Barium Compounds; Toxic Chemical Release Reporting; Community Right-to-Know

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: [email protected],

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