366 Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules

three additional sanitized copies must

also be submitted. Nonconfidential

versions of comments will be placed in

the record for this action and will be

available for public inspection.

Comments should include the docket

control number for the ANPR, OPPTS400106 and the EPA contact. Unit II. of

this document contains additional

information on submitting comments

containing information claimed as CBI.

Comments and data may also be

submitted electronically by sending

electronic mail (e-mail) to:

oppt.ncic@epamail.epa.gov. Electronic

comments must be submitted as an

ASCII file avoiding the use of special

characters and any form of encryption.

Comments and data will also be

accepted on disks in WordPerfect 5.1

file format or ASCII file format. All

comments and data in electronic form

must be identified by the docket number

OPPTS–400106. No CBI should be

submitted through e-mail. Electronic

comments on this ANPR may be filed

online at many Federal Depository

Libraries. Additional information on

electronic submissions can be found in

Unit IV. of this document.

FOR FURTHER INFORMATION CONTACT: Matt

Gillen at 202-260-1801, e-mail:

gillen.matthew@epamail.epa.gov for

specific information regarding this

Notice. For further information on

EPCRA section 313 contact the

Emergency Planning and Community

Right-to-Know 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:

800-553-7672.

SUPPLEMENTARY INFORMATION: Electronic

Availability: An electronic copy of the

documents listed in Unit I of this

document are available from the EPA

Public Access gopher (gopher.epa.gov)

at the Environmental SubSet entry

under ‘‘Rules and Regulations.’’

I. Introduction

In 1986, Congress enacted the

Emergency Planning and Community

Right-to-Know Act (EPCRA). Section

313 of EPCRA requires certain

businesses to submit reports each year

on the amounts of toxic chemicals their

facilities release into the environment or

otherwise manage. The information is

placed in a publicly accessible data base

known as the Toxics Release Inventory

(TRI). The purpose of this requirement

is to inform the public, government

officials, and industry about the

chemical management practices of

specified toxic chemicals.

EPA is interested in expanding the

information available via TRI to include

chemical use information such as

materials accounting data. The Agency

began reviewing this issue in 1993 and

held public meetings in 1994 and 1995.

On August 8, 1995, President Clinton

directed EPA to develop and

implement, on an expedited schedule, a

process for consideration of reporting

use information under TRI. In response,

EPA has begun the regulatory

development process for additional

review of chemical use reporting, which

the Agency believes may provide a more

detailed and comprehensive picture to

the public about environmental

performance and about toxic chemicals

in their communities. EPA published

the ANPR on October 1, 1996 (61 FR

51322) (FRL–5387–6), to give notice of

EPA’s consideration of this issue and to

solicit comments on all aspects of

chemical use and the collection of

chemical use data. At the same time, the

Agency also released ‘‘Issues Paper No.

3’’ which describes previous

stakeholder comments on chemical use

reporting. EPA also held three public

meetings in October and December of

1996 to provide public forums for

interested parties to provide input on

the issues raised by the ANPR. This

issues paper and ANPR can be obtained

from the EPCRA hotline at the

telephone numbers listed in the FOR

FURTHER INFORMATION CONTACT

unit of this document, or electronically

via the EPA’s TRI Homepage at: http:/

/www.epa.gov/opptintr/tri.

The original comment period for the

ANPR was due to expire on December

30, 1996. However, on November 26,

1996, the Department of Energy

submitted a request for an extension of

the comment period to allow time to

gather and consolidate comments from

various DOE facilities, and to account

for DOE’s need to comment on another

EPA reporting initiative during the same

period. EPA has decided to grant this

request and to extend the comment

period for an additional 60 days, or

until February 28, 1997.

II. Rulemaking Record and Electronic

Filing of Comments

A record has been established for the

ANPR under docket number ‘‘OPPTS400106’’ (including comments and data

submitted electronically as described

below). A public version of this record,

including printed paper versions of

electronic comments, which does not

include any information claimed as CBI,

is available for inspection from noon to

4 p.m., Monday through Friday,

excluding legal holidays. The public

record is located in the TSCA

Nonconfidential Information Center,

Room NE-B607, 401 M St., SW.,

Washington, DC 20460.

Any person who submits comments

claimed as CBI must mark the

comments as ‘‘confidential,’’ ‘‘CBI,’’ or

other appropriate designation.

Comments not claimed as confidential

at the time of submission will be placed

in the public file. Any comments

marked as confidential will be treated in

accordance with the procedures in 40

CFR part 2. Any person submitting

comments claimed to be confidential

must prepare a nonconfidential public

version of the comments in triplicate

that EPA can place in the public file.

Electronic comments can be sent

directly to EPA at

oppt.ncic@epamail.epa.gov. Electronic

comments must be submitted as an

ASCII file avoiding the use of special

characters and any form of encryption.

The official record for this action, as

well as the public version, as described

above will be kept in paper form.

Accordingly, EPA will transfer all

comments received electronically into

printed paper form as they are received

and will place the paper copies in the

official record which will also include

all comments submitted directly in

writing. The official record is the paper

record maintained at the address in

ADDRESSES at the beginning of this

document.

List of Subjects in 40 CFR Part 372

Environmental protection,

Community right-to-know, Reporting

and recordkeeping requirements, Toxic

chemicals.

Dated: December 23, 1996.

Lynn R. Goldman,

Assistant Administrator for Prevention,

Pesticides and Toxic Substances.

[FR Doc. 97–57 Filed 1–2–97; 8:45 am]

BILLING CODE 6560–50–F

40 CFR Part 372

[OPPTS–400107; FRL–5581–1]

RIN 2070–AC00

Barium Compounds; Toxic Chemical

Release Reporting; Community Rightto-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
Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules 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.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

This action is taken under sections

313(d) and (e)(1) of the Emergency

Planning and Community Right-toKnow 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 °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. 300f300j-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
368 Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules

(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
Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules 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 bariuminduced 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 deathrates (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 contaminantfree 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
370 Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules

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
Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules 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-
372 Federal Register / Vol. 62, No. 2 / Friday, January 3, 1997 / Proposed Rules

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); KirkOthmer 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

FEDERAL COMMUNICATIONS

COMMISSION

47 CFR Part 73

[MM Docket No. 96–259; RM–8970]

Radio Broadcasting Services; Moscow,

ID

AGENCY: Federal Communications

Commission.

ACTION: Proposed rule.

SUMMARY: This document requests

comments on a petition for rule making

filed by Darin L. Siebert requesting the

allotment of Channel 277A to Moscow,

Idaho, as that community’s second local

commercial FM service. Coordinates

used for Channel 277A at Moscow are

46–42–24 and 116–55–08. As Moscow,

Idaho, is located within 320 kilometers

(199 miles) of the Canadian border, the

Commission must obtain the

concurrence of the Canadian

government to this proposal.

DATES: Comments must be filed on or

before February 18, 1997, and reply

comments on or before March 5, 1997.

ADDRESSES: Secretary, Federal

Communications Commission,

Washington, D.C. 20554. In addition to

filing comments with the FCC,

interested parties should serve the

petitioner, as follows: Darin L. Siebert,

S. 605 Grand Ave., Pullman, WA 99163.

FOR FURTHER INFORMATION CONTACT:

Nancy Joyner, Mass Media Bureau, (202)

418–2180.

SUPPLEMENTARY INFORMATION: This is a

synopsis of the Commission’s Notice of

Proposed Rule Making, MM Docket No.

96–259, adopted December 20, 1996,

and released December 27, 1996. The

full text of this Commission decision is

available for inspection and copying

during normal business hours in the

FCC’s Reference Center (Room 239),

1919 M Street, NW, Washington, DC

The complete text of this decision may

also be purchased from the

Commission’s copy contractors,

International Transcription Service,

Inc., (202) 857–3800, 2100 M Street,

NW., Suite 140,Washington, DC 20037.

Provisions of the Regulatory

Flexibility Act of l980 do not apply to

this proceeding.

Members of the public should note

that from the time a Notice of Proposed

Rule Making is issued until the matter

is no longer subject to Commission

consideration or court review, all ex

parte contacts are prohibited in

Commission proceedings, such as this

one, which involve channel allotments.

See 47 CFR 1.1204(b) for rules

governing permissible ex parte contacts.