[Federal Register Volume 78, Number 43 (Tuesday, March 5, 2013)]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2013-04933]
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
Acetonitrile; Community Right-to-Know Toxic Chemical Release
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: [email protected], 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/.
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:
Examples of potentially
Category affected entities
Industry................................. Facilities included in the
(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
limitations exist for these
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,
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.
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.
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
(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
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
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
hazardous waste (U003) under the Resource Conservation and Recovery Act
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
In September 2000, based on additional reviews, EPA reversed its
previous position that acetonitrile was a chronic neurotoxicant (Ref.
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).
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 ([ap]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/kg-day) 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 high-concentration
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
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/kg-day) 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
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
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
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.
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/kg-day (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
long-term 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
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).
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
1. U.S. EPA. 2000. OPPT/RAD Decision on Neurotoxicity Endpoint for
Acetonitrile. Office of Pollution Prevention and Toxics, Washington,
2. U.S. EPA, 2012. Technical Review of Acetonitrile (Methyl Cyanide).
Office of Environmental Information. Washington, DC. November 5, 2012.
3. Freeman, J.J. and E.P. Hayes. 1988. Microsomal metabolism of
acetonitrile to cyanide. Biochem. Pharmacol. 37:1153-1159.
4. Ahmed, A.E., J.P. Loh, B. Ghanayem et al. 1992. Studies on the
mechanism of acetonitrile toxicity: I. Whole body autoradiographic
distribution and macromolecular interaction of 214C-acetonitrile in
mice. Pharmacol. Toxicol. 70:322-330.
5. Feierman, D.E. and A.I. Cederbaum. 1989. Role of cytochrome P-450
IIE1 and catalase in the oxidation of acetonitrile to cyanide. Chem.
Res. Toxicol. 2:359-66.
6. Willhite, C.C. and R.P. Smith. 1981. The role of cyanide liberation
in the acute toxicity of aliphatic nitriles. Toxicol. Appl. Pharmacol.
7. Hartung, R. 1982. Cyanides and nitriles. In: Patty's Industrial
Hygiene and Toxicology, 3rd Rev. Ed. Patty, F.A., G.D. Clayton, F.E.
Clayton et al., eds. New York: Wiley. pp. 4845-4900.
8. U.S. EPA. 1999. Toxicological Review of Acetonitrile. Office of
Research and Development. Washington, DC. January, 1999. Available at
9. WHO (World Health Organization). 1993. Environmental Health Criteria
154: Acetonitrile. International Programme on Chemical Safety, Geneva,
Switzerland. Available at http://www.inchem.org/documents/ehc/ehc/ehc154.htm.
10. Ballantyne, B. 1983. Artifacts in the definition of toxicity by
cyanides and cyanogens. Fundam. Appl. Toxicol. 3:400-408.
11. Way, J.L. 1981. Pharmacologic aspects of cyanide and its
antagonism. In: Cyanide in Biology. Vennesland, B., E.E. Conn, C.J.
Knowles et al., eds. New York, NY: Academic Press. pp. 29-49.
12. Moore, N.P., R.J. Hilaaski, T.D. Morris et al. 2000. Acute and
subacute toxicological evaluation of acetonitrile. Int. J. Toxicol.
13. NTP (National Toxicology Program). 1996. Toxicology and
carcinogenesis studies of acetonitrile (CAS NO. 75-05-8) in F344/N rats
and B6C3F1 mice (inhalation studies). NTP Technical Report Series 447.
14. Willhite, C.C. 1983. Developmental toxicology of acetonitrile in
the Syrian golden hamster. Teratology. 27:313-325.
15. Saillenfait, A.M. and J.P. Sabat[eacute]. 2000. Comparative
developmental toxicities of aliphatic nitriles: In vivo and in vitro
observations. Toxicol. Appl. Pharmacol. 163:149-163.
16. Argus Research Laboratories, Inc. 1984. Embryofetal toxicity and
teratogenicity study of acetonitrile in New Zealand White rabbits
(Segment II evaluation). Washington, DC: Office of Toxic Substances
submission. Microfiche No. OTS 507279.
17. Saillenfait, A.M., P. Bonnet, J.P. Guenier et al. 1993. Relative
developmental toxicities of inhaled aliphatic mononitriles in rats.
Fundam. Appl. Toxicol. 20:365-375.
18. Johannsen, F.R., G.J. Levinskas, P.E. Berteau et al. 1986.
Evaluation of the teratogenic potential of three aliphatic nitriles in
the rat. Fundam. Appl. Toxicol. 7:33-40.
19. U.S. EPA. 1991. Guidelines for Developmental Toxicity Risk
Assessment. Risk Assessment Forum, Washington, DC. EPA/600/FR-91/001.
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