[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 

[[Page 44001]]
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 

[[Page 44002]]
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