524.2. Measurement of Purgeable
Organic Compounds in Water by Capillary Column Gas Chromatography/Mass
Spectrometry. Revision 4.0. Method detection limit= 0.093 ug/L.
EAD Method 1624. Volatile Organic Compounds by
Isotope Dilution GCMS. Minimum level= 10 ug/l.
OSW Method 8240B. Determination of Volatile
Organics Compounds by Gas Chromatography/Mass Spectrometry (GC/MS). This method
is applicable to various type of samples, regardless of water content, including
ground water, aqueous sludge, caustic liquors, acid liquors, waste solvents, and
oily waste. Estimated quantitation limit= 100 ug/l.
AOAC Method 966.5. Fumigant Mixtures by Gas
Chromatographic Method.
SFSAS Method SFSAS_29. Extraction and Analysis
of Organics in Biological Tissue. Limit of quantitation= 0.050 mg/kg.
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.
EPA Method 8015. For the analysis of solid
waste, a representative sample (solid or liquid) is collected in a standard 40
ml glass screw-cap vial equipped with Teflon-faced silicone septum. Sample
agitation, as well as contamination of the sample with air, must be avoided. Two
vials are filled per sample location, then placed in separate plastic bags for
shipment and storage.
Special References:
Special Reports:
COPPOCK RW ET AL; VET HUM TOXICOL 23 (5): 331
(1981). A REVIEW ON TOXICOLOGY OF CARBON DISULFIDE.
NEAL RA, HALPERT J; ANNU REV PHARMACOL TOXICOL
22: 321 (1982). REVIEW OF TOXICOLOGY ON THIO-SULFUR-CONTAINING COMPOUNDS.
SAMUELS SW; LAST, JM MAXCY-ROSENAU PUBLIC
HEALTH AND PREVENTIVE MEDICINE, 11TH EDITION. XXV+1926P.
APPLETON-CENTURY-CROFTS: NEW YORK, NY, USA ILLUS MAPS ISBN 0-8385-6186-1; 0(0)
822 (1980). REVIEW OF CARCINOGENS, CHEMICALS, TOOLS, WORKPLACE DESIGN,
SURVEILLANCE, INTERVENTION PROGRAM.
NIOSH; Criteria Document: Carbon
Disulfide (1977) DHEW Pub NIOSH 77-156
WHO; Environmental Health Criteria 10: Carbon
disulide (1979)
DHHS/ATSDR; Toxicological Profile for Carbon
Disulfide TP-91/09 (1992)
Santodonato J; Monograph on Human Exposure to
Chemicals in the Workplace: Carbon Disulfide 7 (1986).
Synonyms and Identifiers:
Synonyms:
CARBON BISULFIDE
**PEER REVIEWED**
CARBON BISULPHIDE
**PEER REVIEWED**
CARBON DISULPHIDE
**PEER REVIEWED**
CARBONE (SULFURE DE) (FRENCH)
**PEER REVIEWED**
CARBONIO (SOLFURO DI) (ITALIAN)
**PEER REVIEWED**
CARBON SULFIDE
**PEER REVIEWED**
Caswell No 162
**PEER REVIEWED**
DITHIOCARBONIC ANHYDRIDE
**PEER REVIEWED**
Pesticide Code: 016401
**QC REVIEWED**
EPA Pesticide Chemical Code 016401
**PEER REVIEWED**
KOHLENDISULFID (SCHWEFELKOHLENSTOFF)
(GERMAN)
**PEER REVIEWED**
KOOLSTOFDISULFIDE (ZWAVELKOOLSTOF) (DUTCH)
**PEER REVIEWED**
NCI-C04591
**PEER REVIEWED**
SCHWEFELKOHLENSTOFF
(GERMAN)
**PEER REVIEWED**
SULPHOCARBONIC ANHYDRIDE
**PEER REVIEWED**
SULPHURET OF CARBON
**PEER REVIEWED**
WEEVILTOX
**PEER REVIEWED**
WEGLA DWUSIARCZEK (POLISH)
**PEER REVIEWED**
Formulations/Preparations:
GENERALLY USED ALONE BUT, FOR SOIL TREATMENT,
EMULSIONS OR SOLN WITH ALKALI (THIOCARBONATES) HAVE BEEN MARKETED.
GRADE: 99.9%, SPECTROPHOTOMETRIC
Grades: technical; reagent
Liquid grade
Modern plants generally produce carbon
disulfide of about 99.99% purity.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1131; Carbon disulfide
IMO 6.1; Carbon disulfide
Standard Transportation Number:
49 081 25; Carbon bisulfide
EPA Hazardous Waste Number:
P022; An acute hazardous waste when a
discarded commercial chemical product or manufacturing chemical intermediate or
an off-specification commercial chemical product or a manufacturing chemical
intermediate.
D003; A waste containing sulfide cmpd may (or
may not) be characterized a hazardous waste following testing for the reactivity
characteristics as prescribed by the Resource Conservation and Recovery Act (RCRA)
regulations. /Sulfide cmpd/
F005; A hazardous waste from nonspecific
sources when a spent solvent.
Administrative Information:
Hazardous Substances Databank Number: 52
Last Revision Date: 20030305
Last Review Date: Reviewed by SRP on 5/7/1998
Update History:
Complete Update on 03/05/2003, 5 fields
added/edited/deleted.
Field Update on 02/14/2003, 1 field added/edited/deleted.
Field Update on 11/08/2002, 1 field added/edited/deleted.
Field Update on 10/31/2002, 1 field added/edited/deleted.
Complete Update on 07/22/2002, 1 field added/edited/deleted.
Complete Update on 01/18/2002, 6 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 05/15/2001, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 07/20/1999, 5 fields added/edited/deleted.
Complete Update on 05/04/1999, 1 field added/edited/deleted.
Complete Update on 03/29/1999, 3 fields added/edited/deleted.
Field Update on 03/19/1999, 1 field added/edited/deleted.
Field Update on 03/17/1999, 1 field added/edited/deleted.
Complete Update on 03/01/1999, 1 field added/edited/deleted.
Complete Update on 02/01/1999, 1 field added/edited/deleted.
Complete Update on 01/20/1999, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 10/07/1998, 1 field added/edited/deleted.
Complete Update on 08/04/1998, 79 fields added/edited/deleted.
Field Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 10/17/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 03/27/1997, 2 fields added/edited/deleted.
Complete Update on 03/11/1997, 3 fields added/edited/deleted.
Complete Update on 02/26/1997, 1 field added/edited/deleted.
Complete Update on 02/05/1997, 2 fields added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 05/10/1996, 1 field added/edited/deleted.
Complete Update on 04/23/1996, 1 field added/edited/deleted.
Complete Update on 04/16/1996, 7 fields added/edited/deleted.
Complete Update on 01/18/1996, 1 field added/edited/deleted.
Complete Update on 10/23/1995, 1 field added/edited/deleted.
Complete Update on 08/21/1995, 1 field added/edited/deleted.
Complete Update on 01/18/1995, 1 field added/edited/deleted.
Complete Update on 12/19/1994, 1 field added/edited/deleted.
Complete Update on 08/11/1994, 1 field added/edited/deleted.
Complete Update on 07/20/1994, 1 field added/edited/deleted.
Complete Update on 06/30/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 11/05/1993, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Complete Update on 08/04/1993, 1 field added/edited/deleted.
Complete Update on 04/27/1993, 1 field added/edited/deleted.
Field update on 12/10/1992, 1 field added/edited/deleted.
Complete Update on 11/26/1992, 1 field added/edited/deleted.
Complete Update on 07/02/1992, 86 fields added/edited/deleted.
Field Update on 04/16/1992, 1 field added/edited/deleted.
Field Update on 01/13/1992, 1 field added/edited/deleted.
Complete Update on 10/10/1990, 1 field added/edited/deleted.
Field update on 05/18/1990, 1 field added/edited/deleted.
Complete Update on 04/16/1990, 2 fields added/edited/deleted.
Field update on 03/06/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 3 fields added/edited/deleted.
Field Update on 05/05/1989, 1 field added/edited/deleted.
Complete Update on 12/09/1988, 2 fields added/edited/deleted.
Complete Update on 10/20/1988, 104 fields added/edited/deleted.
Complete Update on 10/03/1986
GLCC
RELATED TOXIC SUBSTANCES FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND
2004
GREAT LAKES CHEMICAL CORPORATION AND THE PATHFINDERS CAMP