BARIUM – A HIGHLY TOXIC METAL
by Dr. Lawrence Wilson
© March 2019, LD Wilson Consultants, Inc.
All
information in this article is solely the opinion of the author and for
educational purposes only. It is
not for the diagnosis, treatment, prescription or cure of any disease or health
condition.
Contents
Young Men Most Affected
Sources
Metabolism
Acute Symptoms
Chronic Symptoms
Removal
Prevention
Interaction With Other Minerals
Barium And Hair Mineral Testing
V. A TECHNICAL ARTICLE ABOUT BARIUM
__________________________________
Barium is a very toxic metal that is a serious problem on earth today. It is an interesting mineral, in that it mainly affects men in their twenties.
Other toxic metals such as Zirconium have a greater effect upon women, especially women in their twenties and thirties, and the effects are different.
SOURCES OF BARIUM
The most important source of barium is the chemtrails that are seen in the skies over many cities in America and other nations. Barium sprayed from the air lands in the water supplies and in the food supply.
This is a Rogue project that is completely illegal and an invasion of the earth by advanced beings who do not want the people of earth to be healthy. The dusting of the planet with barium has been going on for at least 50 years, and longer in some areas.
Dusting with barium is now done throughout the planet, although most experts say there are more chemtrails over America than over any other nation. Food-growing areas of the world such as California and mid-western states of America such as Iowa and Nebraska often have the most chemtrails.
Contrast medium. The other large source of barium is x-ray studies of the digestive tract. These radiologic tests are toxic for this reason and should be avoided, whenever possible. They also damage digestion by irradiating the vital organs such as the stomach, small and large intestines, liver, spleen, pancreas, and intestinal lymph nodes.
II. METABOLISM AND SYMPTOMS OF BARIUM
TOXICITY
METABOLISM OF BARIUM
Absorption. Most barium is absorbed through the intestines from food and beverages. Once absorbed, barium has an affinity for the bones and for the brain.
Barium is located underneath calcium on the periodic table of the elements. This means that the barium atom ÒlooksÓ like a calcium atom in that the outer electron shell has the same number of electrons as does the calcium atom.
As a result, barium can replace calcium in certain enzyme binding sites and other places, including the bones, teeth and in the blood. Blood contains a lot of calcium, which is used as a muscle relaxant and regulator of metabolism. We call calcium the structural mineral because it gives strength and good structure to all tissues.
Cardiovascular and nervous system effects. Barium has toxic affects on many body systems. However, among the most important are the cardiovascular system and the nervous system.
Central nervous system effects. Barium replaces some calcium in the brain. This causes an unsteadiness in a person that weakens the will and causes general malaise, as well.
For some reason, young men aged 15-30 are the most prone to this toxic effect of barium. In them, it also causes a mental dullness and emotionally flat personality.
Cardiovascular effects. Barium weakens the heart muscle and the arterial wall muscles. It may have other cardiovascular toxicity as well.
Other acute toxicity. At
low doses, barium acts as a muscle stimulant, and at higher doses affects the
nervous system eventually leading to paralysis.
Other acute symptoms are cardiac irregularities, weakness, tremors, anxiety, and difficulty breathing. It can also cause a slow pulse, high blood pressure, diarrhea and vomiting.
CHRONIC SYMPTOMS
These are similar to the acute symptoms in that they mainly affect the cardiovascular and nervous systems of the body. In addition, there is evidence that barium toxicity can result in reduced sperm motility and birth defects. Excess barium is also associated with more cancers.
These effects may be due to the antagonism between barium and zinc. Zinc is required for the health of sperm and is protective against birth defects.
Symptoms worse in vegetarians, junk food eaters and those with
sexual fluid loss.
Symptoms of barium toxicity are worse in:
1. Vegetarians
2. Those who have a lot of regular sex with
fluid loss.
3. Those who are malnourished. (The effects of exposure to many toxic
metals are worse in those who are malnourished.)
One reason for the
above is that vegetarians, those who have a lot of sexual fluid loss, and
poorly nourished people all tend to be deficient in zinc. Adequate zinc protects one to a degree against
barium toxicity.
REMOVING BARIUM
A development program. This program will remove excess barium
from the body. The removal process
is slow, however, and requires at least 10 years on a complete program.
The key to the program
is the simultaneous used of about 20 methods of detoxification. These include enhancing the eliminative
organs, enhancing adaptive energy, making the body more yang in macrobiotic
terms, reducing exposure, and improving hydration, oxygenation and circulation.
Other methods used in
this program are balancing and strengthening the autonomic nervous system,
balancing key mineral levels and ratios, putting the person into a more
parasympathetic state, increasing rest and sleep, antagonist therapy, very mild
chelation therapy, improving the activity of the digestive organs, and
improving the overall lifestyle and nutrition of a person.
A major reason that correction
is slow is that it is impossible today to eliminate all exposure to
barium. Through the food and
water, everyone is re-exposed and this slows detoxification. However, at least a development program
can help and is very safe.
Other methods. Most physicians and nutritionists are
using just one or two detoxification methods listed above. In our experience, this is much less
safe and less effective. These
include:
Antagonist therapy. This
is a simple method of giving a person barium antagonists, such as zinc and
calcium, to help eliminate barium.
The problem is that one can unbalance the body by just giving minerals
in a fairly random manner. It is
also not too powerful a method by itself.
This method works to a
slight degree, only. It will help
reduce barium absorption and this method is incorporated into all development
programs. That is, everyone on a
development program receives a diet high in calcium and zinc and receives
supplements of these two minerals as well.
Chelation.
Synthetic and natural chelating agents can lower barium levels in the
body. However, by itself, this method
is not too effective. Chelation is
also toxic. For details, read Chelation Therapy.
PREVENTING BARIUM TOXICITY
It is difficult or
impossible on earth to avoid the effects of chemtrails. However, one can:
1. Reduce exposure to barium. Ways to do this are:
A. Eat organically grown food. This food tends to be lower in barium
because it is higher in zinc, calcium and other minerals that compete with
barium for absorption.
B. Minimize your exposure to x-ray contrast media containing
barium.
These are mainly x-rays of the digestive tract such as the stomach,
small intestine and large intestine.
C. Avoid occupational exposure, although this is uncommon.
2. Maintain good zinc status in the body. This requires a diet of all natural
foods, preferably organically grown.
Also, avoid vegetarian
and vegetarian-leaning diets. In
other words, eat animal protein every day and eat red meat, which has the most
zinc, twice per week.
Also, minimize ordinary
sex with orgasm. Down Sex is much more healthful.
INTERACTION WITH OTHER MINERALS
Calcium. As mentioned earlier, barium is found beneath calcium on the Periodic Table Of The Elements. When an element is found beneath another element on this table, it usually means that the element has some of the same chemical properties of the elements above it and may replace the element above it. This is the case with barium.
Barium interferes with calcium metabolism and can replace calcium in some enzyme binding sites. This is one way it affects the cardiovascular and nervous systems of the human and animal body.
Potassium. Barium lowers potassium, as can calcium. With severe acute exposure, this antagonism can cause death from cardiovascular and respiratory collapse.
The antagonism between calcium and potassium is well established in development science.
Zinc. Zinc is a powerful barium antagonist and protects the body to a degree against barium toxicity.
Barium replaces zinc in some enzyme systems. This may be a reason why barium is particularly toxic for young men, who require excellent zinc levels to function well.
Most young men are very deficient in zinc due to deficiency in all of the food supply and due to poor quality diets. Most young men are also deficient in calcium and other minerals. As a result, they are extremely prone to barium toxicity.
BARIUM AND HAIR MINERAL ANALYSIS
The hair level of barium often reflects the degree of barium toxicity inside the body. In some cases, barium may not be elevated on an initial hair mineral test. However, as some of it is removed through the skin and hair during a development program, the hair level will often elevate on retest mineral analyses.
At this time (December 2019), Analytical Research Labs does not read hair barium levels. A few other laboratories do read barium levels, but these labs do less accurate testing, so we cannot rely upon them.
In development science, fortunately we do not need to measure barium, although it would be nice. The program will remove all toxic metals.
Ideal ranges too high. A hidden problem is that the Ònormal rangeÓ of barium used by laboratories that read this mineral in the hair are too high, in our view. The reason for this is that toxicity with barium is epidemic.
In general, we use lower ideal or normal limits for toxic metals compared to other physicians and laboratories.
V. A TECHNICAL ARTICLE ABOUT BARIUM TOXICITY
The following is a
technical article about barium. We
may not agree with all of it, but we believe it is a very good article.
This material was
researched and compiled by A. A. Francis, M.S., D.A.B.T., and Carol
S. Forsyth, Ph.D. They are members
of the Chemical Hazard Evaluation Group in the Biomedical and Environmental
Information Analysis Section, Health Sciences Research Division, Oak Ridge
National Laboratory.
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.
Acute Toxicity. 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.
Sub-chronic 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
Òbaritosis.Ó 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 μg/L, and 28.6 μg/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 (and effects upon calcium) 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
Òbaritosis.Ó 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 Human
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(s)
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
ÒbaritosisÓ 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
CLASSIFICATION
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.
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