- Toxicity Profiles
- Toxicity Summary for BARIUM
-
- NOTE - Although the toxicity values presented in these
toxicity
- profiles were correct at the time they were produced,
these values
- are subject to change. Users should always refer to the
Toxicity Value
- Database for the currect toxicity values.
-
- EXECUTIVE SUMMARY
- 1. INTRODUCTION
- 2. METABOLISM AND DISPOSITION
- 2.1 ABSORPTION
- 2.2
-
- DISTRIBUTION
- 2.3 METABOLISM
- 2.4 EXCRETION
- 3. NONCARCINOGENIC HEALTH EFFECTS
- 3.1 ORAL EXPOSURES
-
-
- INHALATION EXPOSURES
- 3.3 OTHER ROUTES OF EXPOSURE
- 3.4 TARGET ORGANS/CRITICAL EFFECTS
- 4. CARCINOGENICITY
- 4.1 ORAL EXPOSURES
-
-
- INHALATION EXPOSURES
- 4.3 OTHER ROUTES OF EXPOSURE
- 4.4 EPA WEIGHT-OF-EVIDENCE
- 4.5 CARCINOGENICITY SLOPE FACTORS
-
- REFERENCES
-
-
- Prepared by A. A. Francis, M.S., D.A.B.T., and Carol
S. Forsyth, Ph.D., Chemical Hazard Evaluation Group in the Biomedical and
Environmental Information Analysis Section, Health Sciences Research Division,
*.
-
- Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION
PROGRAM
-
- *Managed by Martin Marietta Energy Systems, Inc., for
the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
-
- EXECUTIVE SUMMARY
-
- The soluble salts of barium, an alkaline earth metal,
are toxic in mammalian systems. They are absorbed rapidly from the gastrointestinal
tract and are deposited in the muscles, lungs, and bone. Barium is excreted
primarily in the feces.
-
- At low doses, barium acts as a muscle stimulant and at
higher doses affects the nervous system eventually leading to paralysis.
Acute and subchronic oral doses of barium cause vomiting and diarrhea,
followed by decreased heart rate and elevated blood pressure. Higher doses
result in cardiac irregularities, weakness, tremors, anxiety, and dyspnea.
A drop in serum potassium may account for some of the symptoms. Death can
occur from cardiac and respiratory failure. Acute doses around 0.8 grams
can be fatal to humans.
-
- Subchronic and chronic oral or inhalation exposure primarily
affects the cardiovascular system resulting in elevated blood pressure.
A lowest-observed-adverse-effect level (LOAEL) of 0.51 mg barium/kg/day
based on increased blood pressure was observed in chronic oral rat studies
(Perry et al. 1983), whereas human studies identified a no-observed-adverse-effect
level (NOAEL) of 0.21 mg barium/kg/day (Wones et al. 1990, Brenniman and
Levy 1984). The human data were used by the EPA to calculate a chronic
and subchronic oral reference dose (RfD) of 0.07 mg/kg/day (EPA 1995a,b).
In the Wones et al. study, human volunteers were given barium up to 10
mg/L in drinking water for 10 weeks. No clinically significant effects
were observed. An epidemiological study was conducted by Brenniman and
Levy in which human populations ingesting 2 to 10 mg/L of barium in drinking
water were compared to a population ingesting 0 to 0.2 mg/L. No significant
individual differences were seen; however, a significantly higher mortality
rate from all combined cardiovascular diseases was observed with the higher
barium level in the 65+ age group. The average barium concentration was
7.3 mg/L, which corresponds to a dose of 0.20 mg/kg/day. Confidence in
the oral RfD is rated medium by the EPA.
-
-
- Subchronic and chronic inhalation exposure of human populations
to barium-containing dust can result in a benign pneumoconiosis called
"baritosis." This condition is often accompanied by an elevated
blood pressure but does not result in a change in pulmonary function. Exposure
to an air concentration of 5.2 mg barium carbonate/m3 for 4 hours/day for
6 months has been reported to result in elevated blood pressure and decreased
body weight gain in rats (Tarasenko et al. 1977). Reproduction and developmental
effects were also observed. Increased fetal mortality was seen after untreated
females were mated with males exposed to 5.2 mg/m3 of barium carbonate.
Similar results were obtained with female rats treated with 13.4 mg barium
carbonate/m3. The NOAEL for developmental effects was 1.15 mg/m3 (equivalent
to 0.8 mg barium/m3). An inhalation reference concentration (RfC) of 0.005
mg/m3 for subchronic and 0.0005 mg/m3 for chronic exposure was calculated
by the EPA based on the NOAEL for developmental effects (EPA 1995a). These
effects have not been substantiated in humans or other animal systems.
-
- Barium has not been evaluated by the EPA for evidence
of human carcinogenic potential (EPA 1995b).
-
-
- 1. INTRODUCTION
-
- Barium (CAS registry number 7440-39-3) is a divalent
alkaline-earth metal found only in combination with other elements in nature.
The most important of these combinations are the peroxide, chloride, sulfate,
carbonate, nitrate, and chlorate. The pure metal oxidizes readily and reacts
with water emitting hydrogen; it is chemically similar to calcium (Weast
et al. 1987). The most likely source of barium in the atmosphere is from
industrial emissions. Since it is usually present as a particulate form,
it can be removed from the atmosphere by wet precipitation and deposition.
Due to the element's tendency to form salts with limited solubility in
soil and water, it is expected to have a residence time of hundreds of
years and is not expected to be very mobile. Acidic conditions, however,
will increase the solubility of some barium compounds facilitating their
movement from the soil to the groundwater (EPA 1984). Trace amounts of
barium were found in more than 99% of the surface waters and finished drinking
water samples (average values of 43 g/L, and 28.6 g/L, respectively) across
the United States (National Academy of Sciences 1977).
-
-
- 2. METABOLISM AND DISPOSITION
-
-
- 2.1 ABSORPTION
-
- The soluble forms of barium salts are rapidly absorbed
into the blood from the intestinal tract. The rates of absorption of a
number of barium salts have been measured in rats following oral exposure
to small quantities (30 mg/kg body weight). The relative absorption rates
were found to be: barium chloride barium sulfate barium carbonate. Large
doses of barium sulfate do not increase the uptake of this salt because
of its low solubility (McCauley and Washington 1983, EPA 1984).
-
- Systemic toxic effects have been observed following both
oral and inhalation exposure. No absorption kinetics are available following
inhalation exposure, although it is obvious that absorption does occur
(EPA 1984).
-
- 2.2 DISTRIBUTION
- Barium absorbed into the bloodstream disappears in about
24 hours; however, it is deposited in the muscles, lungs, and bone. Very
little is stored in the kidneys, liver, spleen, brain, heart, or hair.
It remains in the muscles about 30 hours after which the concentration
decreases slowly. The deposition of barium into bone is similar to calcium
but occurs at a faster rate (Beliles 1994). The half life of barium in
bone is estimated to be about 50 days (Machata 1988).
-
- 2.3 METABOLISM
- About 54% of the barium dose is protein bound. Barium
is known to activate the secretion of catecholamines from the adrenal medulla
without prior calcium deprivation. It may displace calcium from the cell
membranes, thereby increasing permeability and providing stimulation to
muscles. Eventual paralysis of the central nervous system can occur (Beliles
1994).
-
- 2.4 EXCRETION
- A tracer study in rats using 140Ba demonstrated that
7% and 20% of the barium dose was excreted in 24 hours in the urine and
feces, respectively. In contrast, calcium is primarily excreted in the
urine. The clearance of barium is enhanced with saline infusion (Beliles
1994). Following intravenous injection of barium into six healthy men,
excretion was mainly fecal with the total relative fecal:urinary clearance
for 14 days ranging from 6 to 15 (Newton et al. 1991).
-
- 3. NONCARCINOGENIC HEALTH EFFECTS
- 3.1 ORAL EXPOSURES
- 3.1.1 Acute Toxicity
-
-
- 3.1.1.1 Human
-
-
- A number of accidental barium poisonings have occurred
following the ingestion of barium salts. The estimated fatal dose of barium
carbonate, a rodenticide, is about 5 grams for a 70 kg human (Arena 1979).
The LD50 for barium chloride is estimated at about 1 gram for a 70 kg human
(Machata 1988), and the LDLo (lowest published lethal dose) is reported
to be about 0.8 grams (Lewis and Sweet 1984). The acute symptoms include
excess salivation, vomiting, diarrhea, increased blood pressure, muscular
tremors, weakness, paresis, anxiety, dyspnea, and cardiac irregularities.
A severe loss of potassium can account for some of the symptoms. Convulsions
and death from cardiac and respiratory failure can occur. Magnesium and
sodium sulfate are antidotal if taken soon after ingestion since either
salt will result in the formation of insoluble barium sulfate and prevent
further absorption. Survival for more than 24 hours is usually followed
by complete recovery (Arena 1979).
-
- Complications occurred in a woman following a barium
swallow investigation for severe dysphagia. Direct aspiration of a large
amount of barium into the right main bronchus resulted in tachycardia,
tachypnoea, fever, and an oxygen saturation of 82%; two weeks later the
woman still had a moist cough with widespread rales but continued to recover
(Penington 1993).
-
- A family was accidentally poisoned with barium from eating
their evening meal. The mother had fried fish breaded with a flour-like
substance that turned out to be rat poison containing barium carbonate.
All seven family members, aged 2 to 48 years, developed nausea, vomiting,
diarrhea, and crampy abdominal pain within minutes of consuming the meal;
the parents also developed ventricular tachycardia, flaccid paralysis of
the extremities, shortness of breath (mother), and respiratory failure
(father). Patients were treated symptomatically and all fully recovered
(Johnson and VanTassell 1991).
-
-
- 3.1.1.2 Animal
-
-
- Similar acute symptoms occur in animals; however, higher
doses are usually involved. The LD50 for rats is listed as 630 mg/kg for
barium carbonate, 118 mg/kg for barium chloride, and 921 mg/kg for barium
acetate (Lewis and Sweet 1984).
- 3.1.2 Subchronic Toxicity
-
- 3.1.2.1 Human
-
-
- An experiment testing the subchronic toxicity of barium
chloride on human volunteers was conducted by Wones et al. (1990). The
diets of 11 male subjects were controlled. They were given 1.5 L/day of
distilled and charcoal-filtered drinking water that contained 0 mg/L barium
for weeks 1 and 2, 5 mg/L for weeks 3 to 6, and 10 mg/L for weeks 7 to
10. No clinically significant effects were observed in blood pressures,
serum chemistry, urinalysis, or electrocardiograms. The 10 mg/L (0.21 mg/kg/day)
dose was identified as a NOAEL.
-
-
- 3.1.2.2 Animal
-
-
- Groups of 30 male and 30 female Charles River rats were
exposed to barium chloride at 0, 10, 50, or 250 ppm in drinking water for
90 days (Tardiff et al. 1980). The highest average dose in this study was
calculated to be 45.7 mg/kg/day for female rats. No significant clinical
signs of toxicity were observed. Blood pressure was not measured.
-
- McCauley et al. (1985) conducted drinking water studies
in which six male Sprague-Dawley rats/group were given water containing
0, 10, 100, or 250 mg/L barium for 36 weeks, or 1, 10, 100, or 1000 mg/L
barium for 16 weeks. Female rats were given 0 or 250 mg/L for 46 weeks.
Animals receiving the 1000 mg/L dose developed ultrastructural changes
in the kidney glomeruli. No other effects were reported.
-
- Tardiff et al. (1980) exposed groups of 30 male and 30
female Charles River rats to 0, 10, 50, or 250 ppm barium (given as barium
chloride) in drinking water for 90 days. A slight reduction in adrenal
weights was seen in female rats with the 250 ppm (45.7 mg/kg/day) dose
at 13 weeks, and no other adverse effects were observed in male rats with
the 50 ppm (8.1 mg/kg/day) and the 250 ppm (38.1 mg/kg/day) doses at 8
weeks. No clear dose effect or dose duration effect was seen with the adrenal
weight decrease; therefore, the clinical significance is uncertain.
- 3.1.3 Chronic Toxicity
-
- 3.1.3.1 Human
-
-
- An epidemiology study conducted by Brenniman and Levy
(1984) compared a human population ingesting barium levels of 2 to 10 mg/L
in their drinking water to a population ingesting 0 to 0.2 mg/L. Although
significantly higher mortality rates from all cardiovascular diseases were
observed with the higher barium level in the 65 and over age group, there
were no significant individual differences in blood pressures, strokes,
or heart and renal diseases within the two groups. The average barium concentration
for the mortality study was 7.3 mg/L, which corresponds to a dose of 0.20
mg/kg/day assuming drinking water consumption of 2 L/day for a 70 kg human.
-
-
- 3.1.3.2 Animal
-
-
- A series of experiments were performed in which groups
of 52 male and female Long-Evans rats and 42 male and female Swiss mice
were exposed to 5 mg barium/L (given as barium acetate) in drinking water
for their lifetime (Schroeder and Mitchener 1975a,b). The barium doses
were about 0.25 and 0.825 mg/kg/day for rats and mice, respectively. No
adverse clinical effects were observed; however, blood pressure was not
measured. A slight but significant reduction in longevity of treated male
mice was noted when measured as the mean age at death of the last surviving
10% of animals. The overall average life span of the group, however, was
about the same as the control group (EPA 1984, 1989).
-
- Perry et al. (1983) exposed 12 to 13 female weanling
rats/group to 0, 1, 10, or 100 ppm barium (given as barium chloride) for
up to 16 months. Average doses were calculated to be 0, 0.051, 0.51, and
5.1 mg/kg/day (EPA 1985). A clinically significant increase in average
blood pressure was observed in the highest dose group; a slight but statistically
significant increase was seen in the 10 ppm (0.51 mg/kg/day) dose group.
The controlled diet, which restricted the intake of trace metals, calcium,
and potassium, may have contributed to the effect.
- 3.1.4 Developmental and Reproductive Toxicity
- Information on developmental and reproductive toxicity
in humans or
- animals following oral exposure was unavailable.
- 3.1.5 Reference Dose
-
- 3.1.5.1 Subchronic
-
-
- ORAL RfDs: 0.07 mg/kg/day (EPA 1995a)
-
- UNCERTAINTY FACTOR: 3
-
- NOAEL: 0.21 mg/kg/day
-
- PRINCIPAL STUDIES: The same studies and comments apply
to both the
- subchronic and chronic RfD derivations. See Sect. 3.1.5.2.
-
-
- 3.1.5.2 Chronic
-
-
- ORAL RfDc: 0.07 mg/kg/day (EPA 1995b)
-
- UNCERTAINTY FACTOR: 3
-
- MODIFYING FACTOR: 1
-
- NOAEL: 0.21 mg/kg/day
-
- CONFIDENCE:
-
- Study: Medium
-
- Data Base: Medium
-
- RfD: Medium
-
- VERIFICATION DATE: 06/21/90
-
- PRINCIPAL STUDIES: Wones et al. (1990); Brenniman and
Levy (1984).
-
-
- COMMENTS: The RfD values are based on a weight-of-evidence
approach using subchronic to chronic human drinking water studies. The
uncertainty factor accounts for protecting sensitive individuals and is
reduced from the usual factor of 10 because the selected studies examined
the population judged most at risk.
-
- 3.2 INHALATION EXPOSURES
- 3.2.1 Acute Toxicity
-
- 3.2.1.1 Human
-
-
- Barium carbonate dust has been reported to be a bronchial
irritant. Barium oxide dust is considered a dermal and nasal irritant (Beliles
1994). The effect of barium dusts on welders was investigated under simulated
working conditions over a one-week time period (Zschiesche et al. 1992).
Barium fume concentrations were 4.4 and 2.0 mg/m3 during welding with stick
electrodes and flux cored wires, respectively. No adverse health effects
on the welders were attributable to barium exposure, but there was a slight
decrease in plasma potassium levels at the end of the work shift.
-
-
- 3.2.1.2 Animal
-
-
- Information on the acute inhalation toxicity of barium
in animals
- was not available.
- 3.2.2 Subchronic Toxicity
-
- 3.2.2.1 Human
-
-
- Industrial workers exposed to barium dust, usually in
the form of barium sulfate or carbonate, often develop a benign pneumoconiosis
referred to as "baritosis." Because of the radiopacity of barium
compounds, this condition can be specifically diagnosed radiologically.
After removal from the sources of exposure, baritosis is reversible in
most cases. Baritosis results in a significantly higher incidence of hypertension,
but no changes are usually seen in pulmonary function (Stokinger 1981,
EPA 1995b).
-
-
- 3.2.2.2 Animal
-
-
- Male rats were exposed to 1.15 and 5.2 mg/m3 of barium
carbonate dust for 4 hours/day for 6 months. The high dose animals developed
increased arterial pressure; decreased body weight gain; decreased blood
levels of hemoglobin, sugar, protein, cholinesterase and thrombocytes;
increased blood levels of leukocytes, phosphorous and alkaline phosphatase;
increased urine calcium; and perivascular and peribronchial sclerosis in
the lungs. (EPA 1984, Tarasenko et al. 1977).
-
- 3.2.3 Chronic Toxicity
-
- 3.2.3.1 Human
-
-
- Baritosis and bronchial irritation have been reported
in workers chronically exposed to barium containing dust (Beliles 1994).
-
-
- 3.2.3.2 Animal
-
-
- Information on the chronic inhalation toxicity of barium
in animals was not available.
- 3.2.4 Developmental and Reproductive Toxicity
- Tarasenko et al. (1977) performed a series of experiments
in rats designed to test for possible reproductive and developmental effects.
Increased fetal mortality was observed following the mating of males exposed
to barium carbonate (5.2 mg/m3 air) with untreated females. Decreased sperm
motility was observed in males treated with 22.6 mg/m3. The mating of females
exposed to 13.4 mg/m3 for 4 months also resulted in increased fetal mortality
and a general under development of the newborn pups. Ovarian follicle atresia
was seen in female rats exposed to 3.1 mg/m3. No significant adverse effects
were noted with the 1.15 mg/m3 concentration (EPA 1984).
- 3.2.5 Reference Concentration/Dose
-
- 3.2.5.1 Subchronic
-
-
- INHALATION RfCs: 0.005 mg/m3; 0.001 mg/kg/day (EPA 1995a)
-
- UNCERTAINTY FACTOR: 100
-
- NOEL: 0.8 mg Ba/m3 given 4 hr/day (EPA 1995a)
-
- PRINCIPAL STUDY: The same study and comments apply to
the subchronic
- and chronic RfC. The study is described in Sect. 3.2.4.
-
-
- 3.2.5.2 Chronic
-
-
- INHALATION RfCc: 0.0005 mg/m3; 0.0001 mg/kg/day (EPA
1995a)
-
- UNCERTAINTY FACTOR: 1000
-
- NOEL: 0.8 mg Ba/m3 given 4 hr/day (EPA 1995a)
-
- PRINCIPAL STUDY: Tarasenko et al. 1977
-
- COMMENTS: The dose of 1.15 mg BaCO3/m3 was given as the
NOEL in the principal study, which is equivalent to 0.8 mg barium/m3 used
as the basis for the RfC calculations. An inhalation risk assessment for
barium is under review by an EPA work group (EPA, 1995b).
-
- 3.3 OTHER ROUTES OF EXPOSURE
-
-
- 3.3.1 Acute Toxicity
-
- 3.3.1.1 Humans
-
-
- Barium oxide dust is considered to be a dermal and nasal
irritant
- (Beliles 1994).
-
-
- 3.3.1.2 Animal
-
-
- A number of experiments have used intravenous and subcutaneous
injections to measure lethal levels of soluble barium compounds. LD50 values
for barium chloride, nitrate, and acetate were determined in two strains
of mice by intravenous injection (Syed and Hosain 1972). The affected animals
either died within one hour or survived the treatment. The LD50 values
obtained were 8.12, 8.49, and 11.32 mg barium/kg for the chloride, nitrate,
and acetate, respectively, in Swiss-Webster mice, and 19.20, 20.10, and
23.31 mg barium/kg for the chloride, nitrate, and acetate, respectively,
in ICR mice. Although the relative toxicity of the barium salts remained
the same, there was an unexplained two-fold difference in the LD50 values
between the two mice strains.
-
- The LDLo has been determined by subcutaneous injection
in mice to be 10 mg/kg for the barium nitrate and chloride salts. The LDLo
in rabbits was 55 mg/kg for the chloride and 96 mg/kg for the acetate salts.
The LDLo values vary widely with the route and test animal. For example,
with barium chloride the LDLo value for oral administration to rabbits
is 170 mg/kg, whereas the value for subcutaneous injection is 55 mg/kg.
Subcutaneous injection in mice results in a value of 10 mg/kg, which is
higher than the LD50 value for intravenous injection in the Swiss-Webster
strain (Lewis and Sweet 1984).
- 3.3.2 Subchronic Toxicity
- Information on the subchronic toxicity of barium in humans
and
- animals was not available.
- 3.3.3 Chronic Toxicity
- Information on the chronic toxicity of barium in humans
and animals
- was not available.
- 3.3.4 Developmental and Reproductive Toxicity
- Information on the developmental and reproductive toxicity
of barium
- in humans and animals was not available.
-
- 3.4 TARGET ORGANS/CRITICAL EFFECTS
-
-
- 3.4.1 Oral Exposures
-
- 3.4.1.1 Primary Target Organs
-
-
- 1. Cardiovascular system: Subchronic to chronic symptoms
include increased blood pressure and increased incidence of cardiovascular
disease in humans. An acute overdose can result in cardiac irregularities.
Convulsions and death from cardiac and respiratory failure can occur.
-
-
- 2. Nervous system: Acute to subchronic symptoms include
weakness, tremors, anxiety, and dyspnea. An acute overdose can result in
convulsions and death from cardiac and respiratory failure.
-
-
- 3.4.1.2 Other targets
-
-
- Gastrointestinal system: Acute to subchronic symptoms
include excess salivation, vomiting, and diarrhea in humans.
- 3.4.2 Inhalation Exposures
-
- 3.4.2.1 Primary target(s)
-
-
- 1. Cardiovascular system: Symptoms include increased
blood pressure in humans.
-
- 2. Reproduction and development: Subchronic exposure
of rats resulted in decreased sperm motility and ovarian follicle atresia.
Increased fetal mortality and underdevelopment of newborn pups were also
reported.
-
-
- 3.4.2.2 Other target(s)
-
-
- Lungs: Subchronic to chronic exposure in humans results
in a pneumoconiosis known as "baritosis" that usually does not
adversely affect pulmonary function.
-
- 4. CARCINOGENICITY
- 4.1 ORAL EXPOSURES
-
-
- 4.1.1 Human
- Information on the carcinogenicity of barium in humans
was not
- available.
- 4.1.2 Animal
- No significant differences in tumor incidence were found
in either rats or mice in the lifetime exposure experiments of Schroeder
and Mitchener (1975a,b), as described in Sect. 3.1.3.2.
-
- 4.2 INHALATION EXPOSURES
- Information on the carcinogenicity of barium in humans
and animals
- was not available.
-
- 4.3 OTHER ROUTES OF EXPOSURE
- Information on the carcinogenicity of barium in humans
and animals
- was not available.
-
- 4.4 EPA WEIGHT-OF-EVIDENCE
- Barium has not been evaluated by the EPA for evidence
of human
- carcinogenic potential (EPA 1995b).
-
- 4.5 CARCINOGENICITY SLOPE FACTORS
- Data are insufficient to calculate a slope factor for
barium.
-
- 5. REFERENCES
- Arena, J. M. 1979. Poisoning - Toxicology - Symptoms
- Treatments.
- Charles C. Thomas, Publisher, Springfield, Ill. pp. 173-179.
-
- Beliles, R. P. 1994. The Metals. In: Patty's Industrial
Hygiene and
- Toxicology, 4th ed., G.D. Clayton and F. E. Clayton,
eds. John Wiley
- & Sons, New York. pp. 1925-1929.
-
- Brenniman, G. R. and P. S. Levy. 1984. High barium levels
in public
- drinking water and its association with elevated blood
pressure. In:
- Advances in Modern Toxicology IX, E. J. Calabrese, Ed.
Princeton
- Scientific Publications, Princeton, NJ. pp. 231-249.
-
- EPA (United States Environmental Protection Agency).
1984. Health
- Effects Assessment for Barium. Prepared by the Office
of Health and
- Environmental Assessment, Environmental Criteria and
Assessment
- Office, Cincinnati, OH, for the Office of Emergency and
Remedial
- Response, Washington, D.C.
-
- EPA. 1985. Drinking Water Health Effects Criteria Document
on
- Barium. NTIS PB 86-118031. Prepared by the Office of
Health and
- Environmental Assessment, Environmental Criteria And
Assessment
- Office, Cincinnati, OH for the Office of Drinking Water,
Washington, D.C.
-
-
- EPA. 1989. Reportable Quantity Document for Barium and
Compounds.
- Prepared by the Office of Health and Environmental Assessment,
- Environmental Criteria and Assessment Office, Cincinnati,
OH, for
- the Office of Solid Waste and Emergency Response, Washington,
D.C.
-
- EPA. 1995a. Health Effects Assessment Summary Tables.
Annual FY-95.
- Prepared by the Office of Health and Environmental Assessment,
- Environmental Criteria and Assessment Office, Cincinnati,
OH, for
- the Office of Emergency and Remedial Response, Washington
D.C.
-
-
- EPA. 1995b. Integrated Risk Information System (IRIS).
Health Risk
- Assessment for Barium. On line. (Verification date 6/21/90.)
Office
- of Health and Environmental Assessment, Environmental
Criteria and
- Assessment Office, Cincinnati, OH. Retrieved 4/5/95.
-
- Johnson, C. H. and V. J. VanTassell. 1991. Acute barium
poisoning
- with respiratory failure and rhabdomyolysis. Ann. Emer.
Med.
- 20:1138-1142.
-
- Lewis, R. J. and D. V. Sweet, eds. 1984. Registry of
Toxic Effects
- of Chemical Substances, Vol. 1. U.S. Department of Health
and Human
- Services, Public Health Service, Centers for Disease
Control,
- National Institute for Occupational Safety and Health,
Cincinnati, OH.
-
-
- Machata, G. 1988. Barium. In: Handbook on Toxicity of
Inorganic
- Compounds, H. G. Seiler and H. Sigel, eds., Marcel Dekker,
Inc. pp.
- 97-101.
-
- McCauley, P. T. and I. S. Washington. 1983. Barium bioavailability
- as the chloride, sulfate or carbonate salt in the rat.
Drug Chem.
- Toxicol. 6(2):209-217.
-
- McCauley, P. T., B. H. Douglas, R. D. Laurie, and R.
J. Bull. 1985.
- Investigations into the effect of drinking water barium
on rats.
- Environ. Health Perspect. Vol. IX, E. J. Calabrese, ed.
Princeton
- Scientific Publications, Princeton, NJ. pp.197-210.
-
- National Academy of Sciences. 1977. Drinking Water and
Health. Safe
- Drinking Water Committee, Advisory Center on Toxicology,
Assembly of
- Life Sciences, National Research Council. Washington,
D.C. pp
- 211-212.
-
- Newton, D., G. E. Harrison, C. Kang, and A. J. Warner.
1991.
- Metabolism of injected barium in sex healthy men. Health
Physics
- 61:191-201.
-
- Penington, G. R. 1993. Severe complications following
a "barium
- swallow" investigation for dysphagia. Med. J. Aust.
159:764-765.
-
-
- Perry, H. M., S. J. Kopp, M. W. Erlanger, and E. F. Perry.
1983.
- Cardiovascular effects of chronic barium ingestion. In:
Trace
- Substances in Environmental Health, XVII, D. D. Hemphill,
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-
- Retrieve Toxicity Profiles Condensed Version
-
-
- Last Updated 10/07/97
-
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- <mailto:fdolislager@utk.eduFred Dolislager.
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