Federal Register / Vol. 75, No. 38 / Friday, February 26, 2010 / Proposed Rules 8889 

and included as part of the public 

comment. 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. 

Docket: The index to the docket for 

this action is available electronically at 

http://www.regulations.gov and in hard 

copy at EPA Region IX, 75 Hawthorne 

Street, San Francisco, California. While 

all documents in the docket are listed in 

the index, some information may be 

publicly available only at the hard copy 

location (e.g., copyrighted material), and 

some may not be publicly available in 

either location (e.g., CBI). To inspect the 

hard copy materials, please schedule an 

appointment during normal business 

hours with the contact listed in the FOR

FURTHER INFORMATION CONTACT section. 

FOR FURTHER INFORMATION CONTACT: Mae 

Wang, EPA Region IX, (415) 947–4124, 

wang.mae@epa.gov. 

SUPPLEMENTARY INFORMATION: 

This document concerns the 

delegation of unchanged NESHAP to the 

Maricopa County Air Quality 

Department, the Nevada Division of 

Environmental Protection, and the 

Washoe County District Health 

Department, Air Quality Management 

Division. In the Rules and Regulations 

section of this Federal Register, EPA is 

amending regulations to reflect the 

current delegation status of NESHAP in 

Arizona and Nevada. EPA is taking 

direct final action without prior 

proposal because the Agency believes 

this action is not controversial. If we 

receive adverse comments, however, we 

will publish a timely withdrawal of the 

direct final rule and address the 

comments in subsequent action based 

on this proposed rule. Please note that 

if we receive adverse comment on an 

amendment, paragraph, or section of 

this rule and if that provision may be 

severed from the remainder of the rule, 

we may adopt as final those provisions 

of the rule that are not the subject of an 

adverse comment. 

We do not plan to open a second 

comment period, so anyone interested 

in commenting should do so at this 

time. If we do not receive adverse 

comments, no further activity is 

planned. For further information, please 

see the direct final action. 

Authority: This action is issued under the 

authority of Section 112 of the Clean Air Act, 

as amended, 42 U.S.C. Section 7412. 

Dated: January 20, 2010. 

Deborah Jordan, 

Director, Air Division, Region IX. 

[FR Doc. 2010–4077 Filed 2–25–10; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 372 

[EPA–HQ–TRI–2009–0844; FRL–9119–2] 

RIN 2025–AA27 

Hydrogen Sulfide; Community Rightto-Know Toxic Chemical Release 

Reporting 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Intent to consider lifting 

administrative stay; opportunity for 

public comment. 

SUMMARY: EPA is announcing that it is 

considering whether to lift the 

Administrative Stay of the Emergency 

Planning and Community Right-toKnow 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: oei.docket@epa.gov. 

• 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 


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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 (202) 

566–1744, and the telephone number for 

the OEI Docket is (202) 566–1752. 

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: 202–566– 

0743; fax number: 202–566–0677; 

e-mail: bushman.daniel@epa.gov, for 

specific information on this document. 

For general information on EPCRA 

section 313, contact the Emergency 

Planning and Community Right-toKnow Hotline, toll free at (800) 424– 

9346 or (703) 412–9810 in Virginia and 

Alaska or toll free, TDD (800) 553–7672, 

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 


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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/m3)) are lifethreatening 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 


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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 weightof-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/m3) and the likely indicator of 

neurotoxic effects reported by Hannah 

and Roth (Ref. 7) at 20 ppm (28 mg/m3)), 

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-doseresponse, 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. SpragueDawley 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 


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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/m3

to 41.7 mg/m3). 

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/m3 (20 

ppm) and 41.7 mg/m3 (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 


sroberts on DSKD5P82C1PROD with PROPOSALS
8894 Federal Register / Vol. 75, No. 38 / Friday, February 26, 2010 / Proposed Rules 

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] 

BILLING CODE 6560–50–P 


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