[Federal Register Volume 62, Number 2 (Friday, January 3, 1997)]
[Proposed Rules]
[Pages 366-372]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-56]
-----------------------------------------------------------------------
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[OPPTS-400107; FRL-5581-1]
RIN 2070-AC00
Barium Compounds; Toxic Chemical Release Reporting; Community
Right-to-Know
AGENCY: Environmental Protection Agency (EPA).
ACTION: Denial of petition.
-----------------------------------------------------------------------
SUMMARY: EPA is denying a petition to remove the barium compounds
category from the list of chemicals subject to the reporting
requirements under section 313 of the Emergency Planning and
[[Page 367]]
Community Right-to-Know Act of 1986 (EPCRA) and section 6607 of the
Pollution Prevention Act of 1990 (PPA). This action is based on EPA's
conclusion that barium compounds do not meet the deletion criterion of
EPCRA section 313(d)(3). Specifically, EPA is denying this petition
because EPA's review of the petition and available information resulted
in the conclusion that barium ion (Ba+2) can become available from
the barium compounds subject to reporting and that barium ion can
reasonably be anticipated to cause chronic toxicity. Therefore, barium
compounds meet the criteria for inclusion on the list of chemicals
subject to reporting under section 313 of EPCRA.
FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Acting Petitions
Coordinator, 202-260-3882 or e-mail: bushman.daniel@epamail.epa.gov,
for specific information regarding this document. For further
information on EPCRA section 313, contact the Emergency Planning and
Community Right-to-Know Information Hotline, Environmental Protection
Agency, Mail Stop 5101, 401 M St., SW., Washington, DC 20460, Toll
free: 1-800-535-0202, in Virginia and Alaska: 703-412-9877, or Toll
free TDD: 1-800-553-7672.
0SUPPLEMENTARY INFORMATION:
I. Introduction
A. Statutory Authority
This action is taken under sections 313(d) and (e)(1) of the
Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA), 42
U.S.C. 11023. EPCRA is also referred to as Title III of the Superfund
Amendments and Reauthorization Act of 1986 (SARA) (Pub. L. 99-499).
B. Background
Section 313 of EPCRA requires certain facilities manufacturing,
processing, or otherwise using listed toxic chemicals to report their
environmental releases of such chemicals annually. Beginning with the
1991 reporting year, such facilities also must report pollution
prevention and recycling data for such chemicals, pursuant to section
6607 of the Pollution Prevention Act of 1990 (PPA), 42 U.S.C. 13106.
Section 313 established an initial list of toxic chemicals that was
comprised of more than 300 chemicals and 20 chemical categories.
Barium-containing substances were included on the initial list, under
the chemical category entitled ``barium compounds.'' Section 313(d)
authorizes EPA to add or delete chemicals from the list, and sets forth
criteria for these actions. EPA has added and deleted chemicals from
the original statutory list. Under section 313(e)(1), any person may
petition EPA to add chemicals to or delete chemicals from the list.
Pursuant to EPCRA section 313(e)(1), EPA must respond to petitions
within 180 days, either by initiating a rulemaking or by publishing an
explanation of why the petition is denied.
EPCRA section 313(d)(2) states that a chemical may be listed if any
of the listing criteria are met. Therefore, in order to add a chemical,
EPA must demonstrate that at least one criterion is met, but does not
need to examine whether all other criteria are also met. Conversely, in
order to remove a chemical from the list, EPA must demonstrate that
none of the criteria are met.
EPA issued a statement of petition policy and guidance in the
Federal Register of February 4, 1987 (52 FR 3479), to provide guidance
regarding the recommended content and format for submitting petitions.
On May 23, 1991 (56 FR 23703), EPA issued guidance regarding the
recommended content of petitions to delete individual members of the
section 313 metal compound categories. EPA has also published a
statement clarifying its interpretation of the section 313(d)(2)
criteria for adding and deleting chemical substances from the section
313 list (59 FR 61439, November 30, 1994) (FRL-4922-2).
II. Description of Petition and Regulatory Status of Barium and
Barium Compounds
Barium-containing substances are on the list of toxic chemicals
subject to the annual reporting requirements of EPCRA section 313 and
PPA section 6607. Barium-containing substances comprise the ``barium
compounds'' category on the EPCRA section 313 list of toxic chemicals.
The presence of barium in a compound defines its inclusion in the
barium compounds category. As with all the metal compound categories on
the EPCRA section 313 list of toxic chemicals, the basis for inclusion
of the individual metal-containing substances within these categories
is the toxicity which may be exhibited by the intact substance, or by
the metal or metal ion which may be liberated from the intact substance
within an organism, by biological fluids, or in the environment. EPA
published a detailed discussion on the Agency's policies related to the
metal compound categories on the EPCRA section 313 list of toxic
chemicals in the Federal Register of May 23, 1991 (56 FR 23703).
EPA recently deleted barium sulfate (also known as barite) from the
barium compounds category (59 FR 33205, June 28, 1994) (FRL-4767-5).
EPA concluded that barium sulfate does not meet the toxicity criteria
of EPCRA sections 313(d)(2)(A), (B) or (C), and that barium ion is
available from barium sulfate only under low sulfate, anaerobic
conditions in stagnant water bodies that are cut-off from surface and
ground waters (i.e., conditions that cannot reasonably be anticipated
to cause ecotoxicity or lead to human exposure to the ion). EPA
believes that the low toxicity of barium sulfate can be mainly ascribed
to the very low water solubility (2.4 milligrams per liter (mg/L) at 25
deg.C) of barium sulfate, barium ion's strong affinity for sulfate,
and correspondingly, the low availability of barium ion.
Barium is regulated under the Safe Drinking Water Act, (42 U.S.C.
300f-300j-26); the current maximum contaminant level (MCL) is 2 mg/L (2
parts per million (ppm)) (40 CFR 141.62(b)(3)).
On June 28, 1996, EPA received a petition from the Chemical
Products Corporation (CPC) to delete the entire barium compounds
category from the EPCRA section 313 list of toxic chemicals. With this
action, CPC petitioned EPA to delete all barium compounds from the list
of toxic chemicals subject to the annual reporting requirements of
EPCRA section 313 and PPA section 6607. In the petition, data are
presented from various toxicity studies on a limited number of barium
compounds. The petitioner contends that all barium compounds should be
deleted because the available toxicity data show that barium ion does
not meet the criteria for inclusion on the list of EPCRA section 313
chemicals. The petitioner also asserts that under environmental
conditions barium ion is largely unavailable from barium compounds
because of the presence of sulfate ion in the environment; sulfate ion
will react quickly with barium ion to form barium sulfate.
III. EPA's Technical Review of Barium Compounds
The technical review of the petition to delete barium compounds
from the reporting requirements of EPCRA section 313 and PPA section
6607 included an analysis of the chemistry, health effects, ecological
effects, and environmental fate data available for barium compounds.
A. Chemistry and Use
Barium is a metallic substance that occurs in nature as its
divalent cation
[[Page 368]]
(ion), Ba+2. Barium compounds are those substances that contain
barium as part of their molecular formula. EPA has published a
discussion on the chemistry of barium ion (Ref. 1). Barium ion is
highly electropositive, and reacts readily with anions (sulfate
(SO4-2), chloride (Cl-1), carbonate (CO3-2),
nitrate (NO3-2), etc.) to form the corresponding barium salt.
The water solubility of the salt and, therewith, its ability to
dissociate to barium ion is largely dependent on the affinity between
barium ion and the anion. Barium chloride is highly water soluble (317
grams per liter (g/L)), whereas barium carbonate and barium sulfate are
considerably less soluble, having water solubilities of 24 mg/L and 2.4
mg/L, respectively (Ref. 2). Barium carbonate is soluble in diluted
solutions of hydrochloric, nitric or acetic acid. These acids react
with barium carbonate to form barium chloride, barium nitrate, and
barium acetate, respectively, which are all freely soluble in water
(Ref. 2).
Another important factor controlling the availability of barium ion
from a barium compound is the presence of sulfate ion. In waters, the
availability of barium ion from a barium compound is governed largely
by the concentration of sulfate ion present in solution. The
availability of barium ion is inversely related to the concentration of
sulfate; barium ion availability is suppressed in the presence of
sulfate, and enhanced when sulfate concentration is low. This is
because sulfate has a high affinity for barium ion and will form barium
sulfate which precipitates out of solution (Ref 1). A more detailed
discussion of factors that control barium ion availability in waters is
provided below in Unit III.C. of this notice ``Environmental Fate of
Barium Compounds.''
The most common natural form of barium is barium sulfate (barite).
The greater natural occurrence of barium sulfate with respect to other
barium salts is likely to be due to the relatively stronger affinity
between Ba+2 and SO4-2, when compared to the affinity
between Ba+2 and other naturally occurring anions.
Barium carbonate is another naturally occurring barium compound. It
is also produced commercially from barium sulfate. Barium carbonate is
often added to brick and clay products to precipitate sulfates. Barium
carbonate is used also in the production of ceramic materials and glass
products, and to produce other barium compounds. Barium compounds
produced from barium carbonate include: barium acetate; barium bromide;
barium chloride; barium 2-ethylhexanoate; barium hydroxide; barium
hydrosulfide; barium iodide; barium metaborate; barium nitrate; barium
nitrite; barium oxide; barium peroxide; barium sodium niobium oxide;
barium sulfide; barium titanate; and higher purity grades of barium
sulfate (Ref. 3). The uses of most of these barium compounds are
summarized in Ref. 3.
B. Toxicological Evaluation
EPA's toxicological evaluation of barium compounds consisted of an
analysis of health and environmental data pertaining to barium-
containing substances included on the EPCRA section list of toxic
chemicals as part of the barium compounds category. Data were obtained
from: studies found in the literature (Refs. 4-12); the Hazardous
Substances Data Bank (Ref. 13); EPA's Integrated Risk Information
System (IRIS) (Ref. 14); a previous Federal Register Notice on barium
sulfate (Ref. 15); a 1992 report published by the U.S. Department of
Health and Human Services' Agency for Toxic Substances and Disease
Registry entitled Toxicological Profile for Barium (Ref. 16); a 1993
report published by the U.S. Department of Health and Human Services'
National Toxicology Program entitled Toxicology and Carcinogenesis
Studies of Barium Chloride Dihydrate in F4344 Rats and B6C3F1 Mice
(Ref. 17); and a 1990 EPA document entitled The Drinking Water Criteria
Document for Barium (Ref. 18). The health and environmental portions of
these reference sources are summarized below. Detailed discussions can
be found in the publications and in the technical reports (Refs. 19-22)
prepared by the EPA scientists who reviewed the publications. EPA's
toxicological evaluation of barium compounds also included a review of
the analysis of health and environmental data stated in the petition
and the petitioner's interpretation of such data.
1. Acute mammalian toxicity. In humans, symptoms of acute barium
toxicity after accidental or intentional oral ingestion of 1-15 grams
of soluble barium salts include: muscular paralysis; respiratory
failure; arterial hypertension; cardiac arrhythmias; profound
hypokalemia and death (Refs. 5 and 18). The threshold of a toxic oral
dose in adults has been estimated to be 200-500 milligrams (mg) or 2.86
- 7.14 milligrams per kilogram (mg/kg) of body weight. This quantity
applies to the equivalent weight of the barium ion absorbed from the
gut from the barium compound. The digestive system is extremely
permeable to the barium ion. Acute lethal oral doses for barium in
adults have been estimated to be 3-4 grams (calculated 43 - 57 mg/kg)
(Refs. 13 and 18). Animal studies support similar cardiotoxic effects
following acute exposure.
Ogen, et al. summarized the results of two large outbreaks of food
poisoning that occurred following consumption of sausage that contained
barium carbonate which was accidentally substituted for potato starch
during sausage preparation (Ref. 12). The authors estimate that the
amount of barium carbonate ingested in most of the affected individuals
was 2-3 grams per person. The characteristic symptoms occurred within 8
hours after ingestion of the contaminated sausage, and included:
vomiting, diarrhea, general weakness, paresthesia, difficulty in
breathing, and, in the more severe cases, paralysis of the limbs and
respiratory muscles. Most of the 144 affected individuals received
treatment and recovered within a few days, however, 19 individuals
required hospitalization, and one patient died. The authors of the
study attribute the observed toxicity of barium carbonate to its
reaction with hydrochloric acid in the stomach to yield barium
chloride, which dissociates readily to barium ion and is absorbed
systemically. These authors cite other studies involving food poisoning
from barium carbonate.
The acute oral lethality of barium in animals has been well
documented. There is a wide variability in the lethal dose of barium
among species and age, as well as between strains of the same species.
Nevertheless, the acute lethality of various barium salts is a function
of their solubility in water or acid. In rats, acute oral toxicities of
barium chloride, fluoride, nitrate and acetate have median lethal dose
(LD50) values of 118, 250, 355 and 921 mg barium/kg, respectively
(Refs. 4, 13, and 17).
2. Subchronic and chronic mammalian toxicity. EPA's review of the
available toxicity data for barium compounds identified kidney toxicity
as the toxicological endpoint of concern. There are also varying
reports on cardiovascular effects in humans and test animals from
subchronic and chronic exposure to barium.
The U.S. Department of Health and Human Services' National
Toxicology Program (NTP) conducted toxicology and carcinogenicity
studies in F344/N rats and B6C3F1 mice by administering barium chloride
dihydrate (99 percent pure) in drinking water for 15 days, 13 weeks,
and 2 years (Ref. 17). Under the conditions of the study, there was no
evidence of carcinogenic activity in any of the test animals. There
were chemical-related increased incidences of kidney toxicity
(nephropathy) in male and female mice. The Lowest Observed Adverse
Effect Level (LOAEL) for
[[Page 369]]
kidney toxicity in mice is approximately 180 milligrams per kilogram
per day (mg/kg/day) (Refs. 19 and 20). Kidney toxicity was observed in
rats, but the data are conflicting (kidney effects were seen in the 13-
week study, but not in the 2-year study). Test animals and their
offspring were not observed for reproductive or developmental effects.
The results of the NTP study are summarized below. A more detailed
summary is provided in Ref. 19.
In groups of 60 male and 60 female mice receiving 0, 500, 1,250, or
2,500 mg/L barium chloride dihydrate in drinking water for 2 years,
dose-related nephropathy was observed. The incidence of nephropathy was
significantly increased in mice of both genders that received 2,500 mg/
L. The nephropathy consisted of extensive regeneration of cortical and
medullary renal tubule epithelium, tubule dilatation, hyaline cast
formation, multifocal interstitial fibrosis and in some kidneys,
glomerulosclerosis. These lesions were accompanied by brown crystals
(barium precipitated salts) located within the kidney's tubules lumen
and interstitium throughout the cortex and medulla. The kidney lesions
were considered the cause of death in most animals. The absolute and
relative spleen weights in female rats in the highest dose were lower
compared to controls. Based on the renal toxicity, the LOAEL is 160 mg/
kg/day for male mice and 200 mg/kg/day for female mice. The No Observed
Adverse Effect Level (NOAEL) is 75 mg/kg/day for male mice and 90 mg/
kg/day for female mice.
Groups of 10 male and 10 female F344/N rats received barium
chloride dihydrate in drinking water at doses of 0, 125, 500, 1,000,
2,000 or 4,000 mg/L, 7 days a week for 13 weeks (Ref. 17). Drinking
water levels were estimated to deliver daily doses of 10, 30, 65, 110,
or 200 mg/kg for male rats and 10, 35, 65, 115, or 180 mg/kg body
weight to females. Three male rats and one female rat that received
4,000 mg/L died during the last week of the study. A significant
decrease in motor activity was observed in rats that received the
highest dose.
The absolute and relative kidney weights of female rats that
received 2,000 and 4,000 mg/L and the relative kidney weight of male
rats in the 4,000 mg/L groups were greater than controls and were
associated with barium-induced renal lesions. Barium-induced renal
lesions occurred in three male and three female rats in the highest
dose groups. Gross pathology revealed kidneys that were pale and had
roughened surfaces. Microscopically, the kidney lesion appeared as a
minimal to mild focal to multifocal dilatation of the proximal
convoluted tubules in the outer medulla and the renal cortex. Tubule
dilatation observed in this study was different from the common
spontaneous lesions observed in the kidney of rats.
In a similar 13-week study on mice (Ref. 17), barium-induced
nephropathy was observed in 10 male and 9 female mice in the highest
dose group. Gross pathology revealed kidneys that were pale and had
roughened surfaces. The nephropathy consisted of mild to moderate
multifocal tubule dilatation, regeneration and atrophy with crystals in
the lumens of the atrophic tubules. An increased amount of fibrous
connective tissue was present in the affected kidneys. The LOAEL in
male mice was 450 mg/kg/day and in female mice was 495 mg/kg/day based
on the mortality, lower final mean body weights and water consumption,
presence of renal, thymic and splenic lesions. The NOAEL was 205 mg/kg/
day for male mice and 200 mg/kg/day for female mice.
In a 13-week drinking water study (Ref. 11), barium chloride
dihydrate was given to groups of 10 male and 10 female F344/N rats and
B6C3F1 mice at levels of 0, 125, 500, 1,000, 2,000, and 4,000 mg/L
(ppm). The estimated average barium doses for rats were 0, 5.1, 20.0,
39.0, 70.0, and 128 mg/kg/day and for mice were 0, 12.0, 45.0, 83.0,
165, and 399 mg/kg/day. Mortality ranged from 60 to 70 percent in mice
and from 10 to 30 percent in rats in the 4,000 mg/L groups. Deaths in
mice were associated with barium-induced renal toxicity. Renal lesions
in rats were much less severe than in mice and did not contribute to
the barium-induced deaths seen in the high dose group. In both species
the highest dose produced marginal decreases in motor activity, grip
strength, and thermal sensitivity. The authors attributed these effects
to secondary changes resulting from barium chloride toxicity at this
dose. In mating trials, no anatomical effects on offspring of rats or
mice were noted. Rats given 4,000 mg/L had marginal reductions in pup
weights. No effects were noted on reproductive indices. Based on the
mortality and renal toxicity at 4,000 mg/L in both rats and mice, the
NOAEL was 70 mg/kg/day in rats and 165 mg/kg/day in mice.
Reports on the cardiovascular effects of subchronic and chronic
exposure to barium in humans and animals vary. Brenniman et al. (Ref.
7) conducted an epidemiological study in which death-rates (established
from death certificates) in communities with high levels of barium in
their drinking water (2 -10 mg/L) were compared to communities that
were exposed to low levels of barium in water (0.0 - 0.2 mg/L). While
an initial analysis of the data indicated statistical differences in
blood pressure between the communities, extensive analysis did not. No
statistically significant differences were found in blood pressure
between individuals in the two cities even when adjustments for
duration of exposure, use of water softeners and the use of
antihypertensive drugs were made (Ref. 17) .
In a human study conducted by Wones et al. (Ref. 8), 11 healthy men
were enrolled in a 10-week barium drinking water dose-response
protocol. Diet and lifestyle were controlled and the barium content of
the drinking water was varied from 0 mg/L (first 2 weeks) to 5 mg/L
(next 4 weeks) to 10 mg/L (last 4 weeks). There were no changes in
morning or evening systolic or diastolic blood pressures, plasma
cholesterol or lipoprotein, serum potassium or calcium or glucose
levels. There were no arrythmias related to barium exposure.
Consumption of barium in drinking water at a dose of 0.21 mg barium/kg/
day did not appear to affect any of the cardiovascular parameters
monitored in this study (Ref. 17). This study was considered limited by
the EPA's Office of Drinking Water due to its small study population
and short duration of exposure (4 weeks) and because there was no
lowest effect dose.
Perry et al. (Ref. 9) studied the effect of barium in drinking
water on blood pressure in rats. A total of 195 female weanling Long-
Evans rats were subdivided into a control group of 26 animals (0 mg/L)
and 3 exposure groups of 13 rats. Each group was provided drinking
water containing 1, 10, or 100 mg/L of barium chloride for 1, 4, or 16
months. There were significant increases in mean systolic blood
pressure in rats receiving the highest dose at 1 and 4 months (7.1 and
6.3 mg/kg/day, respectively). In the 16-month study, rats exposed to
0.51 and 5.1 mg/kg/day had significant increases in blood pressure as
well. Also at the highest dose, there was a decrease in contractility
and excitability of cardiac muscle fiber. The LOAEL for the 16-month
study was 0.51 mg/kg/day as evidenced by increase in blood pressure and
the NOAEL was 0.051 mg/kg/day. However, the test animals were
maintained on a special contaminant-free diet that restricted their
intake of certain beneficial trace metals, such as calcium and
potassium. This restriction may have contributed to the observed
hypertensive effects. Several other studies with rats and mice lasting
from
[[Page 370]]
13 weeks to 2 years show no increase in blood pressure or any other
cardiovascular effects.
3. Ecotoxicity. Barium compounds have low toxicity to aquatic
organisms and plants (Refs. 15 and 22). The low toxicity of barium
compounds to aquatic species is attributable to the presence of sulfate
in waters; barium ion liberated from a barium compound reacts with
sulfate to form barium sulfate, which precipitates from solution.
C. Environmental Fate of Barium Compounds
EPA's environmental fate evaluation of barium compounds consisted
of an analysis of environmental fate data pertaining to barium-
containing substances included on the EPCRA section 313 list of toxic
chemicals as part of the barium compounds category. Data were obtained
from studies found in the literature (Refs. 23, 26-29, 31, and 32) and
several government documents (Refs. 24, 25, and 30). The portions of
these reference sources that are relevant to EPA's review of the
environmental fate of barium compounds are summarized below. Detailed
discussions can be found in the publications and in Ref. 33, EPA's
technical review of these publications.
1. Air. Most barium compounds released to the environment from
industrial sources are in forms that do not become widely dispersed
(Ref. 23). In the atmosphere, barium compounds are likely to be present
in particulate form. Although chemical reactions may cause changes in
speciation of barium in air, the main mechanisms for the removal of
barium compounds from the atmosphere are likely to be wet and dry
deposition (Ref. 24).
Elemental barium is oxidized readily in moist air (Refs. 25 and
26). The residence time of barium in the atmosphere may be several
days, depending on the size of the particulate formed, the chemical
nature of the particulate, and environmental factors such as rainfall
(Ref. 24).
2. Water. In aquatic media, barium compounds are likely to
precipitate out of solution as barium sulfate (BaSO4) or barium
carbonate (BaCO3). Waterborne barium may also adsorb to suspended
particulate matter (Refs. 24, 27, and 28). Precipitation of barium
sulfate is accelerated when rivers enter ocean waters. This is due to
the higher sulfate content in ocean waters (Ref. 33). Sedimentation
removes a large portion of barium compounds that are suspended in
surface waters (Ref. 29).
Appreciable quantities of barium sulfate or carbonate precipitate
may occur in aquatic environments. This is because natural waters
usually contain sulfate or carbonate concentrations that are sufficient
to react with barium ion to form barium sulfate or carbonate, which
precipitates from solution (Ref. 30). In natural waters at pH levels of
9.3 or below, barium ion will react to form barium sulfate (Ref. 27).
At pH above 9.3 formation of barium carbonate is favored.
3. Soil. Barium is not very mobile in most soils. The rate of
transportation of barium in soils is dependent on soil characteristics.
Soil properties that influence the transportation of barium to
groundwaters are cation exchange capacity and calcium carbonate
(CaCO3) content. In soils with a high cation exchange capacity
(e.g., fine textured mineral soils or soils with high organic matter
content), barium mobility will be limited by adsorption (Ref. 28). High
calcium carbonate content limits mobility by precipitation of the
element as barium carbonate. In soils, barium will also precipitate as
barium sulfate in the presence of sulfate ions (Refs. 27 and 28).
Barium is more mobile and is more likely to be leached from soils in
the presence of chloride due to the increased solubility of barium
chloride as compared to other chemical compounds of barium (Ref. 28).
Barium can form compounds with fatty acids (e.g., in acidic landfill
leachate) with enhanced mobility in soils due to the lower charge of
these compounds and subsequent reduction in adsorption capacity (Ref.
28). The significance of these mobility enhancing processes is thought
to be minor overall, and it is likely that in the presence of sulfate
or carbonate in soils, barium ion will react to form a solid (barium
sulfate or barium carbonate) with relatively low mobility.
4. Barium solubility in anaerobic environments. Although the
formation of barium sulfate precipitate is thought to be the major fate
pathway for barium ion in aqueous environments containing adequate
levels of sulfate, there is evidence indicating that under anaerobic,
low sulfate conditions, enhanced barium solubility from barium sulfate
can occur. Barium ion concentrations greater than those expected based
on the solubility of barium sulfate can result through a series of
steps in which available sulfate is reduced to sulfide by anaerobic
bacteria (Ref. 31).
The existence of anaerobic, sulfate poor aquatic environments where
enhanced barium solubility may occur has been documented (Ref. 32).
However, these environments are often found in northern glaciated
regions in water bodies that are isolated from flowing surface waters
and groundwaters. As these areas tend to be remote, the likelihood of
releases of barium compounds entering these environments with
subsequent attainment of barium ion concentrations of environmental
significance is low.
D. Acute Exposure
Because barium compounds have been associated with acute effects in
humans, EPA conducted a limited exposure analysis. (See discussion of
use of exposure in listing decisions, 59 FR 61440, November 30, 1994.)
Based on the TRI data, EPA has determined that the concentration levels
of barium compounds likely to exist beyond facility site boundaries are
low compared to the levels that would be required to induce the acute
toxicities discussed above. Therefore, EPA does not believe that
adverse acute human health effects are reasonably likely to occur as a
result of continuous, or frequently recurring releases of barium
compounds from facilities (Ref. 33).
IV. Technical Summary
EPA's technical review shows that many barium compounds are known
to produce toxic effects in humans and experimental animals with the
main target organ being the kidneys. Several barium compounds are
acutely toxic to humans; however, EPA's exposure analysis indicates
that the concentrations required to produce these acute toxicities are
not reasonably likely to exist beyond facility site boundaries as a
result of continuous, or frequently recurring releases of barium
compounds from facilities. With regard to chronic toxicity, the data
from animal studies support a LOAEL of approximately 180 mg/kg/day for
renal toxicity. Based on these data, EPA considers barium ion to have
moderately high chronic toxicity. From its technical review EPA
concludes that: barium ion is bioavailable from barium compounds,
including some compounds with low water solubility (e.g, barium
carbonate); and that barium ion is responsible for the toxic effects
produced by barium compounds. Available data indicate that barium
compounds are not ecotoxic. EPA's previous determination (59 FR 33205,
June 28, 1994) (FRL-4767-5) that barium sulfate is essentially non-
toxic to humans and the environment, and thus does not meet the EPCRA
section 313(d)(2) criteria for listing remains unchanged.
V. Rationale for Denial
With the exception of barium sulfate, barium-containing substances
are chemicals subject to EPCRA section 313
[[Page 371]]
(listed under the category of ``barium compounds'') and PPA section
6607 reporting requirements. The petition to delist barium compounds is
based on the petitioner's contention that barium compounds are not
toxic and do not meet any of the statutory criteria under section
313(d)(2). In addition, the petitioner contends that due to an
abundance of sulfate in the environment, barium ion is not available
from barium compounds released into the environment because
environmental sulfate will combine with barium ion to form barium
sulfate.
EPA's review of available data has led the Agency to conclude that
in experimental animals and humans: (1) Barium ion is available from
barium compounds, including some compounds that have low water
solubility; and (2) barium ion causes moderately high toxicity to the
kidney.
Based on available data, EPA concludes that barium compounds can
reasonably be anticipated to cause chronic toxicity in humans because
of their ability to liberate barium ion, which in turn causes adverse
chronic health effects. Therefore, barium compounds meet the criteria
of EPCRA section 313(d)(2)(B). EPA concludes that barium compounds
should not be deleted from the section 313 list of toxic chemicals, and
the petition should be denied. Because barium compounds can reasonably
be anticipated to cause moderately high chronic toxicity, EPA does not
believe that an exposure assessment is necessary to conclude that
barium compounds meet the toxicity criterion of EPCRA section
313(d)(2)(B). For a discussion of the use of exposure in EPCRA section
313 listing/delisting decisions, see 59 FR 61440, November 30, 1994.
EPA agrees with the petitioner that sulfate is a ubiquitous
substance in the environment, and that sulfate reacts with barium ion
to form barium sulfate. EPA also agrees that barium sulfate does not
meet the criteria for listing on the section 313 list of toxic
chemicals. EPA does not agree, however, that the presence of sulfate in
the environment ensures that barium compounds cannot be toxic to
humans. In its review of the toxicity of barium compounds, EPA
concludes that environmental presence of barium ion is not a necessary
prerequisite for toxicity from a barium compound. In the technical
review portion of this notice, EPA describes studies in which adverse
effects were observed following exposure to an intact barium compound.
The toxicity occurs as a consequence of barium ion release in vivo.
Therefore, exposure to an intact barium compound can reasonably be
anticipated to cause toxicity as a result of the release of barium ion
in the body.
In addition, EPA does not agree that the presence of sulfate in the
environment automatically ensures that barium ion availability will not
result from barium compounds released into the environment. EPA feels
that continuous releases of a barium compound (particularly a highly
soluble one) to a given area could deplete sulfate in that area. Once
sulfate depletion takes place, continued release of the barium compound
could lead to availability of barium ion.
EPA's denial of this petition is consistent with the Agency's
published policy and guidance on metal compound categories under
section 313 of EPCRA (56 FR 23703, May 23, 1991). This policy and
guidance articulated EPA's determination that the toxicity of a metal-
containing compound that dissociates or reacts to generate the metal
ion can be expressed as a function of the toxicity induced by the
intact species and the availability of the metal ion. Thus, EPA stated
that for petitions to exempt individual metal-containing compounds from
the EPCRA section 313 list of toxic chemicals, EPA bases its decisions
on the evaluation of all chemical and biological processes that may
lead to metal ion availability, as well as on the toxicity exhibited by
the intact species. EPA stated that the Agency will deny petitions for
chemicals that dissociate or react to generate the metal ion at levels
which can reasonably be anticipated to cause adverse effects to human
health or the environment and for which the metal ion availability
cannot be properly characterized.
In summary, EPA's review of information pertaining to barium
compounds resulted in the conclusion that in mammals: (1) Barium ion is
available from barium compounds (including some compounds that have low
water solubility); and (2) barium ion causes chronic toxic effects.
Thus, barium compounds can reasonably be anticipated to cause chronic
toxicity in humans because of their ability to liberate barium ion. EPA
believes that the available data satisfy the criterion in EPCRA section
313(d)(2)(B). Accordingly, EPA is denying the petition.
VI. References
1. USEPA. 1991. Barium Sulfate: Toxic Chemical Release Reporting
(Withdrawal of Proposed Rule); Community Right-to-Know. Federal
Register, Vol. 56, No. 100, May 23, 1991; pages 23668-23672.
2. USEPA, OPPTS. 1996. Raksphal, Ram; ``Chemistry Report on Barium
Compounds.''
3. USEPA, OPPTS. 1996. Arnold, Fred; ``Economic Report on Barium
Compounds.''
4. RTECS. 1996. Registry of Toxic Effects of Chemical Substances
(database). US Department of Health and Human Services, National
Institute for Occupational Safety and Health, Washington, DC.
5. Rosa, O., Berman, L.B.; ``The Pathophysiology of Barium:
Hypokalemic and Cardiovascular Effects.'' J. Pharmacol Exp Ther. v.
177, (1971), pp. 433-439.
6. Klassen, C.D., Amdur, M.O., Doull, J., (eds); Casarett and
Doull's Toxicology 5th ed., New York: Macmillan Co. Inc., (1995), p.
726.
7. Brenniman G.R., Namekata, T., Kojola, W.H., Carnow, B.W., Levy,
P.S.; ``Cardiovascular Disease Death Rates in Communities with Elevated
Levels of Barium in Drinking Water.'' Environ. Res. v. 20, (1979), pp.
318-324.
8. Wones, R.G., Stadler, B.L., Frohman, L.A.; 1990. ``Lack of
Effect of Drinking Water Barium on Cardiovascular Risk Factors.'' Env.
Health Perspect. v. 85, (1990), pp. 355-359.
9. Perry, H.M, Kopp, S.J., Perry E.F., Erlanger, M.W.;
``Hypertension and Associated Cardiovascular Abnormalities Induced by
Chronic Barium Feeding.'' J. Toxicol. Environ. Health v. 28, (1989),
pp. 373-388.
10. Kopp, S.J., Perry. H.M., Feliksik, J.M., Erlanger, M., Perry,
E.F.; ``Cardiovascular Dysfunction and Hypersensitivitiy to Sodium
Pentobarbital Induced by Chronic Barium Chloride Ingestion.'' Toxicol.
Appl. Pharmacol. v. 77, (1984), pp. 303-314.
11. Dietz, D.D., Elwell, M.R., Davies, W.E., Meirhenry, E.F.;
``Subchronic Toxicity of Barium Chloride Dihydrate Administered to Rats
and Mice in the Drinking Water.'' Fundam. Appl. Toxicol. v. 19, (1992),
pp. 527-537.
12. Ogen, S., Rosenbluth, S., Eisenberg, A.; ``Food Poisoning Due
to Barium Carbonate in Sausage.'' Isr. J. Med. Sci. v. 3, (1967), pp.
565-568.
13. HSDB 1996. Hazard Substances Data Bank. MEDLARS online
Information Retrieval System. National Library of Medicine.
14. U.S. Environmental Protection Agency's Integrated Risk
Information System (IRIS) file pertaining to Barium (CAS No. 7440-39-
3).
15. USEPA. 1993. Barium Sulfate: Toxic Chemical Release Reporting
(Proposed Rule); Community Right-to-
[[Page 372]]
Know. Federal Register, Vol. 58, No. 111, June 11, 1993; pp. 32622-
32628.
16. ATSDR. 1992. Toxicological Profile for Barium. U.S. Department
of Health and Human Services, Public Health Service, Agency for Toxic
Substances and Disease Registry (ATSDR), Atlanta, GA, report no. ATSDR/
TP-91/03.
17. U.S. Department of Health and Human Services. 1993 NTP
Technical Report 432. Toxicology and Carcinogenesis Studies of Barium
Chloride Dihydrate in F4344 Rats and B6C3F1 mice. NIH Publication # 93-
3163.
18. USEPA, ODW. 1990. The Drinking Water Criteria Document on
Barium. Office of Drinking Water, U.S. Environmental Protection Agency,
Washington, DC; report no. TR-1242-62A.
19. USEPA, OPPTS. 1996. Memorandum from Dr. Nicole Paquette,
Toxicologist, Health and Environmental Review Division. Subject: Human
Health Assessment of Barium for Review of the Petition to Delist Barium
Compounds from the Toxics Release Inventory. (August 22, 1996).
20. USEPA, OPPTS. 1996. Memorandum from Lorraine Randecker, Hazard
Integrator, Chemical Screening and Risk Assessment Division. Subject:
Hazard Assessment of Barium for Review of the Petition to Delist Barium
Compounds from the Toxics Release Inventory. (August 1996).
21. USEPA, OPPTS. 1996. Memorandum from Dr. Leonard Keifer, Health
and Environmental Review Division. Subject: Bioavailability of Barium
from Soluble Barium Salts. (August 15, 1996).
22. USEPA, OPPTS. 1996. Memorandum from Dr. Ossi Meyn, Biologist,
Health and Environmental Review Division. Subject: Ecological
Assessment for Petition to Delist Barium Compounds from the Toxics
Release Inventory. (August, 1996).
23. Ng, A., Patterson, C.C. ``Changes of Lead and Barium With Time
in California Offshore Basin Sediments.'' Geochim Cosmochim Acta v. 46
(1982) pp. 2307-2321
24. USEPA, ECAO. 1984. Health effects assessment for barium.
Prepared by Environmental Criteria and Assessment Office, Cincinnati,
OH: US Environmental Protection Agency, Office of Solid Waste and
Emergency Response, Washington, DC: EPA/540/1-86/021.
25. USEPA. 1987. Code of Federal Regulations. 40 CFR Part 264,
Appendix IX.
26. Kunesh, C.J. ``Barium.'' In: Grayson, M., Eckroth, D., (eds);
Kirk-Othmer Encyclopedia of Chemical Technology. Volume 3, 3rd ed. New
York, NY: John Wiley and Sons, (1978) pp. 457-463.
27. Bodek, I., Lyman, W.J., Reehl, W.F. (eds). Environmental
Inorganic Chemistry: Properties, Processes, and Estimation Methods. New
York, NY: Pergamon Press (1988).
28. Lagas, P., Loch, J.P.G., Bom, C.M., et al. ``The Behavior of
Barium in a Landfill and the Underlying Soil.'' Water, Air, Soil
Pollut. v. 22, (1984), pp. 121-129.
29. Benes, P., Sebesta, F., Sedlacek, J., et al. ``Particulate
Forms of Radium and Barium in Uranium Mine Waste Waters and Receiving
River Waters.'' Water Res v. 17, (1983), pp. 619-624.
30. USNAS. 1977. Drinking water and health. Vol. 1. National
Academy of Sciences. Washington, DC: National Academy Press, p. 229.
31. Deuel, L.E., Freeman, B.D.; ``Amendment to the Louisiana
Statewide Order 29-B Suggested Modifications for Barium Criteria, SPE/
IADC,'' (1989), pp. 461-466.
32. Shannon, R.D., White, J.R. ``Spatial and Temporal Variations in
Methane Cycling in Bog Ecosystems,'' Preprint Extended Abstract:
Presented before the Division of Environmental Chemistry, American
Chemical Society, Atlanta, Georgia, April 14-19 (1991).
33. USEPA, OPPTS. 1996. Lynch, David; ``Exposure Assessment for TRI
Barium Compounds Category.''
VIII. Administrative Record
The record supporting this decision is contained in docket control
number OPPTS-400107. All documents, including the references listed in
Unit VI. above and an index of the docket, are available to the public
in the TSCA Non-Confidential Information Center (NCIC), also known as
the Public Docket Office, from noon to 4 p.m., Monday through Friday,
excluding legal holidays. The TSCA NCIC is located at EPA Headquarters,
Rm. NE-B607, 401 M St., SW., Washington, DC 20460.
List of Subjects in 40 CFR Part 372
Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, and Toxic chemicals.
Dated: December 23, 1996.
Lynn R. Goldman,
Assistant Administrator, for Prevention, Pesticides and Toxic
Substances.
[FR Doc. 97-56 Filed 1-2-97; 8:45 am]
BILLING CODE 6560-50-F
