[Federal Register Volume 60, Number 164 (Thursday, August 24, 1995)]
[Proposed Rules]
[Pages 44000-44003]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 95-21039]
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DEPARTMENT OF AGRICULTURE
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[OPPTS-400094; FRL-4954-6]
Toxic Chemical Release Reporting; Community Right-To-Know; Denial
of Petition
AGENCY: Environmental Protection Agency (EPA).
ACTION: Denial of Petition.
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SUMMARY: EPA is denying a petition to delete manganese and manganese
compounds contained in iron-making and carbon steel making slags from
the list of toxic chemicals subject to section 313 of the Emergency
Planning and Community Right-to-Know Act of 1986 (EPCRA). This action
is based on EPA's conclusion that manganese and manganese compounds in
slags do not meet the EPCRA section 313(d)(3) deletion criteria.
FOR FURTHER INFORMATION CONTACT: Maria J. Doa, Petitions Coordinator,
202-260-9592, e-mail: [email protected], for specific
information on this Denial of Petition, or for more information on
EPCRA section 313, the Emergency Planning and Community Right-to-Know
Hotline, Environmental Protection Agency, Mail Code 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 issued 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.
Section 313(d) authorizes
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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), any person may petition
EPA to add chemicals to or delete chemicals from the list. EPA must
respond to petitions within 180 days either by initiating a rulemaking
or by publishing an explanation of why the petition is denied.
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 published 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).
II. Description of Petition
The American Iron and Steel Institute (AISI) petitioned the Agency
on October 20, 1993, to qualify the listings of manganese and manganese
compounds to exempt reporting of these substances when they are
contained in slag generated from iron and carbon steel manufacturing
operations. AISI (the petitioner) claims that, due to the tightly bound
nature of the manganese-slag complex, the complex is relatively inert
and does not present an unreasonable risk to human health or the
environment. Moreover, the petitioner asserted that the manganese ion
is not available to be leached from the complex due, again, to its
tightly bound nature.
III. EPA's Technical Review of the Petition
The technical review of the petition to delete manganese and
manganese compounds contained in iron-making slags and carbon steel-
making slags included an analysis of the toxicological effects of
manganese compounds as contained in the aforementioned slags. Based on
the guidance published by EPA on petitions to delist individual members
of the metal compound categories (56 FR 23703, May 23, 1991), EPA also
reviewed the toxicity of manganese ion, as well as the availability of
the ion from the aforementioned slags, (Refs. 1, 2, 3, and 4).
A. Chemistry Profile
1. Manganese ion. Manganese is a naturally occurring substance
found in many rocks and as a constituent in several freshwaters and the
ocean. Although pure manganese is silvery, much like iron in its
appearance, manganese is rarely found in its pure state. Generally, it
exists combined with other chemicals (such as oxygen, sulfur, and
chlorine) (Ref. 5). As present in the slag, manganese is typically
found as oxides and are relatively insoluble compounds.
2. Manganese in slags. Although manganese can be added directly
into the iron and steel manufacturing process, generally the manganese
found in the slags originates from iron ore. Slags containing manganese
compounds can be generated from three processes: blast furnace; basic
oxygen furnace; and electric arc furnaces. Slags are produced as the
lighter fraction in each of the processes and are separated during the
tapping procedure. After separation, the slag is cooled with water
sprays and broken into smaller pieces. These smaller pieces are
generally loaded in a truck for transport to an on-site landfill.
The slag may be used in concrete manufacture, as roadbed fill, as
railroad ballasts, and as fertilizer components.
B. Toxicological Evaluation of Manganese Ion
It is generally recognized that manganese uptake and elimination
are under homeostatic control, allowing for a wide range of dietary
intakes considered to be safe. Further, manganese is an essential
element, being required for normal human growth and maintenance of
health (Refs. 3 and 4).
It has been reported that the average daily dose of manganese in
the United States, England, and Holland ranges from 2.3 to 8.8
milligrams per day (mg/day). The Food and Nutrition Board of the
National Research Council has determined a safe level of intake of
manganese to be 2 to 5 mg/day for adults. In the normal adult,
approximately 3 to 10 percent of dietary manganese is absorbed.
However, dietary deficiencies of calcium and iron can increase that
percentage. Therefore, it appears as if certain subpopulations, such as
children, individuals with dietary deficiencies, pregnant women, and
the elderly, may have an increased potential for heightened body
burdens of manganese (Refs. 3, 4, and 6).
Manganese has been shown to readily penetrate the bloodbrain and
placental barriers (Refs. 3 and 4). These findings are significant with
respect to the well-known effects of manganese on the central nervous
system (CNS) of adult humans and, probably, developing humans.
Manganese elimination from the body is slow, and the clearance half-
time from the brain is considerably longer than that for the whole body
(Ref. 6).
1. Acute toxicity. In 1984, the Agency generated a comprehensive
health assessment for manganese in which median lethal dose (LD50)
values for several inorganic manganese compounds were calculated. These
values range from 400 to 830 milligrams per kilogram (mg/kg) by the
oral route and 38 to 64 mg/kg by parenteral injection (Ref. 6).
2. Neurotoxicity. The CNS effects of manganese compounds have long
been known. The first medical description of chronic manganese
neurotoxicity (manganism) in workers is generally credited to Couper in
the 1830s (Ref. 6). The disorder, manganism, has been described in
workers in industries that typically involve exposure to manganese
oxide fumes. Such industries include: Ore crushing; ferroalloy
production; steel making; dry cell battery manufacture; and, welding
rod manufacture. Those who develop chronic manganese poisoning
initially exhibit a hyperactive maniacal state that progresses through
lassitude and weakness to a later stage characterized by parkinsonism,
dystonia, and cerebellar ataxia. Although the course and degree of
manganese intoxication can vary greatly among individuals, the chronic
state can develop without an initial manic state. However, once the
chronic stage has developed, the neurologic dysfunction is irreversible
(Ref. 6).
There is evidence of neurotoxic effects in adult humans and
animals. These effects are also a probable hazard to human fetal and
neonatal nervous systems (i.e., developmental neurotoxicity) based on
circumstantial human data and on test data in animals. There is also
human and animal evidence of acute toxicity (manganese pneumonia, metal
fume fever in humans, severe lung damage in animals) and human and
animal data on chronic pulmonary effects (Ref. 6).
Several studies have noted neurotoxic effects from soluble forms of
manganese. As specified in the Integrated Risk Information System
(IRIS) and other sources, neurotoxicity is the critical endpoint of
concern. There are two epidemiological studies describing toxicologic
responses in humans from excess amounts of manganese dissolved in
drinking water (Ref. 6). The first, Kondakis et al. (1989) studies
three
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areas in northwest Greece (Ref. 6). The total population of the three
areas (A, B, C) studied ranged from 3,200 to 4,350 people and manganese
concentration in well water ranged from 3.6 micrograms per litre (ug/1)
to 2300 ug/1. Individuals chosen for the study were submitted to
neurological examination; whole blood and hair manganese concentration
were also determined. The concentration of manganese in the whole blood
did not differ between the three areas, but this is not considered to
be a reliable indicator of manganese exposure. However, there was a
significant difference noted in neurological scores for area C versus
area A even when both age and sex are taken into account. A lowest
observed adverse effect level (LOAEL) of 0.06 mg Mn/kg-day and a no
observed adverse effect level (NOAEL) of 0.005 mg Mn/kg-day for the
study were estimated from concentrations using default values (a water
consumption of 2 litres/day, and a 70 Kg assumed adult body weight)
(Ref. 6).
The second report is by Kawamura et al. (1941) and is the only
epidemiological study describing toxicologic responses in humans
consuming large amounts of manganese in drinking water (Ref. 6).
Twenty-five cases of manganese poisoning were reported, with symptoms
including lethargy, increased muscle tonus, tremors and mental
disturbances. Elderly people showed the most severe symptoms. Although
the intake of manganese in the diet was not determined, the approximate
intake estimated for the study was 0.8 mg/kg-day. This supports the
LOAEL estimated from the Kondakis et al. (1989) study (Ref. 6). It
should be noted that the well water in the study was contaminated with
zinc, and that this could have effected the results. The impacts of the
zinc contamination were not evaluated.
Use of the Greek study is supported upon review in context of
additional information. The spectrum of neurological dysfunction
observed in chronic manganese neurotoxicity effects in humans can be
reproduced, in part, in different animal species, including rats,
rabbits, and monkeys (characteristic CNS signs were produced in monkeys
exposed to manganese dioxide) (Ref. 6).
Roels et al. (1992) reported that workers who had chronically been
exposed to manganese (0.215 mg manganese/m3) for respirable dust
and 0.948 mg manganese/m3 for total dust with a duration of
employment ranging from 0.2 to 17.7 years) performed worse than
controls on several measures of neurobehavioral function (such as
visual reaction time, eye-hand coordination, uncertainty, etc.) (Ref.
6). A LOAEL of 0.05 mg/m3 was derived from the study. A previous
study performed by Roels et al. (1987) found significant differences in
mean scores between manganese-exposed and referenced subjects for
visual reaction time, eye-hand coordination, hand steadiness, and
audio-verbal short-term memory (Ref. 6). Total airborne manganese dust
ranged from 0.07 to 8.61 mg/m3 for a duration of employment
spanning from 1 to 19 years. During the study it was also noted that
there were a significantly greater prevalence of coughs during the cold
season and episodes of acute bronchitis in the manganese-exposed group.
A LOAEL of 0.34 mg/m3 was derived from the study (Ref. 6).
As noted in IRIS (November 1993), there is a consistent pattern of
evidence indicating that neurotoxicity is associated with low-level
occupational manganese exposure (Ref. 6). More detail on the neurotoxic
effects observed from chronic exposure to manganese is given above.
3. Respiratory toxicity. As specified in IRIS (November 1993), as a
route of exposure, the respiratory tract is the most important route of
entry (Ref. 6). Particles which deposit in the extrathoracic and
tracheobronchial regions (greater than 2.5 micrometers (um)) are
predominantly cleared by the mucociliary escalator into the
gastrointestinal tract where absorption is low. Smaller mode particles
(greater than 2.5 um) are deposited in the pulmonary region where 100
percent absorption is assumed. However, some researchers have suggested
that neurotoxic metals can be directly transported to the brain
olfactory bulbs (Ref. 6).
After absorption by the respiratory tract, manganese is transported
directly to the brain via the blood stream, bypassing the liver. This
direct path has been suggested to account for the difference in
toxicity between inhaled and ingested manganese (Ref. 6).
4. Reproductive/developmental toxicity. There is insufficient
information on the developmental toxicity of manganese by inhalation
exposure, and the same is true for information on the female
reproductive function. The study of the female reproductive toxicity of
inhaled manganese in males also needs to be characterized more fully
(Ref. 6).
5. Carcinogenicity. Manganese has been identified as Class D or not
classifiable as to human carcinogenicity. Existing studies are
inadequate to assess the carcinogenicity of manganese (Ref. 6).
6. Ecological effects. Manganese ion exhibits a moderate toxicity
to aquatic and terrestrial organisms and has a high potential to
bioaccumulate. Manganese is an essential tract element or micronutrient
for microorganisms, plants and animals. It is a functional component of
nitrate assimilation, in the Hill reaction of photosynthesis, and is an
essential catalyst of many enzyme systems.
Acquatic chronic toxicity values are as low as 3.2 to 5.7 parts per
million (ppm) for invertebrates and as low as 12 ppm for fish.
Concentrations as low as 0.2 to 0.3 ppm were toxic to some marine
algae. Aquatic chronic toxicity data are more limited. The no observed
effect concentration (NOEC) for rainbow trout eggs exposed to manganese
for 29 days is less than 370 parts per billion (ppb). The lowest
observed effect concentration (LOEC) in this study was calculated to be
approximately 370 ppb (Ref. 7).
Marine plants and animals may bioaccumulate manganese;
bioconcentration values have been reported to be approximately 3,000.
Furthermore, bioconcentraton values for shellfish range from 1,000 to
10,000; and for fish, marine algae, and plants, from 100 to 100,000
(Ref. 7).
C. Toxicological Evaluation of Manganese in Slags
1. Human health effects. The Agency has identified some potential
hazards resulting from exposure to the manganese-slag complex.
Generally, these hazards are associated with the slag in a granular or
powdered form and are consistent with typical concerns of particulate
exposure. These include: Eye irritation; lung overload; and lung
irritation. The insolubility of the manganese-slag complex allays most
systemic toxicity concerns with the exception of lung overload. The
Agency does not consider the hazard of lung overload to be significant
(Refs. 3 and 4).
2. Ecological effects. Manganese levels in leachate from slags as
reported in the petition exceed the range of manganese reported in most
natural freshwaters. The upper leachate level reported in the petition
ranged from 28 to 32 ppm, with averages as high as 7 and 11 ppm.
Manganese concentrations in natural freshwaters around the world
normally range from 10 to 850 ppb, with an average of 35 ppb. However,
some reservoirs may have concentrations of up to 150 ppm; subsurface
and acid mine waters may contain 10 ppm (Ref. 7).
The petitioner contends that ``manganese compounds in slags do not
[[Page 44003]]
dissociate or react to yield metal ions because the metal ion is
tightly bound in a calcium-silica matrix and cannot be released.''
However, this conclusion is inconsistent with the information from
other studies presented in the petition indicating high levels of
manganese from leaching are possible.
D. Availability of Manganese ion from Slags
Although it is established that leaching of manganese from the slag
occurs, there is insufficient information regarding the ultimate fate
of the leachate for a detailed characterization. A variety of
conditions (i.e., geology, pH, soil organic content, etc.) combine in a
complex manner to severely limit modeling of the fate of the leachate.
Manganese may be leached from slags under acidic and reducing
conditions, which are the conditions expected to prevail in landfilled
slags that are in contact with the aquatic environment. Further, these
same conditions are conducive to reduction of the manganese oxides
normally found in slags to the water soluble manganous ion,
(Mn+2). Although Mn+2 often precipitates with carbonate ions
as MnCO3, this is not always the case, and various lines of
evidence suggest that Mn+2 may enter ground water supplies and/or
may reach surface waters. Evidence also shows that sorption of
manganese to soil is highly variable, and that release may actually
occur under certain conditions (Ref. 1). Thus, it cannot be concluded
that ``any manganese leached from slags is quickly adsorbed by the
surrounding soil'' as the petitioner claims.
The petitioner reports the slag to have a pH of 9 to 11 in which
the manganese is present in an insoluble oxide form. Slag piles are
generally fully exposed to weather conditions and are present in a wide
range of sizes, very small particulates to large blocks. Under acidic
conditions, such as those present in acid rain (pH 5.5), the
predominant species of manganese is not the insoluble oxide form but
the soluble ion form, manganese+2. The petitioner also reports a
range of manganese leachate measured from a variety of slag sources;
the upper level being 22 to 32 mg/1 (ppm) of manganese ion (Refs. 1 and
6).
The soluble manganese ion can then hydrolyze, form insoluble
oxides, exist as Mn+2 in solution, precipitate with carbonates and
other anions, and form insoluble sulfides depending on the redox
potential of the water media, pH, temperature, and the mix of anions
present. Most of these reactions are catalyzed by biota. Adsorption of
Mn+2 is favored in soils with a large percentage of clay particles
and organic material. Anaerobic conditions and acidified conditions
favor resolubilization of Mn+2 (Refs. 1 and 6).
E. Technical Summary
EPA's toxicological evaluation of manganese ion indicates that
manganese can cause neurotoxic effects in humans, exhibits moderate
toxicity to aquatic and terrestrial organisms, and has a high potential
to bioaccumulate. EPA's assessment of the availability of manganese ion
from iron-making and carbon steel-making slags indicates that a wide
range of manganese leachate from slag piles has been documented (noted
in the petition). This indicates that leaching of the manganese ion is
expected. Measured leachate levels, as specified in the petition,
exceed acute and chronic aquatic toxicity values and those reported as
toxic to certain plants. Evidence also shows that sorption of manganese
to soils is highly variable, and that release may actually occur under
certain conditions (Refs. 1, 6, and 7).
IV. Rationale for Denial
EPA is denying the petition to delete manganese and manganese
compounds in iron-making and carbon steel-making slag from the EPCRA
section 313 list. EPA believes that manganese ion can become available
at levels which can reasonably be anticipated to induce adverse human
health and environmental effects. EPA believes that manganese and
manganese compounds in iron-making and carbon steel-making slag meet
the toxicity criteria of EPCRA section 313(d)(2)(B) based on available
neurotoxicity data, and that they meet the toxicity criteria of EPCRA
section 313(d)(2)(C) based on the available acute environmental
toxicity and bioconcentration data.
V. References
(1) USEPA/OPPT, Boethling, Bob, Environmental Fate of Manganese
dated January 18, 1994.
(2) USEPA/OPPT, Macek, Greg, Final Report: Engineering Support for
EPA Review of Section 313(e) Petition on Manganese and Manganese
Compounds in Iron-Making and Carbon Steel-Making Slags dated January
27, 1994.
(3) USEPA/OPPT, Murphy, James J., Preliminary Review of Systemic
Toxicity for EPCRA Section 313 Delisting Petition on Manganese and its
Compounds in Slags dated November 19, 1993.
(4) USEPA/OPPT, Murphy, James J., Review of Systemic Toxicity of
Manganese with Particular Reference to Manganese-Containing Slag dated
December 29, 1993.
(5) USEPA/OPPT, Rakshpal, Ram, Section 313(e) Petition on Manganese
and Manganese Compounds in Iron-Making Slags and Carbon Steel-Making
Slags (Chemistry Report) dated December 9, 1993.
(6) USEPA/OPPT, Rusak, Linda, Technical Integrator Report dated
April 1995.
(7) USEPA/OPPT, Smerchek, Jerry C., Ecological Hazard Review of the
American Iron and Steel Institute Petition to Delist Manganese and
Manganese Compounds Contained in Iron-Making Slags and Carbon Steel-
Making Slags dated December 9, 1993.
VI. Administrative Record
The record supporting this denial of petition is contained in the
docket number OPPTS-400094. All documents, including an index of the
docket, are available in the TSCA Nonconfidential Information Center
(NCIC), also known as the TSCA Public Docket Office, from noon to 4
p.m., Monday through Friday, excluding legal holidays. The TSCA Public
Docket Office 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, Chemicals, Community right-to-know, Reporting
and reccordkeeping requirements, and Toxic chemicals.
Dated: August 15, 1995.
Lynn R. Goldman,
Assistant Administrator for Prevention, Pesticides and Toxic
Substances.
[FR Doc. 95-21039 Filed 8-23-95; 8:45 am]
BILLING CODE 6560-50-F