[Federal Register: February 26, 2010 (Volume 75, Number 38)]
[Proposed Rules]
[Page 8889-8894]
[DOCID:fr26fe10-21]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 372

[EPA-HQ-TRI-2009-0844; FRL-9119-2]
RIN 2025-AA27

Hydrogen Sulfide; Community Right-to-Know Toxic Chemical Release
Reporting

AGENCY: Environmental Protection Agency (EPA).

ACTION: Intent to consider lifting administrative stay; opportunity for
public comment.

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SUMMARY: EPA is announcing that it is considering whether to lift the
Administrative Stay of the Emergency Planning and Community Right-to-
Know Act (EPCRA) section 313 toxic chemical release reporting
requirements for hydrogen sulfide (Chemical Abstracts Service Number
(CAS No.) 7783-06-4). Hydrogen sulfide was added to the EPCRA section
313 list of toxic chemicals in a final rule published in the Federal
Register on December 1, 1993. However, on August 22, 1994, EPA issued
an Administrative Stay of the reporting requirements for hydrogen
sulfide in order to evaluate issues brought to the Agency's attention
after promulgation of the final rule concerning the human health effect
basis for the listing and the Agency's use of exposure analysis in
EPCRA section 313 listing decisions. Although the final rule listing
hydrogen sulfide under section 313 of EPCRA remained in force, the stay
deferred the reporting requirements for hydrogen sulfide while EPA
completed this further evaluation. EPA has now completed its further
evaluation, including a consideration of additional information that
has become available since the stay was put in place regarding the
human health and environmental effects of hydrogen sulfide. Based on
this further evaluation, EPA believes that the Administrative Stay
should be lifted. By this current action, EPA is not revisiting the
original listing decision, which was accomplished by final rule on
December 1, 1993. Rather, EPA is merely presenting its rationale for
why the Administrative Stay of the reporting requirements for hydrogen
sulfide should be lifted. After consideration of comments received, the
Agency will issue another Federal Register document responding to
comments and taking appropriate action.

DATES: Comments must be received on or before April 27, 2010.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
TRI-2009-0844, by one of the following methods:
     www.regulations.gov: Follow the on-line instructions for
submitting comments.
     E-mail<EMAIL_ADDRESS>     Mail: Office of Environmental Information (OEI) Docket,
Environmental Protection Agency, Mail Code: 28221T, 1200 Pennsylvania
Ave., NW., Washington, DC 20460
     Hand Delivery: EPA Docket Center (EPA/DC), EPA West, Room
3334, 1301 Constitution Ave., NW., Washington, DC 20460. Such
deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-TRI-
2009-0844. EPA's policy is that all comments received will be included
in the public docket without change and may be made available online at
www.regulations.gov, including any personal information provided,
unless the comment includes information claimed to be Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute. Do not submit information that you consider to
be CBI or otherwise protected through www.regulations.gov or e-mail.
The www.regulations.gov Web site is an ``anonymous access'' system,
which means EPA will not know your identity or contact information
unless you provide it in the body of your comment. If you send an e-
mail comment directly to EPA without going through www.regulations.gov,
your e-mail address will be automatically captured and included as part
of the comment that is placed in the public docket and made available
on the Internet. If you submit an electronic comment, EPA recommends
that you include your name and other contact information in the body of
your comment and with any disk or CD-ROM you submit. If EPA cannot read
your comment due to technical difficulties and cannot contact you for
clarification, EPA may not be able to consider your comment. Electronic
files should avoid the use of special characters, avoid any form of
encryption, and be free of any defects or viruses.
    Docket: All documents in the docket are listed in the
www.regulations.gov index. Although listed in the index, some
information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly

available only in hard copy. Publicly available docket materials are
available either electronically in www.regulations.gov or in hard copy
at the OEI Docket, EPA/DC, EPA West, Room 3334, 1301 Constitution Ave.,
NW., Washington, DC. This Docket Facility is open from 8:30 a.m. to
4:30 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the Public Reading Room is<PHONE_NUMBER>, and the
telephone number for the OEI Docket is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Environmental
Analysis Division, Office of Information Analysis and Access (2842T),
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460; telephone number:<PHONE_NUMBER>; fax number: 202-
566-0677; e-mail<EMAIL_ADDRESS>for specific information on
this document. For general information on EPCRA section 313, contact
the Emergency Planning and Community Right-to-Know Hotline, toll free
at<PHONE_NUMBER> or<PHONE_NUMBER> in Virginia and Alaska or toll
free, TDD<PHONE_NUMBER>, http://www.epa.gov/epaoswer/hotline/.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does This Action Apply to Me?

    You may be potentially affected by this action if you manufacture,
process, or otherwise use hydrogen sulfide. Potentially affected
categories and entities may include, but are not limited to:

------------------------------------------------------------------------
           Category            Examples of potentially affected entities
------------------------------------------------------------------------
Industry.....................  Facilities included in the following
                                NAICS manufacturing codes (corresponding
                                to SIC codes 20 through 39): 311*, 312*,
                                313*, 314*, 315*, 316, 321, 322, 323*,
                                324, 325*, 326*, 327, 331, 332, 333,
                                334*, 335*, 336, 337*, 339*, 111998*,
                                211112*, 212324*, 212325*, 212393*,
                                212399*, 488390*, 511110, 511120,
                                511130, 511140*, 511191, 511199, 512220,
                                512230*, 519130*, 541712*, or 811490*.
                               *Exceptions and/or limitations exist for
                                these NAICS codes.
                               Facilities included in the following
                                NAICS codes (corresponding to SIC codes
                                other than SIC codes 20 through 39):
                                212111, 212112, 212113 (correspond to
                                SIC 12, Coal Mining (except 1241)); or
                                212221, 212222, 212231, 212234, 212299
                                (correspond to SIC 10, Metal Mining
                                (except 1011, 1081, and 1094)); or
                                221111, 221112, 221113, 221119, 221121,
                                221122, 221330 (Limited to facilities
                                that combust coal and/or oil for the
                                purpose of generating power for
                                distribution in commerce) (correspond to
                                SIC 4911, 4931, and 4939, Electric
                                Utilities); or 424690, 425110, 425120
                                (Limited to facilities previously
                                classified in SIC 5169, Chemicals and
                                Allied Products, Not Elsewhere
                                Classified); or 424710 (corresponds to
                                SIC 5171, Petroleum Bulk Terminals and
                                Plants); or 562112 (Limited to
                                facilities primarily engaged in solvent
                                recovery services on a contract or fee
                                basis (previously classified under SIC
                                7389, Business Services, NEC)); or
                                562211, 562212, 562213, 562219, 562920
                                (Limited to facilities regulated under
                                the Resource Conservation and Recovery
                                Act, subtitle C, 42 U.S.C. 6921 et seq.)
                                (correspond to SIC 4953, Refuse
                                Systems).
Federal Government...........  Federal facilities.
------------------------------------------------------------------------

    This table is not intended to be exhaustive, but rather provides a
guide for readers regarding entities likely to be affected by this
action. Some of the entities listed in the table have exemptions and/or
limitations regarding coverage, and other types of entities not listed
in the table could also be affected. To determine whether your facility
would be affected by this action, you should carefully examine the
applicability criteria in part 372 subpart B of Title 40 of the Code of
Federal Regulations. If you have questions regarding the applicability
of this action to a particular entity, consult the person listed in the
preceding FOR FURTHER INFORMATION CONTACT section.

B. How Should I Submit CBI to the Agency?

    Do not submit CBI information to EPA through www.regulations.gov or
e-mail. Clearly mark the part or all of the information that you claim
to be CBI. For CBI information in a disk or CD ROM that you mail to
EPA, mark the outside of the disk or CD ROM as CBI and then identify
electronically within the disk or CD ROM the specific information that
is claimed as CBI. In addition to one complete version of the comment
that includes information claimed as CBI, a copy of the comment that
does not contain the information claimed as CBI must be submitted for
inclusion in the public docket. Information so marked will not be
disclosed except in accordance with procedures set forth in 40 CFR part
2.

II. Introduction

    Section 313 of EPCRA, 42 U.S.C. 11023, requires certain facilities
that manufacture, process, or otherwise use listed toxic chemicals in
amounts above reporting threshold levels to report their environmental
releases and other waste management quantities of such chemicals
annually. These facilities must also report pollution prevention and
recycling data for such chemicals, pursuant to section 6607 of the
Pollution Prevention Act (PPA), 42 U.S.C. 13106. EPCRA section 313
established an initial list of toxic chemicals composed of more than
300 chemicals and 20 chemical categories.
    EPCRA section 313(d) authorizes EPA to add or delete chemicals from
the list and sets forth criteria for these actions. Specifically, EPCRA
section 313(d)(2) states that EPA may add a chemical to the list if
``there is sufficient evidence to establish any one'' of the listing
criteria. Therefore, to add a chemical, EPA must demonstrate that at
least one criterion is met, but need not determine whether any other
criterion is met. Conversely, EPCRA section 313(d)(3) states that to
remove a chemical from the list, EPA must determine that ``there is not
sufficient evidence to establish any'' of the Section 313(d)(2)
criteria. Therefore, to remove a chemical, EPA must demonstrate that
none of the criteria are met. The EPCRA section 313(d)(2) criteria are:

    (A) The chemical is known to cause or can reasonably be
anticipated to cause significant adverse acute human health effects
at concentration levels that are reasonably likely to exist beyond
facility site boundaries as a result of continuous, or frequently
recurring, releases.
    (B) The chemical is known to cause or can reasonably be
anticipated to cause in humans--
    (i) Cancer or teratogenic effects, or
    (ii) Serious or irreversible--
    (I) Reproductive dysfunctions,
    (II) Neurological disorders,
    (III) Heritable genetic mutations, or
    (IV) Other chronic health effects.
    (C) The chemical is known to cause or can be reasonably
anticipated to cause, because of
    (i) Its toxicity,
    (ii) Its toxicity and persistence in the environment, or
    (iii) Its toxicity and tendency to bioaccumulate in the
environment, a significant adverse effect on the environment of
sufficient seriousness, in the judgment of

the Administrator, to warrant reporting under this section.

EPA often refers to the section 313(d)(2)(A) criterion as the ``acute
human health effects criterion;'' the section 313(d)(2)(B) criterion as
the ``chronic human health effects criterion;'' and the section
313(d)(2)(C) criterion as the ``environmental effects criterion.''
    Under EPCRA section 313(e)(1), any person may petition EPA to add
chemicals to or delete chemicals from the list. 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 under EPCRA section 313(e). EPA
also issued guidance in the Federal Register of May 23, 1991 (56 FR
23703) regarding the recommended content of petitions to delete
individual members of the section 313 metal compound categories. In
addition, EPA published in the Federal Register of November 30, 1994
(59 FR 61432) a statement clarifying its interpretation of the section
313(d)(2) and (d)(3) criteria for modifying the section 313 list of
toxic chemicals.

III. Background Information

A. What is the History of the Listing of Hydrogen Sulfide Under EPCRA
Section 313?

    In response to a petition from the Natural Resources Defense
Council and the Governor of New York, hydrogen sulfide, along with 20
other chemicals and two chemical categories, was added to the EPCRA
section 313 list of toxic chemicals as part of a 1993 final rule
(December 1, 1993, 58 FR 63500). Hydrogen sulfide was listed under the
criteria of EPCRA section 313(d)(2)(B) (chronic human health effects)
based on chronic neurotoxic effects in humans and under EPCRA section
313(d)(2)(C) (environmental effects) based on acute aquatic toxicity.
However, on August 22, 1994 (59 FR 43048), EPA issued an Administrative
Stay of the EPCRA section 313 reporting requirements for hydrogen
sulfide. Although the final rule listing hydrogen sulfide under section
313 of EPCRA remained in force, the stay deferred the reporting
requirements for hydrogen sulfide.

B. What Was the Basis for the Administrative Stay?

    After the final rule was issued adding hydrogen sulfide to the
EPCRA section 313 list of toxic chemicals, some members of the
regulated community expressed a concern that the ``chronic human health
effects'' basis for listing hydrogen sulfide under EPCRA section
313(d)(2)(B) changed between the proposed rule (September 8, 1992, 57
FR 41020) and the final rule (December 1, 1993, 58 FR 63500), and that
commenters on the proposed rule therefore did not have an opportunity
to comment on that individual basis for the listing. Specifically,
although the Agency cited the same acute aquatic toxicity as an
``environmental effects'' basis for the listing under EPCRA section
313(d)(2)(C) in both the proposed and final rules, the Agency also
cited chronic respiratory effects as a ``chronic human health effects''
basis under EPCRA section 313(d)(2)(B) in the proposed rule, but
chronic neurotoxic effects as a ``chronic human health effects'' basis
under that same provision in the final rule. In addition, after
issuance of the final rule, some members of the regulated community
expressed concern that EPA's decision not to include an exposure
analysis in deciding to list hydrogen sulfide on the basis of chronic
human health effects was inconsistent with past Agency practice.
    Although EPA did not agree that it had been inconsistent in its use
of exposure analyses, and notwithstanding the fact that the listing
decision was dictated by the acute aquatic toxicity finding alone under
EPCRA section 313(d)(2)(C), the Agency issued an Administrative Stay of
the reporting requirements for hydrogen sulfide in order to review the
concerns raised after issuance of the final rule by some members of the
regulated community.

C. What Is the Purpose of This Document?

    The purpose of this document is to provide the public with the
opportunity to comment on EPA's review of the currently available data
on the human health and environmental effects of hydrogen sulfide--
specifically, chronic respiratory effects, chronic neurotoxic effects,
and acute, chronic and early-life stage aquatic toxicity--and EPA's
belief that the Administrative Stay should be lifted based on that
data. EPA's analysis of the toxicity of hydrogen sulfide is based on
the Agency's latest Toxicological Review of Hydrogen Sulfide (Ref. 1),
as well as a reassessment of the environmental effects of hydrogen
sulfide (Ref. 2). These assessments are discussed in detail in Unit IV.
of this document. In addition, this document addresses the concerns
raised regarding use of exposure analyses. After consideration of
comments received, the Agency will issue another Federal Register
document responding to comments and taking appropriate action.

IV. What Is EPA's Technical Review of Hydrogen Sulfide?

A. What Is EPA's Evaluation of the Human Health Toxicity of Hydrogen
Sulfide?

    The following assessment of the human health toxicity of hydrogen
sulfide is based on the information contained in EPA's most recent
(June 2003) Integrated Risk Information System (IRIS) Toxicological
Review of Hydrogen Sulfide (Ref. 1).
    Hydrogen sulfide is a colorless, acutely toxic gas at high
concentrations. Hydrogen sulfide gas is absorbed rapidly through the
lungs and can be absorbed through the gastrointestinal tract. Oral
exposure is not likely to occur. In animals and humans, it distributes
to the blood, brain, lungs, heart, liver, spleen, and kidneys.
Oxidation is the primary metabolic pathway for hydrogen sulfide, with
thiosulfate and sulfate as metabolites. Metabolism in laboratory
animals and in humans appears to be similar. Hydrogen sulfide
metabolites are excreted in the urine.
    A considerable body of case studies exists on the human health
impacts resulting from acute exposure to high levels of hydrogen
sulfide. Levels in the range of 500 to 1,000 parts per million (ppm)
(695 to 1,390 milligrams per cubic meter (mg/m\3\)) are life-
threatening and can cause immediate unconsciousness followed by serious
and debilitating neurologic and respiratory sequelae and death (Ref.
1). While complete recovery from a high exposure episode has been
reported, more often long term or even irreversible harmful
neurological effects remain. Several groups of investigators (Tvedt, et
al. (Refs. 3 and 4); Wasch, et al. (Ref. 5)) have reported long-term
persistent adverse neurological effects from hydrogen sulfide-induced
unconsciousness in humans during occupational, accidental, and chronic
exposures, including neuropsychological and neurobehavorial decrements
and brain damage. These irreversible effects are believed to be caused
by an essentially hypoxic (low oxygen) condition existing in persons
who become unconscious from a high exposure to hydrogen sulfide.
Because a loss of oxygen (anoxia) utilization in tissues, particularly
the brain, occurs in such poisonings, it is possible to attribute
persistent neuronal damage to this effect. Permanent (chronic) damage
is commonly observed clinically when

brain tissues have been deprived of oxygen due to inadequate delivery
of the gas or to interrupted utilization of oxygen by cells, as is the
case with hydrogen sulfide poisoning.
    The observed nonirritant effects produced in mammals from exposure
to hydrogen sulfide gas may primarily be attributed to the cellular
anoxia produced by inhibition of cytochrome oxidase (Ref. 1).
Inhibition of cytochrome oxidase reduces the oxygen dependent
metabolism of the cell, reduces cell energy sources (e.g., adenosine
triphosphate (ATP)), increases products of anaerobic metabolism such as
lactic acid, and produces cell death. Hence, cells with a high oxygen
demand such as those in brain and cardiac tissue are thought to be more
sensitive to disruption of oxidative metabolism and may be considered
selected targets for the toxicity of hydrogen sulfide.
    1. Chronic Toxicity. EPA has reviewed the available toxicological
studies on hydrogen sulfide in its most recent IRIS Toxicological
Review of Hydrogen Sulfide (Ref. 1) and concluded that hydrogen sulfide
can cause chronic human health toxicity. As reported in IRIS, the upper
respiratory tract (neuronal and basal cells of the olfactory nasal
epithelium) and neurologic tissues are both targets for hydrogen
sulfide toxicity. The weight-of-evidence from the animal studies
indicates that nasal tract lesions and neurological effects of hydrogen
sulfide are dose-dependent, and both effects are clearly of relevance
to humans. The levels of hydrogen sulfide associated with these effects
appear to be similar for either endpoint (e.g., the no-effect level of
nasal tract lesions reported by Brenneman, et al. (Ref. 6) at 10 ppm
(14 mg/m\3\) and the likely indicator of neurotoxic effects reported by
Hannah and Roth (Ref. 7) at 20 ppm (28 mg/m\3\)), which is some
indication that consideration for one effect will also address the
other (Ref. 1).
    a. Upper Respiratory Tract Toxicity. Several subchronic exposure
studies in rats and mice indicate that low concentrations of hydrogen
sulfide cause nasal lesions of the olfactory mucosa (Brenneman, et al.
(Ref. 6); Dorman, et al. (Ref. 8); Chemical Industry Institute of
Toxicology (Ref. 9); Lopez, et al. (Ref. 10); Dorman, et al. (Ref.
11)). The nasal lesions are consistent with the neurotoxic and irritant
properties of this gas. Based on the demonstrable histopathology,
information available on exposure-dose-response, and the commonality of
the underlying mechanism (cytochrome oxidase inhibition and irritation)
between animals and humans, there is compelling indication that such
effects are reasonably anticipated to occur in humans chronically
exposed to hydrogen sulfide (Hirsch and Zavala (Ref. 12)).
    Brenneman, et al. (Ref. 6) reported significant concentration-
related increases in the incidence and severity of lesions to the nasal
olfactory epithelium in rats exposed to 0, 10, 30, or 80 ppm of
hydrogen sulfide for 10 weeks. The effects consisted of olfactory
neuron loss and basal cell hyperplasia in rats exposed to 30 or 80 ppm,
6 hours/day, 7 days/week for 10 weeks; no adverse effects were observed
at 10 ppm. The severity of the olfactory neuron loss was concentration-
related; however, an inverse relationship between severity and
concentration was observed for the basal cell hyperplasia suggesting
that as the concentration increased, the ability of the olfactory
epithelium to regenerate decreased. In contrast, earlier studies
conducted by the Chemical Industry Institute of Toxicology (CIIT)
(Refs. 13 and 14) where rats and mice were exposed to 0, 10.1, 30.5, or
80 ppm of hydrogen sulfide, 6 hours/day, 5 days/week for 13 weeks, did
not find significant alterations in the nasal turbinates of Fischer-344
(F-344) or Sprague-Dawley rats exposed to 80 ppm or less of hydrogen
sulfide. Inflammation of the squamous portion of the nasal mucosa was
observed in mice exposed to 80 ppm hydrogen sulfide, 6 hours/day, 5
days/week for 13 weeks (CIIT (Ref. 9)); the no-observed-adverse-effect-
level (NOAEL) for this effect is 30.5 ppm. However, a re-examination of
the histological specimens from this study revealed a statistically
significant increase in the incidence of olfactory neuron loss in
Sprague-Dawley rats, F-344 rats, and B6C3F1 mice exposed to 30 or 80
ppm; no lesions were observed at 10 ppm (Dorman, et al. (Ref. 11)). In
addition, increases in the incidence of bronchiolar epithelial
hyperplasia and hypertrophy were observed in female Sprague-Dawley rats
exposed to 30 or 80 ppm and male Sprague-Dawley and F-344 rats exposed
to 80 ppm.
    b. Neurotoxicity. The neurotoxic effects of low level hydrogen
sulfide exposure have been primarily assessed from neurodevelopmental
toxicity studies. Male Sprague-Dawley rats and male B6C3F1 mice exposed
to 80 ppm of hydrogen sulfide (6 hours/day, 5 days/week for 13 weeks)
had a statistically significant decrease in absolute (but not relative)
brain weight (CIIT (Ref. 13) and Dorman, et al. (Ref. 11)) at 80 ppm
but not 30 ppm. In an earlier study, Skrajny, et al. (Ref. 15) examined
the effect of hydrogen sulfide exposure on serotonin and norepinephrine
levels in the developing cerebellum and frontal cortex of Sprague-
Dawley rats. Timed-pregnant rats were exposed to 0, 20 or 75 ppm for 7
hours/day from gestational day 5 until post natal day (PND) 21. There
were statistically significant increases in serotonin levels in the
frontal cortex on PND 21 in pups exposed to 20 ppm hydrogen sulfide and
increases in serotonin levels in the cerebellum and frontal cortex on
postpartum days 14 and 21 in pups exposed to 75 ppm hydrogen sulfide.
Norepinephrine levels were increased at 75 ppm in the cerebellum on
PNDs 7, 14, and 21, and in the frontal cortex on PND 21. At 20 ppm
frontal cortex norepinephrine levels were decreased compared to
controls on days 14 and 21.
    In a similarly designed study using the same exposure protocol as
the CIIT (Refs. 9, 13, and 14) and Dorman, et al. (Ref. 11) studies,
Hannah and Roth (Ref. 7) evaluated the perinatal effect of hydrogen
sulfide on developing cerebellar Purkinje cells. Sprague-Dawley dams
were exposed to 0, 20 or 50 ppm hydrogen sulfide for 7 hr/day from
gestational day 5 until PND 21. Exposure to both 20 and 50 ppm
interrupted normal dendritic growth of Purkinje cells in the brain of
offspring. In later studies using this same experimental protocol,
Hannah, et al. (Refs. 16 and 17) also found decreases in several brain
amino acid levels in Sprague-Dawley rats exposed to 75 ppm of hydrogen
sulfide.
    The significance of the morphological changes and alteration of
brain neurotransmitters in these studies and the Skrajny, et al. (Ref.
15) study to humans is unclear. Since Purkinje cell alterations and
changes in neurotransmitter levels may constitute a hydrogen sulfide-
induced change in the growth or organization of structural (or
neurochemical) elements, they are to be regarded as indicators of a
neurotoxic effect in accordance with guidance in EPA's neurotoxicity
risk assessment guidelines (Ref. 18). The question as to what
functional impairment these alterations might lead to in humans remains
unclear. Predicting particular functional impairments from decreased
brain weight and specific structural alterations such as reported by
the CIIT (Refs. 9, 13, and 14) and Dorman, et al. (Ref. 11) studies and
Hannah and Roth (Ref. 7) is difficult due to the selective nature of
the observed alterations and the dynamic self-organizing response of
the developing brain to injury. Although behavioral testing has not
indicated that alterations of brain neurotransmittters

have a functional impact (Dorman, et al. (Ref. 8)), further examination
of the biochemical and functional aspects of the developing brain in
hydrogen sulfide-exposed animals is warranted and neurotoxic effects
cannot be discounted.
    Available information indicates that the dose-response character of
indicators of neurotoxicity (such as the alterations to cerebellar
Purkinje cells reported by Hannah and Roth (Ref. 7) and nasal olfactory
(neuronal cell) lesions reported by Brenneman, et al. (Ref. 6)) may be
similar to one another, such that consideration of one may be inclusive
of the other. However, more extensive and definitive information on the
neurologic endpoints could reveal that these should be the most
relevant endpoints, more so than nasal tract lesions. The IRIS Summary
for Hydrogen Sulfide (Ref. 1) indicates that such information may
provide sufficient reason to reassess hydrogen sulfide.
    2. Summary. As stated in the IRIS Summary for Hydrogen Sulfide
(Ref. 1) and as discussed above, both nasal tract lesions (upper
respiratory effects) and neurologic effects are chronic effects of
concern. These effects occur in a clear dose concentration manner with
the lowest levels of hydrogen sulfide exposure associated with these
effects ranging from 20 to 30 ppm (28 mg/m\3\ to 41.7 mg/m\3\).

B. What Is EPA's Evaluation of the Environmental Toxicity of Hydrogen
Sulfide?

    A number of ecotoxicity studies have been conducted on hydrogen
sulfide, mainly on freshwater invertebrates and fish. Acute, chronic,
and early-life stage toxicity values for hydrogen sulfide include
numerous values that are well below 1 milligram per liter (mg/L),
indicating that hydrogen sulfide is toxic at very low concentrations.
EPA's ecological assessment (Ref. 2) includes an extensive listing of
the aquatic toxicity values for hydrogen sulfide. Some examples of the
values from Table 2-1 of EPA's ecological assessment (Ref. 2) are
provided below.
    Hydrogen sulfide acute toxicity values (96-hour LC50
(i.e., the concentration that is lethal to 50% of test organisms)) for
freshwater fish ranged from 0.0149 mg/L (fathead minnow) to 0.0448 mg/L
(bluegill). Chronic toxicity values for freshwater fish ranged from a
6-week lowest-observed-effect-concentration (LOEC) (growth rate) of
0.0005 mg/L in a tropical fish (Mystus nemurus) to a 430-day LOEC
(final weight) of 0.009 mg/L for goldfish. Additionally, in early-life
stage toxicity testing with eggs, fry, and juveniles of various
freshwater fish species, endpoint values ranged from a 96-hour
LC50 of <0.002 mg/L (yellow perch sac fry) to a 96-hour
LC50 value of 0.0536 mg/L (fathead minnow). The hydrogen
sulfide 96-hour LC50 values for freshwater invertebrates
ranged from 0.021 mg/L (amphipod) to 1.07 mg/L (isopod), and 48- to 96-
hour LC50 values for estuarine/marine invertebrates ranged
from 0.063 mg/L (saltwater shrimp) to 0.332 mg/L (adult amphipod). The
hydrogen sulfide EC50 (i.e., the concentration that is
effective in producing a sublethal response in 50% of test organisms)
values for estuarine/marine invertebrates included 0.01 mg/L (saltwater
mussel) and 0.019 mg/L (sea urchin). Hydrogen sulfide chronic values
for freshwater invertebrates ranged from a 65-day LOEC (reproduction)
of 0.0031 mg/L to a 10-day LC50 value of 0.042 mg/L, both
for the amphipod Gammarus pseudolimnaeus. For early-life stage toxicity
testing, a 96-hour LC50 value of 0.034 mg/L was available
for juvenile crayfish (freshwater species), and for estuarine/marine
invertebrates, 48-hour LC50 values of 0.0087 mg/L and 0.0185
mg/L were available for white shrimp larvae and juveniles,
respectively.

V. EPA's Use of Exposure Analyses

    The Agency's position on the use of exposure analyses in listing
decisions under EPCRA section 313 was presented in a proposed rule in
the Federal Register of January 12, 1994 (59 FR 1788). The proposed
rule provided the public with the opportunity to comment on the
Agency's interpretation of the statutory listing criteria as it relates
to the use of exposure considerations. After considering the comments
received, EPA published in the Federal Register of November 30, 1994
(59 FR 61432) a statement clarifying its interpretation of the
statutory requirements regarding how exposure will be considered in
listing decisions. Subsequent to the final rule, EPA's interpretation
of the statutory listing criteria as it relates to the consideration of
exposure was upheld in National Oilseed Processors Ass'n. v. Browner,
924 F. Supp. 1193 (D.D.C. 1996), aff'd in part & remanded in part, Troy
Corp. v. Browner, 120 F.3d 277 (D.C. Cir. 1997).
    EPA has determined that hydrogen sulfide can reasonably be
anticipated to cause serious or irreversible chronic human health
effects at relatively low doses and thus is considered to have
moderately high to high chronic toxicity. EPA does not believe that it
is appropriate to consider exposure for chemicals that are moderately
high to highly toxic based on a hazard assessment when determining if a
chemical can be listed for chronic effects pursuant to EPCRA section
313(d)(2)(B) (see 59 FR 61432, 61433, 61440-61442). Hydrogen sulfide
has also been determined to cause ecotoxicity at relatively low
concentrations, and thus is considered to have high ecotoxicity. EPA
believes that chemicals that induce death or serious adverse effects in
aquatic organisms at relatively low concentrations (i.e., they have
high ecotoxicity) have the potential to cause significant changes in
the population of fish and other aquatic organisms, and can therefore
reasonably be anticipated to cause a significant adverse effect on the
environment of sufficient seriousness to warrant reporting. EPA does
not believe that it is required to consider exposure for chemicals that
have high ecotoxicity based on a hazard assessment when determining if
a chemical can be listed for effects pursuant to EPCRA section
313(d)(2)(C) (see 59 FR 61432, 61433, 61440-61442).

VI. What Is EPA's Rationale That the Administrative Stay Should Be
Lifted?

    EPA's technical evaluation of hydrogen sulfide shows that it can
reasonably be anticipated to cause chronic health effects in humans.
The chronic health effects have been observed in laboratory animals at
concentrations as low as 28 mg/m\3\ (20 ppm) and 41.7 mg/m\3\ (30 ppm).
In addition, EPA's technical evaluation of hydrogen sulfide also shows
that it can reasonably be anticipated to cause, because of its
toxicity, significant adverse effects in aquatic organisms. Examples of
hydrogen sulfide's ecological toxicity include acute toxicity (96-hour
LC50) values for freshwater fish that ranged from 0.0149 mg/
L (fathead minnow) to 0.0448 mg/L (bluegill), indicating high aquatic
toxicity. Examples of hydrogen sulfide's chronic ecological toxicity
include freshwater fish values that ranged from a 6-week LOEC (growth
rate) of 0.0005 mg/L in a tropical fish (Mystus nemurus) to a 430-day
LOEC (final weight) of 0.009 mg/L for goldfish, also indicating high
aquatic toxicity.
    Based on the above findings, EPA believes that there is no basis
for continuing the Administrative Stay of the reporting requirements
for hydrogen sulfide, and that the Administrative Stay should therefore
be lifted. As an aside, EPA notes also that it believes that the above
findings clearly demonstrate the correctness of the Agency's final
decision in December 1993 to list hydrogen sulfide on the EPCRA section
313 toxic chemicals list

based on the listing criteria in EPCRA sections 313(d)(2)(B) and (C).
    Finally, in accordance with EPA's stated policy on the use of
exposure assessments (59 FR 61432), EPA does not believe that an
exposure assessment is appropriate for determining whether hydrogen
sulfide meets the criteria of EPCRA section 313(d)(2)(B) or (C), and
therefore the Administrative Stay should not be continued for lack of
an exposure analysis.

VII. What Are the References Cited in This Document?

    EPA has established an official public docket for this action under
Docket ID No. EPA-HQ-TRI-2009-0844. The public docket includes
information considered by EPA in developing this action, including the
documents listed below, which are electronically or physically located
in the docket. In addition, interested parties should consult documents
that are referenced in the documents that EPA has placed in the docket,
regardless of whether these referenced documents are electronically or
physically located in the docket. For assistance in locating documents
that are referenced in documents that EPA has placed in the docket, but
that are not electronically or physically located in the docket, please
consult the person listed in the above FOR FURTHER INFORMATION CONTACT
section.

    1. U.S. Environmental Protection Agency. ``Toxicological Review
of Hydrogen sulfide, (CAS No. 7783-06-4), In Support of Summary
Information on the Integrated Risk Information System.'' Washington,
DC: Integrated Risk Information System. U.S. Environmental
Protection Agency. June, 2003. http://www.epa.gov/ncea/iris/
toxreviews/0061-tr.pdf Integrated Risk Information Summary for
Hydrogen Sulfide available at: http://www.epa.gov/ncea/iris/subst/
0061.htm.
    2. U.S. Environmental Protection Agency, Technical Review of
Hydrogen Sulfide: Chemistry, Environmental Fate and Ecological
Toxicity, CAS Registry Number 7783-06-4; Office of Environmental
Information, Office of Information Access and Analysis,
Environmental Analysis Division, Analytical Support Branch; June 22,
2009.
    3. Tvedt, B., Edland, A., Skyberg, K. et al., ``Delayed
neuropsychiatric sequelae after acute hydrogen sulfide poisoning:
affection of motor function, memory, vision and hearing.'' Acta.
Neurol. Scand. v. 84, (1991), pp. 348-351.
    4. Tvedt, B., Skyberg, K., Aaserud, O., et al., ``Brain damage
caused by hydrogen sulfide: a follow-up study of six patients.'' Am.
J. Ind. Med. v. 20, (1991), pp. 91-101.
    5. Wasch, H.H., Estrin, W.J., Yip, P. et al., ``Prolongation of
the P-300 latency associated with hydrogen sulfide exposure.'' Arch.
Neurol. v. 46, (1989), pp. 902-904.
    6. Brenneman, K.A., James, R.A., Gross, E.A., Dorman, D.C.,
``Olfactory neuron loss in adult male CD rats following subchronic
inhalation exposure to hydrogen sulfide.'' Toxicol. Pathol. v.
28(2), (2000), pp. 326-333.
    7. Hannah, R.S., Roth, S.H., ``Chronic exposure to low
concentrations of hydrogen sulfide produces abnormal growth in
developing Purkinje cells.'' Neurosci. Lett. v. 122, (1991), pp.
225-228.
    8. Dorman, D.C., Brenneman, K.A., Struve, M.F., et al., (2000)
``Fertility and developmental neurotoxicity effects of inhaled
hydrogen sulfide in Sprague-Dawley rats.'' Neurotoxicol Teratol. v.
22, (2000), pp. 71-84.
    9. Chemical Industry Institute of Toxicology, ``90-Day vapor
inhalation toxicity study of hydrogen sulfide in B6C3F1 mice.''
(1983), EPA/OTS 0883-0255.
    10. Lopez, A., Prior, M., Yong, S., et al., ``Nasal lesions in
rats exposed to hydrogen sulfide for four hours.'' Am. J. Vet. Res.
v. 49(7), (1988), pp. 1107-1111.
    11. Dorman, D.C., Struve, M.F., Gross, E.A., et al.,
``Respiratory tract toxicity of inhaled hydrogen sulfide in Fischer-
344 rats, Sprague-Dawley rats, and B6C3F1 mice following subchronic
(90-day) exposure.'' Toxicol Appl Pharmacol v. 198, (2004), pp. 29-
39.
    12. Hirsch, A.R., Zavala, G., ``Long-term effect on the
olfactory system of exposure to hydrogen sulphide.'' Occup. Environ.
Med. v. 56, (1999), pp. 284-287.
    13. Chemical Industry Institute of Toxicology, ``90-Day vapor
inhalation toxicity study of hydrogen sulfide in Fischer-344 rats.''
(1983), EPA/OTS 0883-0255.
    14. Chemical Industry Institute of Toxicology, ``90-Day vapor
inhalation toxicity study of hydrogen sulfide in Sprague-Dawley
rats.'' (1983), EPA/OTS 0883-0255.
    15. Skrajny, B., Hannah, R.S., Roth, S.H., ``Low concentrations
of hydrogen sulphide alter monoamine levels in the developing rat
central nervous system.'' Can. J. Physiol. Pharmacol. v. 70(11),
(1992), pp. 1515-1518.
    16. Hannah, R.S., Hayden, L.J., Roth, S.H., ``Hydrogen sulfide
exposure alters the amino acid content in developing rat CNS.''
Neurosci. Lett. v. 99, (1989), pp. 323-327.
    17. Hannah, R.S., Bennington, R., Roth, S.H., ``A relationship
between hydrogen sulfide exposure and taurine levels in maternal
rats.'' Proc West Pharmacol Soc v. 33, (1990), pp. 177-179.
    18. U.S. Environmental Protection Agency, ``Guidelines for
neurotoxicity risk assessment.'' Federal Register, May 14, 1998,
63(93):26926-26954. http://cfpub.epa.gov/ncea/cfm/
recordisplay.cfm?deid=12479

List of Subjects in 40 CFR Part 372

    Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, and Toxic chemicals.

    Dated: February 19, 2010.
Lisa P. Jackson,
Administrator.
[FR Doc. 2010-4084 Filed 2-25-10; 8:45 am]
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[Federal Register Volume 82, Number 244 (Thursday, December 21, 2017)]
[Rules and Regulations]
[Page 60545]
[FR Doc No: 2017-27426]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R05-OAR-2017-0323; FRL-9972-33-Region 5]

Air Plan Approval; Illinois; Volatile Organic Compounds
Definition; Withdrawal of Direct Final Rule

AGENCY: Environmental Protection Agency (EPA).

ACTION: Withdrawal of direct final rule.

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SUMMARY: Due to the receipt of an adverse comment, the Environmental
Protection Agency (EPA) is withdrawing the November 2, 2017, direct
final rule approving changes to the Illinois Administrative Code
definition of volatile organic material, otherwise known as volatile
organic compound (VOC). The revision would remove recordkeeping and
reporting requirements related to the use of t-butyl acetate as a VOC,
and is in response to an EPA rulemaking that occurred in 2016.

DATES: The direct final rule published at 82 FR 50811 on November 2,
2017, is withdrawn effective December 21, 2017.

FOR FURTHER INFORMATION CONTACT: Charles Hatten, Environmental
Engineer, Control Strategy Section, Air Programs Branch (AR-18J),
Environmental Protection Agency, Region 5, 77 West Jackson Boulevard,
Chicago, Illinois 60604,<PHONE_NUMBER>, [email protected].

SUPPLEMENTARY INFORMATION: In the direct final rule, EPA stated that if
adverse comments were submitted by December 4, 2017, the rule would be
withdrawn and not take effect. EPA received an adverse comment prior to
the close of the comment period and, therefore, is withdrawing the
direct final rule. EPA will address the comment in a subsequent final
action based upon the proposed action also published on November 2,
2017 (82 FR 50853). EPA will not institute a second comment period on
this action.

List of Subjects in 40 CFR Part 52

    Environmental protection, Air pollution control, Incorporation by
reference, Intergovernmental relations, Ozone, Reporting and
recordkeeping requirements, Volatile organic compounds.

    Authority: 42 U.S.C. 7401 et seq.

    Dated: December 11, 2017.
Robert A. Kaplan,
Acting Regional Administrator, Region 5.

PART 52--APPROVAL AND PROMULGATION OF IMPLEMENTATION PLANS

0
Accordingly, the amendment to 40 CFR 52.720 published in the Federal
Register on November 2, 2017 (82 FR 50811) is withdrawn effective
December 21, 2017.

[FR Doc. 2017-27426 Filed 12-20-17; 8:45 am]
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[Federal Register Volume 79, Number 103 (Thursday, May 29, 2014)]
[Notices]
[Pages 30840-30841]
[FR Doc No: 2014-12364]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. CP14-486-000]

East Cheyenne Gas Storage, LLC; Notice of Application for
Amendment, Reaffirmation of Market-Based Rate Authority, and Request To
Vacate, in Part, Prior Authorizations

    Take notice that on May 12, 2014, East Cheyenne Gas Storage, LLC
(East Cheyenne), 10370 Richmond Avenue, Suite 510, Houston, Texas
77042, filed with the Federal Energy Regulatory Commission an
application under Section 7(c) of the Natural Gas Act (NGA) to amend in
part the certificate of public convenience and necessity issued by the
Commission in Docket No. CP10-34-000 (as amended in Docket Nos. CP11-
40-000, CP12-35-000, and CP12-124-000); to increase the certificated
working gas capacity of the West Peetz field; and to construct and
install six injection/withdrawal wells in the West Peetz field. The
Application also requests the Commission issue an order reaffirming its
market-based rate authorization, and vacating in part East

Cheyenne's certificate authorization related to construction of the
Lewis Creek field, all as more fully set forth in the application which
is on file with the Commission and open for public inspection.
    This filing is accessible on-line at http://www.ferc.gov, using the
``eLibrary'' link and is available for review in the Commission's
Public Reference Room in Washington, DC. There is an ``eSubscription''
link on the Web site that enables subscribers to receive email
notification when a document is added to a subscribed docket(s). For
assistance with any FERC Online service, please email
<EMAIL_ADDRESS>or call<PHONE_NUMBER> (toll free). For
TTY, call<PHONE_NUMBER>.
    Any questions concerning this application may be directed to: James
Hoff, Vice President, Reservoir Engineering, East Cheyenne Gas Storage,
LLC, 10370 Richmond Avenue, Suite 510, Houston, Texas 77042; Telephone:
(713) 403-6467; FAX:<PHONE_NUMBER>.
    Pursuant to section 157.9 of the Commission's rules, 18 CFR 157.9,
within 90 days of this Notice the Commission staff will either:
Complete its environmental assessment (EA) and place it into the
Commission's public record (eLibrary) for this proceeding; or issue a
Notice of Schedule for Environmental Review. If a Notice of Schedule
for Environmental Review is issued, it will indicate, among other
milestones, the anticipated date for the Commission staff's issuance of
the final environmental impact statement (FEIS) or EA for this
proposal. The filing of the EA in the Commission's public record for
this proceeding or the issuance of a Notice of Schedule for
Environmental Review will serve to notify federal and state agencies of
the timing for the completion of all necessary reviews, and the
subsequent need to complete all federal authorizations within 90 days
of the date of issuance of the Commission staff's FEIS or EA.
    There are two ways to become involved in the Commission's review of
this project. First, any person wishing to obtain legal status by
becoming a party to the proceedings for this project should, on or
before the comment date stated below, file with the Federal Energy
Regulatory Commission, 888 First Street NE., Washington, DC 20426, a
motion to intervene in accordance with the requirements of the
Commission's Rules of Practice and Procedure (18 CFR 385.214 or
385.211) and the Regulations under the NGA (18 CFR 157.10). A person
obtaining party status will be placed on the service list maintained by
the Secretary of the Commission and will receive copies of all
documents filed by the applicant and by all other parties. A party must
submit 7 copies of filings made in the proceeding with the Commission
and must mail a copy to the applicant and to every other party. Only
parties to the proceeding can ask for court review of Commission orders
in the proceeding.
    However, a person does not have to intervene in order to have
comments considered. The second way to participate is by filing with
the Secretary of the Commission, as soon as possible, an original and
two copies of comments in support of or in opposition to this project.
The Commission will consider these comments in determining the
appropriate action to be taken, but the filing of a comment alone will
not serve to make the filer a party to the proceeding. The Commission's
rules require that persons filing comments in opposition to the project
provide copies of their protests only to the party or parties directly
involved in the protest.
    Persons who wish to comment only on the environmental review of
this project should submit an original and two copies of their comments
to the Secretary of the Commission. Environmental commenters will be
placed on the Commission's environmental mailing list, will receive
copies of the environmental documents, and will be notified of meetings
associated with the Commission's environmental review process.
Environmental commenters will not be required to serve copies of filed
documents on all other parties. However, the non-party commenters will
not receive copies of all documents filed by other parties or issued by
the Commission (except for the mailing of environmental documents
issued by the Commission) and will not have the right to seek court
review of the Commission's final order.
    The Commission strongly encourages electronic filings of comments,
protests, and interventions via the internet in lieu of paper. See 18
CFR 385.2001(a)(1)(iii) and the instructions on the Commission's Web
site (www.ferc.gov) under the ``e-Filing'' link. Persons unable to file
electronically should submit an original and 5 copies of the protest or
intervention to the Federal Energy regulatory Commission, 888 First
Street NE., Washington, DC 20426.
    Comment Date: 5:00 p.m. Eastern Time on June 11, 2014.

    Dated: May 21, 2014.
Kimberly D. Bose,
Secretary.
[FR Doc. 2014-12364 Filed 5-28-14; 8:45 am]
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