Federal Register / Vol. 78, No. 43 / Tuesday, March 5, 2013 / Proposed Rules 14241 

23 Id. at 21. 24Comment of Nicholas Legendre, http:// 

www.mbda.gov/sites/default/files/ 

AAPetitioncomments_asof062912.pdf at 56 (citing 

Arab American Institute Foundation, Quick Facts 

About Arab Americans, http://aai.3cdn.net/ 

afbc33810b07728c5a_oim6bx98f.pdf). 

free enterprise system impaired due to 

diminished capital and credit 

opportunities. 

Specifically, the Petition fails to 

provide evidence of the type MBDA 

requires to establish a relationship 

between any discriminatory treatment 

and business impediments experienced 

by Arab-American businesses as a group 

that are not common to all business 

people in the same or similar market 

place. Section III of the Petition states 

that: 

Arab-Americans suffer from 

discrimination, prejudice and cultural bias in 

the workplace. This employment 

discrimination has produced obstacles in the 

business world for Arab-Americans—both as 

employees and entrepreneurs. Members of 

the group have no control over such 

discrimination. Other entrepreneurs and 

individuals, outside of the group, do not 

suffer from such discrimination and bias.23

But, the Petition does not substantiate 

this assertion by providing evidence to 

support the statement, such as statistical 

measures of the impact that 

employment discrimination complaints 

have on Arab-American business 

success or workplace attainment. The 

EEOC complaints discussed above must 

be coupled with an analysis or study of 

the impact of discrimination on ArabAmericans in the business world. 

In addition, a 2008 Arab American 

Institute Foundation study produced 

results contrary to the Petitioner’s 

arguments. This study found that ArabAmerican households’ mean individual 

income is 27% higher than the national 

average and that the group shows higher 

than average educational attainment.24

These figures are not dispositive, but do 

suggest that prejudice Arab-Americans 

have faced may not have impacted their 

economic opportunities to the extent 

necessary to establish that ArabAmericans’ businesses require the 

technical and outreach services that 

MBDA provides. 

The Petition also does not establish 

with the necessary type of evidence that 

Arab-Americans have experienced 

diminished capital and credit 

opportunities. The descriptions of 

immigration controls, employment 

discrimination complaints, and 

post-9/11 programs that the Petition 

states target Arab-Americans do not 

demonstrate that Arab-Americans are 

unable to compete in the free enterprise 

system due to diminished capital and 

credit opportunities. Statistical or 

empirical evidence demonstrating a 

relationship between the discrimination 

suffered by the group and business 

impediments, or impaired access to 

capital, credit, contracts, and other 

business opportunities experienced by 

the group is necessary to show the 

social or economic conditions required 

to qualify the Petitioners for eligibility 

for MBDA’s programs that assist 

businesses in obtaining access to 

capital, credit, contracting, and other 

business opportunities. The comments 

submitted in support of the Petition 

similarly lack this supporting 

information. 

Accordingly, MBDA does not 

currently have sufficient evidence to 

recognize the Arab-American 

community as a minority group that is 

socially or economically disadvantaged 

within the specific meaning of the 

regulation because the Petition is not 

supported by sufficient evidence to 

meet the necessary elements of social or 

economic disadvantage as required by 

15 CFR 1400.4(a) of the MBDA 

regulations and applicable case law. As 

such, MBDA has returned the Petition to 

ADC for further consideration consistent 

with this response to petition. 

Dated: February 27, 2013. 

David Hinson, 

Director. 

[FR Doc. 2013–04955 Filed 3–4–13; 8:45 am] 

BILLING CODE P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 372 

[EPA–HQ–TRI–2006–0319; FRL–9787–1] 

RIN 2025–AA19 

Acetonitrile; Community Right-toKnow Toxic Chemical Release 

Reporting 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Denial of petition. 

SUMMARY: EPA is denying a petition to 

remove acetonitrile from the list of 

chemicals subject to reporting 

requirements under section 313 of the 

Emergency Planning and Community 

Right-to-Know Act of 1986 (EPCRA) and 

section 6607 of the Pollution Prevention 

Act of 1990 (PPA). EPA has reviewed 

the available data on this chemical and 

has determined that acetonitrile does 

not meet the deletion criterion of 

EPCRA section 313(d)(3). Specifically, 

EPA is denying this petition because 

EPA’s review of the petition and 

available information resulted in the 

conclusion that acetonitrile meets the 

listing criterion of EPCRA section 

313(d)(2)(B) due to its potential to cause 

death in humans. 

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; email: 

bushman.daniel@epa.gov, for specific 

information on this notice. For general 

information on EPCRA section 313, 

contact the Emergency Planning and 

Community Right-to-Know 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 notice apply to me? 

You may be potentially affected by 

this action if you manufacture, process, 

or otherwise use acetonitrile. 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. 


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Category Examples of potentially affected entities 

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 can I get copies of this document 

and other related information? 

EPA has established a docket for this 

action under Docket ID No. EPA–HQ– 

TRI–2006–0319. 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 (202) 566–1744, and 

the telephone number for the OEI 

Docket is (202) 566–1752. 

II. Introduction 

A. Statutory Authority 

This action is taken under sections 

313(d) and 313(e)(1) of EPCRA, 42 

U.S.C. 11023. EPCRA is also referred to 

as Title III of the Superfund 

Amendments and Reauthorization Act 

of 1986 (SARA) (Pub. L. 99–499). 

B. Background 

Section 313 of EPCRA, 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 PPA, 42 

U.S.C. 13106. Congress established an 

initial list of toxic chemicals subject to 

reporting that comprised more than 300 

chemicals and 20 chemical categories. 

EPCRA section 313(d) authorizes EPA 

to add or delete chemicals from the list 

and sets criteria for these actions. 

EPCRA section 313(d)(2) states that EPA 

may add a chemical to the list if any of 

the listing criteria in Section 313(d)(2) 

are met. 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, to remove a chemical from 

the list, EPCRA section 313(d)(3) 

dictates that EPA must demonstrate that 

none of the listing criteria in Section 

313(d)(2) 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.’’ 

EPA issued a statement of petition 

policy and guidance in the Federal 

Register of February 4, 1987 (52 FR 

3479) to provide guidance regarding the 

recommended content and format for 

submitting petitions. On May 23, 1991 

(56 FR 23703), EPA issued guidance 

regarding the recommended content of 

petitions to delete individual members 

of the section 313 metal compounds 

categories. EPA has also 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. What is the description of the 

petition and the regulatory status of 

acetonitrile? 

Acetonitrile is on the list of toxic 

chemicals subject to the annual release 

reporting requirements of EPCRA 

section 313 and PPA section 6607. 

Acetonitrile was among the list of 

chemicals placed on the EPCRA section 

313 list by Congress. Acetonitrile is 

listed under the Clean Air Act (CAA) as 

a volatile organic compound (VOC) and 

a hazardous air pollutant (HAP). 

Acetonitrile is also on the list of 

hazardous constituents (Appendix VIII 

to Part 261) and can qualify as listed 


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hazardous waste (U003) under the 

Resource Conservation and Recovery 

Act (RCRA). 

On February 4, 1998, EPA received a 

petition from BP Chemicals Inc. (BP) 

and GNI Chemicals Corporation 

(GNICC) to delete acetonitrile from the 

list of chemicals reportable under 

EPCRA section 313 and PPA section 

6607, stating that acetonitrile meets all 

of the criteria for delisting under EPCRA 

section 313(d)(3). On March 5, 1999 (64 

FR 10597), EPA denied the petition 

based on a determination that 

acetonitrile meets the listing criteria of 

EPCRA section 313(d)(2)(B) and 

(d)(2)(C) due to its potential to cause 

neurotoxicity and death in humans and 

its contribution to the formation of 

ozone in the environment. 

In September 2000, based on 

additional reviews, EPA reversed its 

previous position that acetonitrile was a 

chronic neurotoxicant (Ref. 1). 

On June 28, 2002, EPA received a 

second petition from BP to delete 

acetonitrile from the list of chemicals 

reportable under EPCRA section 313. 

Specifically, BP argues that acetonitrile 

meets all of the criteria for delisting 

under EPCRA section 313(d)(3) because: 

(1) Under generally accepted scientific 

principles, chronic mortality is not an 

issue for concern; and (2) EPA’s Office 

of Air Quality Planning and Standards 

(OAQPS) has concluded that 

acetonitrile does not have sufficient 

photochemical reactivity to contribute 

to ozone formation. Subsequent to BP’s 

filing of the petition on June 28, 2002, 

BP formed Innovene USA LLC as its 

olefin, derivatives and refining group, 

which was then acquired from BP by 

INEOS USA, LLC (INEOS), which has 

taken over the petition. 

IV. What is EPA’s technical review of 

acetonitrile? 

In response to the petition to delete 

acetonitrile from the list of chemicals 

reportable under EPCRA section 313 

and PPA section 6607, EPA prepared a 

Technical Review of Acetonitrile 

(Methyl Cyanide) (Ref. 2). The sections 

below summarize the human health 

hazard information contained in the 

Technical Review. The review did not 

consider acetonitrile’s status as a 

volatile organic compound (VOC) and 

thus its contribution to the formation of 

ozone in the environment since EPA no 

longer considers these factors as a basis 

for listing under EPCRA section 

313(d)(2) (70 FR 37698). 

A. Metabolism 

Acetonitrile is metabolized to 

inorganic cyanide through the 

intermediate production of hydrogen 

cyanide. Data demonstrate that the 

metabolism to cyanide is oxygen- and 

NADPH-dependent (Ref. 3), and 

mediated by cytochrome P450 isozyme 

2E1 (or P–450j) production of a reactive 

intermediate, methyl cyanohydrine 

(Refs. 4, 5, and 6). Formaldehyde and 

formic acid are also by-products of 

acetonitrile metabolism (Ref. 4). 

Cyanide is further oxidized and 

conjugated to thiocyanate, a less toxic 

compound that is excreted in urine, but 

one that has been shown to interfere 

with thyroid function (Ref. 7). 

B. Toxicity Evaluation 

1. Effects of Acute Exposure 

Humans acutely exposed to sublethal 

doses of acetonitrile developed effects 

that are generally attributed to 

metabolism of acetonitrile to cyanide 

(Ref. 8). Several cases were reported in 

which children or adults ingested large 

amounts of acetonitrile (≈250 to 4,000 

milligrams/kilogram (mg/kg)) (Ref. 9). 

Symptoms exhibited by poisoning 

victims include anxiety, confusion, 

hyperpnea, dyspnea, rapid pulse, 

unconsciousness, and convulsions (Ref. 

9). Cyanide was detected in the blood of 

these individuals. Case reports of acute 

occupational exposure to acetonitrile 

indicate that workers exhibited nausea, 

shallow and/or irregular respiration, 

and impaired motor activity. An 

autopsy of a worker who died shortly 

after exposure revealed cerebral, 

thyroid, liver, splenic, and renal 

congestion (Ref. 9). Gastric erosion has 

been reported in individuals who 

ingested acetonitrile (Refs. 10 and 11). 

In animals, oral LD50 values (i.e., the 

dose of a chemical that is lethal to 50 

percent of the test organisms) have been 

reported for the mouse (269–453 mg/kg) 

and the rat (1,730–4,050 mg/kg) and 

inhalation LC50 values (i.e., the 

concentration of a chemical that is 

lethal to 50 percent of the test 

organisms) of 12,000, 16,000, and 

7,551–12,435 parts per million (ppm) 

have been reported for the rat for 2, 4, 

and 8 hour exposures, respectively, and 

for the mouse following 1–2 hour 

exposures (2,300–5,700 ppm) (Ref. 9). A 

1-hour LC50 estimate for acetonitrile in 

mice was reported to be 2,693 ppm (Ref. 

6). A recent study (Ref. 12) reported a 

slightly higher oral LD50 of 617 mg/kg 

for Crl:CD–1(ICR)BR mice and an 

inhalation LC50 of 3,587 ppm for this 

strain. Observational signs of toxicity 

reported in animals after acute exposure 

to acetonitrile include dyspnea, 

tachypnea, tremors, and convulsions in 

various studies (Ref. 9). 

2. Effects of Subchronic and Chronic 

Exposure 

Subchronic inhalation exposure to 

acetonitrile resulted in an increase in 

mortality in rats at 1,600 ppm 

(calculates to approximately 505 mg/kgday) and in mice at 800 ppm (calculates 

to approximately 402 mg/kg-day) (Ref. 

13). 

Following subchronic inhalation 

exposure in rats, the mortality incidence 

was 0/20 in each of the 0, 100, 200 and 

400 ppm groups, 1/20 in the 800 ppm 

group (one death occurring on day 5), 

and 9/20 in the 1,600 ppm group (four 

deaths occurring on day 2, one each on 

days 7, 9, 10, 11, and 23) (Ref. 13). 

Clinical signs at the two highconcentration groups included 

hypoactivity and ruffled fur during the 

first week. Ataxia, abnormal posture, 

and clonic convulsions occurred in the 

1,600 ppm males that died. In addition, 

a decrease in hematocrit, hemoglobin, 

and erythrocytes was observed in male 

rats at 1,600 ppm and in female rats at 

≥800 ppm. Changes in organ weights 

were also observed, primarily at the 

highest dose in male rats and at ≥800 

ppm in female rats, and include 

decreases in absolute and relative 

thymus weight, increases in absolute 

and/or relative liver and kidney weight, 

and decreases and increases in brain 

and heart weight, respectively. 

Histopathologic effects were limited to 

rats that died at 800 and 1,600 ppm; 

effects observed include congestion, 

edema, and hemorrhage in the lung 

alveoli. 

Following subchronic inhalation 

exposure in mice, the mortality 

incidence was 0/20 in each of the 0, 100 

and 200 ppm groups, 1/20 in the 400 

ppm group (death occurring on day 13), 

5/20 in the 800 ppm group (deaths 

occurring on days 20, 21, 45, 69, 89) and 

20/20 in the 1,600 ppm group (all 

deaths occurring by day 21) (Ref. 13). 

Changes in organ weights were 

observed, including increased absolute 

and/or relative liver weight at ≥100 ppm 

in males and ≥400 ppm in females and 

increased relative lung weight at ≥200 

ppm in males. 

Effects were not observed in rats or 

mice following chronic inhalation 

exposure to 400 ppm (calculates to 

approximately 126 mg/kg-day) 

acetonitrile in rats and 200 ppm 

(calculates to approximately 100 mg/kgday) acetonitrile in mice (Ref. 13). The 

concentrations at which effects were 

observed in the 13-week study were not 

tested in the chronic study, and, in 

addition, two of the three principal 

reviewers of the study suggested that the 

highest exposure concentrations applied 


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in the chronic study (200 ppm-mouse; 

400 ppm-rat) were too low and one 

reviewer suggested concentrations 

should have been as high as 800 ppm 

(Ref. 13). 

3. Carcinogenicity 

There are no studies evaluating the 

carcinogenicity of acetonitrile in 

humans. Other data pertinent to the 

assessment of potential carcinogenicity 

include a National Toxicology Program 

(NTP) cancer bioassay in mice and rats. 

NTP concluded that the evidence for 

carcinogenicity via inhalation of 

acetonitrile in male F344/N rats was 

equivocal (Ref. 13). Although there was 

a statistically significant positive trend 

in the incidences of hepatocellular 

adenomas, carcinomas, and adenomas 

and carcinomas (combined) in male rats 

only, the incidences were not 

statistically significant by pairwise 

comparison or by life table analysis. 

There was no evidence of 

carcinogenicity in female rats or in 

either male or female B6C3F1 mice (Ref. 

13). 

4. Developmental and Reproductive 

Toxicity 

Following acute inhalation exposure 

to 3,800 ppm acetonitrile to hamsters on 

a single day during gestation day 8 

(GD8), an increase in maternal toxicity 

and mortality was observed; at higher 

exposure concentrations (≥5,000 ppm), 

an increase in severe fetal abnormalities, 

including exencephaly, encephalocoele, 

and rib fusions was reported (Ref. 14). 

Following acute oral ingestion of 

acetonitrile in hamsters on a single day 

at GD8, a decrease in fetal body weight 

was observed at the lowest observed 

adverse effect level (LOAEL) of 100 mg/ 

kg (the LOAEL for maternal toxicity was 

300 mg/kg) (Ref. 14). In rats, a single 

oral dose of 2,000 mg/kg on GD10 

resulted in dysmorphogenic features, 

including misdirected allantois and/or 

trunk and caudal extremity (Ref. 15). 

Mortality was not observed in dams 

exposed to 2,000 mg/kg acetonitrile on 

GD10; however, dams exhibited clinical 

signs of toxicity including piloerection, 

prostration, and/or tremors, and caused 

unspecified maternal weight loss 

between GDs 10 and 12 (Ref. 15). In a 

oral gavage study, New Zealand white 

rabbits were administered acetonitrile 

on GDs 6–18, which resulted in a 

decrease in the average number of live 

fetuses per litter at 30 mg/kg-day, as 

well as an increase in maternal 

mortality and anorexia, ataxia, 

decreased motor activity, bradypnea, 

dyspnea, and impaired righting reflex 

(Ref. 16). 

Inhalation and oral exposure in rats 

and rabbits resulted in both maternal 

and developmental toxicity. Maternal 

mortality was observed in rats at 

inhalation concentrations of 1,827 ppm 

(Ref. 17) and oral doses of 275 mg/kgday (Ref. 18), and at 30 mg/kg-day in 

rabbits (Ref. 16). In rats, inhalation 

exposure to 1,827 ppm resulted in an 

increase in the percentage of nonlive 

implants per litter and early resorptions 

(Ref. 17). In rats, there was an increase 

in post-implantation loss and in the 

number of fetuses with unossified 

sternebrae and a decrease in number of 

live fetuses per dam at the oral dose of 

275 mg/kg-day (Ref. 18). A decrease in 

the average number of live fetuses per 

litter was observed in rabbits at 30 mg/ 

kg-day (Ref. 16). While developmental 

toxicity was observed at doses that 

produced maternal toxicity or mortality, 

it is inadequate to assume that the 

developmental effects result only from 

maternal toxicity, and the results may 

indicate that both lifestages, the adult 

and developing offspring, are sensitive 

to the dose level (Ref. 19). 

V. What is EPA’s summary of the 

technical review? 

Based on the available data, and given 

the severity of the effect, mortality, EPA 

concludes that there is sufficient 

evidence to support a concern for 

moderately high toxicity from exposure 

to acetonitrile. In assessing mortality 

following acetonitrile exposure, the 

patterns in the timing of death across 

exposures demonstrates the chronic 

nature of the effect. Mortality was 

observed in the 13-week mouse 

inhalation study in the 800 and 1600 

ppm treatment groups (Ref. 13). The 

first occurrence of mortality in the 800 

ppm treatment group was not observed 

until day 20 and single deaths 

continued on days 21, 45, 69 and 89 of 

the 13-week study. This pattern of 

mortality is dissimilar to that observed 

in the 13-week mouse inhalation study 

at 1,600 ppm, where initial deaths were 

observed in the first week and all mice 

died by day 21 (Ref. 13). 

Based on the observed pattern of 

death in the 800 ppm treatment group 

of the NTP 13-week mouse inhalation 

study, beginning at the end of the third 

week and extending through the 

termination of the study, it can be 

reasonably anticipated that additional 

acetonitrile-induced mortality would 

have continued beyond the termination 

of the study and the sacrifice of 

surviving animals. Because the 

mortalities extended from the third 

week of the study to study termination, 

the data indicates that the mortality 

observed in the 800 ppm treatment 

group is not due to a single acute 

exposure to sufficiently high acetonitrile 

concentrations, but rather is best 

explained as being the result of longterm repeated exposures. The observed 

exposure-response relationship for 

acetonitrile demonstrates that a 

threshold exists at which acetonitrile 

exposure levels are sufficient to cause 

mortality from chronic exposure, and, as 

such, mortality would not necessarily be 

expected following chronic exposure at 

the doses tested in the NTP 2-year study 

because the acetonitrile exposure levels 

in the study design were not sufficient 

to cause mortality. 

In addition, in 1999, EPA’s Integrated 

Risk Information System (IRIS) 

Toxicological Review of Acetonitrile 

(Ref. 8) set the reference concentration 

(RfC) for acetonitrile based on this same 

13-week mouse inhalation study (Ref. 

13). The IRIS Toxicological Review of 

Acetonitrile identified the 400 ppm 

concentration in the NTP (1996) mouse 

study as a frank effect level (FEL) and 

the critical effect in the derivation of the 

reference concentration (RfC), given the 

death of a mouse at week 2 at 400 ppm 

and the increased mortality at 800 ppm. 

The FEL is a level of exposure or dose 

that produces irreversible, adverse 

effects at a statistically or biologically 

significant increase in frequency or 

severity between those exposed and 

those not exposed. The RfC is an 

estimate of a continuous inhalation 

exposure to the human population 

(including sensitive subgroups) that is 

likely to be without an appreciable risk 

of deleterious effects during a lifetime. 

Such a ‘‘lifetime’’ exposure value, set by 

IRIS based on the 13-week mouse 

inhalation study, is based on chronic 

effects, and would be unnecessary if 

IRIS found only acute effects. 

VI. What is EPA’s rationale for the 

denial? 

EPA is denying the petition to delete 

acetonitrile from the EPCRA section 313 

list of toxic chemicals. This denial is 

based on EPA’s conclusion that 

acetonitrile can reasonably be 

anticipated to cause serious or 

irreversible chronic health effects in 

humans. Based on the available data, 

and given the severity of the effect, 

mortality, EPA concludes that there is 

sufficient evidence to support a concern 

for moderately high toxicity from 

chronic exposure to acetonitrile. 

Because EPA believes that acetonitrile 

has moderately high chronic toxicity, 

EPA does not believe that an exposure 

assessment is appropriate for 

determining whether acetonitrile meets 

the criteria of EPCRA section 

313(d)(2)(B). This determination is 


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consistent with EPA’s published 

statement clarifying its interpretation of 

the section 313(d)(2) and (d)(3) criteria 

for modifying the section 313 list of 

toxic chemicals (59 FR 61432, 

November 30, 1994). 

VII. References 

EPA has established an official public 

docket for this action under Docket ID 

No. EPA–HQ–TRI–2006–0319. 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. EPA. 2000. OPPT/RAD Decision 

on Neurotoxicity Endpoint for 

Acetonitrile. Office of Pollution 

Prevention and Toxics, Washington, 

DC. 

2. U.S. EPA, 2012. Technical Review of 

Acetonitrile (Methyl Cyanide). 

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2000. Comparative developmental 

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List of Subjects in 40 CFR Part 372 

Environmental protection, 

Community right-to-know, Reporting 

and recordkeeping requirements, and 

Toxic chemicals. 

Dated: February 25, 2013. 

Arnold E. Layne, 

Director, Office of Information Analysis and 

Access. 

[FR Doc. 2013–04933 Filed 3–4–13; 8:45 am] 

BILLING CODE 6560–50–P 

DEPARTMENT OF THE INTERIOR 

Fish and Wildlife Service 

50 CFR Part 17 

[Docket No. FWS–R8–ES–2009–0062; 

4500030114] 

RIN 1018–AW85 

Endangered and Threatened Wildlife 

and Plants; Designation of Critical 

Habitat for the Buena Vista Lake Shrew 

AGENCY: Fish and Wildlife Service, 

Interior. 

ACTION: Proposed rule; revision and 

reopening of comment period. 

SUMMARY: We, the U.S. Fish and 

Wildlife Service (Service), announce the 

reopening of the comment period on the 

July 10, 2012, revised proposal to 

designate critical habitat for the Buena 

Vista Lake shrew (Sorex ornatus 

relictus) (shrew) under the Endangered 

Species Act of 1973, as amended (Act). 

We announce a revision of the unit map 

labels. We provide maps with correct 

labels for all proposed units herein. We 

also announce the availability of a draft 

economic analysis (DEA) of the revised 

critical habitat proposal, and of an 

amended required determinations 

section of the revised proposal. We are 

reopening the comment period for an 

additional 60 days to allow all 

interested parties an opportunity to 

comment on the revised proposed rule, 

the associated DEA, and the amended 

required determinations section. 

Furthermore, we announce a public 

hearing for the purpose of taking oral or 

written comments on those documents. 

Comments previously submitted need 

not be resubmitted, as they will be fully 

considered in preparation of the final 

rule. 

DATES: Written Comments: We will 

consider comments received on or 

before May 6, 2013. Comments must be 

received by 11:59 p.m. Eastern Time on 

the closing date. Any comments that we 

receive after the closing date may not be 


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