[Federal Register Volume 64, Number 32 (Thursday, February 18, 1999)]
[Proposed Rules]
[Pages 8043-8048]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 99-3993]


-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 82

[FRL-6301-8]
RIN 2060-AG12


Protection of Stratospheric Ozone; Listing of Substitutes for 
Ozone-Depleting Substances

AGENCY: Environmental Protection Agency.

ACTION: Request for data and advance notice of proposed rulemaking.

-----------------------------------------------------------------------

SUMMARY: This action requests comments and information on n-propyl 
bromide (nPB) under the U.S. Environmental Protection Agency's (EPA) 
Significant New Alternatives Policy (SNAP) program. SNAP implements 
section 612 of the amended Clean Air Act of 1990 (CAAA), which requires 
EPA to evaluate substitutes for ozone depleting substances (ODSs) to 
reduce overall risk to human health and the environment. Through these 
evaluations, SNAP generates lists of acceptable and unacceptable 
substitutes for each of the major industrial use sectors. The intended 
effect of the SNAP program is to expedite movement away from ozone 
depleting compounds while avoiding a shift into substitutes posing 
other environmental or health problems.
    Through this Advance Notice of Proposed Rulemaking (ANPR), the 
Agency hopes to receive information as part of the development of 
effective regulatory options on the listing of nPB as acceptable or 
unacceptable for the various submitted end-uses under SNAP. This action 
notifies the public of the availability of information regarding nPB 
and the Agency hopes that this action will provide the public an 
opportunity to provide input at an early stage in the decision-making 
process.
    This notice does not constitute a final, or even preliminary, 
decision by the Agency. Based on information collected as part of this 
ANPR, EPA intends to propose a future determination regarding the 
acceptability or unacceptability of nPB as a substitute for class I and 
class II ozone depleting substances and, if acceptable, an occupational 
exposure limit (OEL) for nPB. This limit would be designed to protect 
worker safety until the Occupational Safety and Health Administration 
(OSHA) sets its own standards under Public Law 91-596. However, until a 
final determination is made, users of nPB should exercise caution in 
the manufacture, handling, and disposal of this chemical.
    EPA has received petitions under CAAA Section 612(d) to add nPB to 
the list of acceptable alternatives for class I and class II ozone 
depleting substances in the solvent sector for general metals, 
precision, and electronics cleaning, as well as in aerosol and adhesive 
applications.

DATES: Written comments on data provided in response to this notice 
must be submitted by April 19, 1999.

ADDRESSES: Comments on and materials supporting this advanced notice 
are collected in Air Docket # A-92-13, U.S. Environmental Protection 
Agency, 401

[[Page 8044]]

M Street, S.W., Room M-1500, Washington, D.C., 20460. The docket is 
located at the address above in room M-1500, First Floor, Waterside 
Mall. The materials may be inspected from 8 am until 4 pm Monday 
through Friday. A reasonable fee may be charged by EPA for copying 
docket materials.

FOR FURTHER INFORMATION CONTACT: The Stratospheric Ozone Hotline at 
(800)-296-1996 or Melissa Payne at (202) 564-9738 or fax (202) 565-
2096, Analysis and Review Branch, Stratospheric Protection Division, 
Mail Code 6205J, Washington, D.C. 20460. Overnight or courier 
deliveries should be sent to our 501 3rd Street, N.W., Washington, DC, 
20001 location.

SUPPLEMENTARY INFORMATION:
    This action is divided into four sections:

I. Section 612 Program
    A. Statutory Requirements
    B. Regulatory History
II. Listing of Substitutes
III. Information Needs
    A. Objective
    B. Ozone Depletion Potential
    C. Toxicity
    D. Potential Use
IV. Regulatory Options
V. References

I. Section 612 Program

A. Statutory Requirements

    Section 612 of the Clean Air Act authorizes EPA to develop a 
program for evaluating alternatives to ozone-depleting substances. This 
program is referred to as the Significant New Alternatives Policy 
(SNAP) program. Section 612(c) requires EPA to publish a list of the 
substitutes unacceptable for specific uses and a corresponding list of 
acceptable alternatives for specific uses. Section 612(d) grants the 
right to any person to petition EPA to add a substitute to or delete a 
substitute from the lists published in accordance with section 612(c).

B. Regulatory History

    On March 18, 1994, EPA published the Final Rulemaking (59 FR 13044) 
which described the process for administering the SNAP program and 
issued EPA's first acceptability and unacceptability lists for 
substitutes in the major industrial use sectors. These sectors include: 
refrigeration and air conditioning; foam blowing; solvent cleaning; 
fire suppression and explosion protection; sterilants; aerosols; 
adhesives, coatings and inks; and tobacco expansion. These sectors 
comprise the principal industrial sectors that historically consume 
large volumes of ozone-depleting compounds.
    The Agency defines a ``substitute'' as any chemical, product 
substitute, or alternative manufacturing process, whether existing or 
new, that could replace a class I or class II substance. Anyone who 
produces a substitute must provide the Agency with health and safety 
studies on the substitute at least 90 days before introducing it into 
interstate commerce for significant new use as an alternative. This 
requirement applies to chemical manufacturers, but may include 
importers, formulators or end-users when they are responsible for 
introducing a substitute into commerce.

II. Listing of Substitutes

    To develop the lists of unacceptable and acceptable substitutes, 
EPA conducts screens of health and environmental risks posed by various 
substitutes for ozone-depleting compounds in each use sector. The 
outcome of these risk screens can be found in the public docket, as 
described above in the Addresses portion of this document.
    Under section 612, the Agency has considerable discretion in the 
risk management decisions it can make in SNAP. The Agency has 
identified five possible decision categories: acceptable; acceptable 
subject to use conditions; acceptable subject to narrowed use limits; 
unacceptable; and pending. Fully acceptable substitutes, i.e., those 
with no restrictions, can be used for all applications within the 
relevant sector end-use. Conversely, it is illegal to replace an ODS 
with a substitute listed by SNAP as unacceptable. A pending listing 
represents substitutes for which the Agency has not received complete 
data or has not completed its review of the data.
    After reviewing a substitute, the Agency may make a determination 
that a substitute is acceptable only if certain conditions of use are 
met to minimize risks to human health and the environment. Such 
substitutes are placed on the ``acceptable, subject to use, 
conditions'' lists. Use of such substitutes in ways that are 
inconsistent with such use conditions renders these substitutes 
unacceptable and subjects the user to enforcement for violation of 
section 612 of the Clean Air Act.
    Even though the Agency can restrict the use of a substitute based 
on the potential for adverse effects, it may be necessary to permit a 
narrowed range of use within a sector end-use because of the lack of 
alternatives for specialized applications. Users intending to adopt a 
substitute acceptable with narrowed use limits must ascertain that 
other acceptable alternatives are not technically feasible. Companies 
must document the results of their evaluation, and retain the results 
on file for the purpose of demonstrating compliance. This documentation 
shall include descriptions of substitutes examined and rejected, 
processes or products in which the substitute is needed, reason for 
rejection of other alternatives, e.g., performance, technical or safety 
standards, and the anticipated date other substitutes will be available 
and projected time for switching to other available substitutes. Use of 
such substitutes in applications and end-uses which are not specified 
as acceptable in the narrowed use limit renders these substitutes 
unacceptable.

III. Information Needs

A. Objective

    As noted above, the purpose of today's notice is to elicit the 
voluntary submission of information on nPB as a substitute for class I 
and class II substances. Listed below are the specific areas of 
information that will be most useful to the Agency in completing the 
risk characterizations needed to make regulatory decisions. However, 
any available data pertaining to nPB will be considered by the Agency. 
Data submitted in response to this request can be designated as 
confidential business information (CBI) under 40 CFR, part 2, subpart 
B.
    EPA has been reviewing the data available on nPB with regard to its 
toxicity and its ozone depletion potential. In order to ascertain the 
extent of potential environmental implications associated with the use 
of this chemical, the Agency is also interested in estimates of nPB 
production and ultimate use in various applications. Based on the 
assessment to date, the Agency believes that additional information in 
all of these areas is needed before regulatory decisions can be 
formulated. This notice is to inform the public of the information gaps 
and to make publicly available the data to which the Agency already has 
access. In this light, EPA is establishing a docket with all available 
information on the environmental and health risks associated with nPB, 
and is asking for comments and data that can supplement this 
information. EPA is seeking public comment regarding nPB in the 
following areas where EPA believes that either significant 
uncertainties exist in the available data or the data are incomplete. 
These areas are critical to EPA's decision-making on the acceptability 
or unacceptability of nPB.

[[Page 8045]]

B. Ozone Depletion Potential

    The ozone depletion potential (ODP) of a chemical compound provides 
a relative measure of the expected impact on stratospheric ozone per 
unit mass of the emission of the compound, as compared to that expected 
from the same mass emission of CFC-11 integrated over time. ODP is a 
benchmark that has been used by the Parties to the Montreal Protocol to 
characterize the relative risks associated with the various ozone-
depleting compounds subject to the Protocol's requirements. Under the 
auspices of the United Nations Environment Programme, every four years 
the world's leading experts in the atmospheric sciences publish a 
scientific assessment, relied upon by the Parties to the Montreal 
Protocol for future decisions regarding protection of the stratospheric 
ozone layer. These assessments evaluate the impacts of ozone depleting 
substances on stratospheric ozone concentrations using ODP. Prior 
analyses of ODP conducted by these experts, as well as by others in the 
field of atmospheric chemistry, have traditionally focused on compounds 
with relatively long atmospheric lifetimes (e.g., three months or 
longer) (WMO, 1994).
    Recently, EPA has been called upon to review compounds of much 
shorter lifetimes, such as nPB, which has an estimated atmospheric 
lifetime of only 11 days. Estimates of ODP for nPB based on the current 
models lie within the range of 0.006-0.027 (Wuebbles et al., 1997 and 
1998). The two-dimensional (2-D) and other models currently used to 
estimate the relative effects of long-lived compounds on stratospheric 
ozone, however, may not be as useful in measuring effects associated 
with compounds with very short atmospheric lifetimes.
    Chemicals previously evaluated for ODP have atmospheric lifetimes 
sufficiently long to be well-mixed in the troposphere, and 2-D models 
have been adequate tools for ODP estimation. Short-lived substances 
(i.e., compounds with atmospheric lifetimes shorter than three months) 
such as nPB can either reach the stratosphere or, unlike long-lived 
compounds, break down in the troposphere. Thus, the amount of bromine 
that would be available to affect stratospheric ozone greatly depends 
on the complex effects of transport and chemical processes in the 
troposphere. Two-dimensional modeling is not designed to accurately 
account for variations in chemical concentration at different latitudes 
or for atmospheric transport of short-lived compounds. As a result, 
there are questions about the adequacy of the ODPs determined with 
these models for short-lived chemicals like nPB. Since current models 
may not accurately evaluate impacts of these short-lived compounds, EPA 
is concerned that it may be difficult to meaningfully compare them to 
the longer-lived compounds already controlled.
    EPA is presently developing a process to more accurately determine 
ODPs for short-lived compounds. Independent atmospheric scientists are 
also in the process of refining current atmospheric models for this 
same purpose. The models are expected to examine a variety of questions 
related to convective transport rates at different latitudes, and the 
relative importance of transient versus steady-state effects. EPA 
expects this work to increase the accuracy of the ODP estimate for nPB, 
as well as for other short-lived compounds, and the Agency anticipates 
that these models will produce preliminary results within the next 
year. In addition, the Agency is interested in receiving from the 
public any other information pertaining to the atmospheric effects and 
ozone depletion potential of short-lived atmospheric chemicals (shorter 
than three months), and any additional information on the ozone 
depletion potential of nPB, specifically. EPA will make any new 
information accessible to the public as it becomes available by placing 
it in the docket identified in the Addresses section of this document, 
and if appropriate, issue a notice of data availability in the Federal 
Register to insure that the public is aware of any new information.

C. Toxicity

    Information on the toxicity of nPB was submitted to the Agency as 
part of the requirements of the SNAP program. Data from the submitters 
included the results of newly performed 28-day and 90-day repeated dose 
studies, both of which included a functional observation battery. A 
consortium of companies interested in nPB was formed after the initial 
data were submitted under the SNAP program. Other studies, not 
previously available to the public, were also submitted by a company 
that is not part of the consortium. Additional studies were available 
from the published scientific journals. A list of the studies received, 
evaluated, and placed in the docket is appended in Section VI.
    EPA reviewed the literature to evaluate the potential metabolites 
of nPB and their expected toxicity following inhalation exposure. A 
structure-activity relationship analysis for potential carcinogenicity 
was part of this evaluation. The pharmacokinetics of nPB and its 
metabolites were also examined, as well as reports of other studies 
performed under non-guideline protocols. Data on structural analogues 
of nPB, such as 2-propyl bromide, were also reviewed. This information, 
and the reports of the acute (less than 14-day) studies, 28-day and 90-
day inhalation studies can be used to estimate a tentative exposure 
limit for the use of nPB in industrial settings. The ``no observed 
adverse effect level'' (NOAEL) for liver effects in the 90-day study of 
2000 milligrams per cubic meter (mg/m\3\), or 400 parts per million 
(ppm), is a possible basis for setting an industrial exposure guideline 
(ICF 1998k). Based on this NOAEL, EPA's preliminary estimate of an 
exposure guideline is in the range of 50-100 ppm as an 8-hour time 
weighted average. Using the NOAEL for effects on sperm counts and 
motility from the Ichihara et al. (1998) study would result in a 
preliminary, estimated guideline of 93 ppm, suggesting that a range 
from 50-100 ppm would be protective of both liver and testicular 
effects. (This limit would be designed to protect worker safety until 
the Occupational Safety and Health Administration (OSHA) sets its own 
standards under P.L. 91-596. The existence of an EPA standard in no way 
bars OSHA from standard-setting under OSHA authorities as defined in 
P.L. 91-596.)
    EPA also examined the potential uses of nPB in the solvent, 
aerosol, and adhesives, coatings and inks sectors and received 
additional personal monitoring data for these sectors. Preliminary 
consideration of the available personal monitoring data (Smith, 1998) 
during solvent, adhesive and aerosol usage indicates that nPB exposures 
can generally be kept within the range of 50-100 ppm, although some of 
the exposure measurements exceeded this range.
    At this time, EPA cannot recommend a firm exposure limit because of 
identified areas of uncertainty. The fact that reproductive system 
effects have been observed in both rats and humans for the similar 
compound, 2-propyl bromide, as well as the report of oligospermia in 
rats exposed to nPB, raises concern that insufficient testing has been 
completed to fully evaluate these significant endpoints. The industry 
consortium has responded to these concerns by initiating studies to 
test the developmental and reproductive system effects of nPB. Results 
from these studies will not be available for another year.

[[Page 8046]]

    Finally, EPA is aware that an isomer of nPB, 2-bromo-propane (2BP; 
also known as iso-propyl bromide), can be present as a contaminant in 
nPB formulations. Occupational exposure to 2BP has been associated with 
anemia and reproductive toxicity (Kim et al., 1996). Reproductive and 
hematopoietic effects of 2BP have also been demonstrated in animal 
studies (Takeuchi et al., 1997; Ichihara et al., 1996, 1997; Kamijima 
et al., 1997a,b). Should nPB be listed as acceptable under SNAP, the 
Agency would consider establishing maximum concentration limits for 2BP 
in applications involving nPB.
    EPA is presenting and making publicly available the information it 
has received so that interested parties may evaluate these data for 
themselves and use it as guidance if they choose to use nPB until a 
proposal and final rule are in place. EPA is also interested in 
receiving additional information on human health and toxicological 
risks associated with exposure to nPB. As EPA receives new data, they 
will be added to the docket, along with notice of data availability in 
the Federal Register, as appropriate.

D. Potential Use

    EPA is requesting information on the anticipated uses for nPB, the 
extent of its use in the different sectors (aerosols, solvents, 
adhesives, coatings, and inks), as well as estimated market potential. 
The Agency is also requesting information on the relative effectiveness 
of nPB versus the chemicals it would potentially replace, and the 
relative quantities of nPB that would be needed in various sectors 
compared to other chemicals that it would potentially replace. This 
information will provide the Agency information needed to assess 
potential environmental effects associated with use of nPB.

IV. Regulatory Options

    EPA believes that notice-and-comment rulemaking is required to 
place any alternative on the list of prohibited substitutes, to list a 
substitute as acceptable only under certain use conditions or narrowed 
use limits, or to remove an alternative from either the list of 
prohibited or acceptable substitutes.
    EPA does not believe that rulemaking procedures are required to 
list alternatives as acceptable with no limitations. Such listings do 
not impose any sanction, nor do they remove any prior license to use a 
substitute. Consequently, EPA adds substitutes to the list of 
acceptable alternatives without first requesting comment on new 
listings. Updates to the acceptable and pending lists are published as 
separate Notices of Acceptability in the Federal Register.

V. References

Barnsely, E. 1966. The formation of 2-hydroxypropylmercapturic acid 
from 1-halogenpropanes in the rat. Biochem J 100:362-372.
Barnsely, E; Grenby, T; Young, L. 1966. Biochemical Studies of Toxic 
Agents: the metabolism of 1- and 2-bromopropane in rats. Biochem J 
100:282-288.
Bors, W; Michel, C; Dalke, C; Stettmaier, K; Saran, M; Andrae, U. 
1993. Radical intermediates during the oxidation of nitropropanes. 
The formation of NO2 from 2-nitropropane, its reactivity 
with nucleosides, and implications for the genotoxicity of 2-
nitropropane. Chemical Research in Toxicology 6:302-309.
ClinTrials. 1997a. A 28-Day Inhalation Study of a Vapor-Formulation 
of ALBTA1 in the Albino Rat. Report No. 91189. Prepared by 
ClinTrials BioResearch Laboratories, Ltd., Senneville, Quebec, 
Canada. May 15, 1997. Sponsored by Albemarle Corporation, Baton 
Rouge, LA.
ClinTrials. 1997b. ALBTA1: A 13-Week Inhalation Study of a Vapor 
Formulation of ALBTA1 in the Albino Rat. Report No. 91190. Prepared 
by ClinTrials BioResearch Laboratories, Ltd., Senneville, Quebec, 
Canada. February 28, 1997. Sponsored by Albemarle Corporation, Baton 
Rouge, LA.
Cunningham, M; Matthews, H. 1991. Relationship of 
hepatocarcinogenicity and hepatocellular proliferation induced by 
mutagenic noncarcinogens vs. carcinogens, II. 1- vs. 2-nitropropane. 
Toxicology and Applied Pharmacology 110:505-513.
Elf Atochem S.A. 1993. Acute Oral Toxicity in Rats. N-Propyl 
Bromide. Study No. 10611 Tar. Study Director, Jack Clouzeau. Study 
performed by Centre International de Toxicologie, Miserey, France. 
November 3, 1993.
Elf Atochem S.A. 1994. Ames test--reverse mutation assay on 
Salmonella typhimurium. n-Propyl Bromide. HIS1005/1005A. Study 
performed by Sanofi Recherche, Service de Toxicologie.
Elf Atochem S.A. 1995a. Micronucleus Test by Intraperitoneal Route 
in Mice. N-Propyl Bromide. Study No. 12122 MAS. Study Director, 
Brigitte Molinier. Study performed by Centre International de 
Toxicologie, Miserey, France. September 6, 1995.
Elf Atochem S.A. 1995b. Acute Dermal Toxicity in Rats. N-Propyl 
Bromide. Study No. 13113 Tar. Study Director, Stephane de Jouffrey. 
Study performed by Centre International de Toxicologie, Miserey, 
France. September 26, 1995.
Elf Atochem S.A. 1995c. Skin Sensitization Test in Guinea-Pigs 
(Maximization method of Magnusson B, and Kligman, A.M.). N-Propyl 
Bromide. Study No. 12094 TSG. Study Director, Stephane de Jouffrey. 
Study performed by Centre International de Toxicologie, Miserey, 
France. June 30, 1995.
Elf Atochem S.A. 1996. Amendment to Protocol. n-Propyl Bromide. 
Study No. 13293 MLY. Amendment No. 01. Study Director, Brigitte 
Molinier. January 29, 1996.
Elf Atochem S.A. 1997a. Study of Acute Toxicity on n-Propyl Bromide 
Administered to Rats by Vapour Inhalation. Determination of the 50% 
Lethal Concentration. L.E.T.E. Study Number 95122. Study performed 
by Laboratoire d'Etudes de Toxicologie Experimentale.
Elf Atochem. 1997b. Safety Data Sheet for N-Propyl Bromide. Elf 
Atochem, Paris, France, 1997.
Elf Atochem. 1997c. Toxicity Data Sheet for N-Propyl Bromide. Elf 
Atochem, Department de Toxicologie Industrielle, France, 1997.
Fiala, E.; Czerniak, R.; Castonguay, A.; Conaway, C.; Rivenson, A. 
1987. Assay of 1-nitropropane, 2-nitropropane, 1-azoxypropane and 2-
azoxypropane for carcinogenicity by gavage in Sprague-Dawley rats. 
Carcinogenesis 8(12):1947-1949.
George, E; Burlinson, B; Gatehouse, D. 1989. Genotoxicity of 1-and 
2-nitropropane in the rat. Carcinogenesis 10(12):2239-2334.
Goggelmann, W; Bauchinger, M; Kulka, U; Schmid, E. 1988. 
Genotoxicity of 2-nitropropane and 1-nitropropane in Salmonella 
typhimurium and human lymphocytes. Mutagenesis 3(2):137-140.
Griffin, T; Stein, A; Coulston, F. 1982. Inhalation exposure of rats 
to vapors of 1-nitropropane at 100 ppm. Ecotoxicology and 
Environmental Safety 1982, 6, 268-282.
Haas-Jobelius, M; Coulston, F; Korte, F. 1992. Effects of short-term 
inhalation exposure to 1-nitropropane and 2-nitropropane on rat 
liver enzymes. Ecotoxicology and Environmental Safety 23:253-259.
Haseman, J; Lockhart, A. 1994. The relationship between use of the 
maximum tolerated dose and study sensitivity for detecting rodent 
carcinogenicity. Fundamentals of Applied Toxicology 22:382-391.
ICF. 1995a. ``Propyl Bromide.'' Memorandum prepared by ICF 
Incorporated, Washington, DC, for EPA, under Contract No. 68-D5-
0147, Work Assignment No. 0-13 (October 17, 1995)
ICF. 1996a. ``1-Bromopropane ODP Estimate.'' Memorandum prepared by 
ICF Incorporated, Washington, DC, for EPA, under Contract No. 68-D5-
0147, Work Assignment No. 0-13 (January 16, 1996).

[[Page 8047]]

ICF. 1996b. ``Estimated ODPs for Brominated Compounds.'' Memorandum 
prepared by ICF Incorporated, Washington, DC, for EPA, under 
Contract No. 68-D5-0147, Work Assignment No. 1-11 (October 2, 1996).
ICF. 1997a. ``Review of ALBTA1 (1-Bromopropane) Toxicity Study.'' 
Memorandum prepared by ICF Incorporated, Washington, DC, for EPA 
under Contract No. 68-D5-0147, Work Assignment No. 1-11 (April 1, 
1997).
ICF. 1997e. ``Comments on Report `Acceptable Industrial Exposure 
Limit for N-Propyl-Bromide'.'' Memorandum prepared by Dr. Elizabeth 
Weisburger under subcontract with ICF Incorporated, Washington, DC, 
for EPA, under Contract No. 68-D5-0147, Work Assignment No. 1-11 
(July 16, 1997).
ICF. 1998c. ``Review of Japanese Study on 1-Bromopropane and 2-
Bromopropane.'' Memorandum prepared by ICF Incorporated, Washington, 
DC, for EPA, under Contract No. 68-D5-0147, Work Assignment No. 2-09 
(February 16, 1998).
ICF. 1998e. ``Estimating Total Adjusted Chlorine Loading Impact of 
N-Propyl Bromide.'' Memorandum prepared by ICF Incorporated, 
Washington, DC, for EPA, under Contract No. 68-D5-0147, Work 
Assignment No. 2-08 (April 10, 1998).
ICF. 1998h. ``Preliminary Exposure Assessment for N-Propyl-
Bromide.'' Memorandum prepared by ICF Incorporated, Washington, DC, 
for EPA, under Contract No. 68-D5-0147, Work Assignment No. 2-06 
(April 30, 1998).
ICF. 1998k. ``Acceptable Industrial Exposure Limit for N-Propyl-
Bromide.'' Memorandum prepared by ICF Incorporated, Washington, DC, 
for EPA, under Contract No. 68-D5-0147, Work Assignment No. 2-09 
(September 24, 1998).
Ichihara G, Asaeda N, Kumazawa T, Tagawa Y, Kamiuima M, Yu X, Kondo 
H, Nakajima T, Kitoh J, Yu IJ, Moon YH, Hisanaga N, Takeuchi Y. 
1996. Testicular toxicity of 2-bromopropane. J Occup Health 38:205-
206.
Ichihara G, Asaeda N, Kumazawa T, et al. 1997. Testicular and 
hematopoietic toxicity of 2-bromopropane, a substitute for ozone 
layer-depleting chlorofluorocarbons. J Occup Health 39:57-63.
Ichihara M, Takeuchi Y, Shibata E, Kitoh J, et al. 1998. 
Neurotoxicity of 1-Bromopropane. Translated by Albemarle 
Corporation.
Jones, A; Walsh, D. 1979. The oxidative metabolism of 1-bromopropane 
in the rat. Xenobiotica 9(12):763-772.
Kamijima M, Ichihara G, Yu X, et al. 1997a. Disruption in ovarian 
cyclicity due to 2-bromopropane in the rat. J Occup Health 39:3-4.
Kamijima M, Ichihara G, Kitoh J, et al. 1997b. Ovarian toxicity of 
2-bromopropane in the nonpregnant female rat. J Occup Health 39:144-
149.
Khan, S; O'Brien, P. 1991. 1-bromoalkanes as new potent nontoxic 
glutathione depletors in isolated rat hepatocytes. Biochemical and 
Biophysical Research Communications 179(1):436-441.
Kim, HY; Chung, YH; Yi, KH; Kim, JG; Yu, IJ. 1996. LC50 
of 2-bromopropane. Industrial Health 34:403-407.
Kim, Y; Jung, K; Hwang, T; Jung, G; Kim, H; Park, J; Kim, J; Park, 
J; Park, D; Park, S; Choi, K; Moon, Y. 1996. Hematopoeitic and 
reproductive hazards of Korean electronic workers exposed to 
solvents containing 2-bromopropane. Scand J Work Environ Health 
22:387-91.
Kliesch, U; Adler, I. 1987. Micronucleus test in bone marrow of mice 
treated with 1-nitropropane, 2-nitropropane and cisplatin. Mutation 
Research 192:181-184.
Kohl, C; Morgan, P; Gescher, A. 1995. Metabolism of the genotoxicant 
2-nitropropane to a nitric oxide species. Chemico-Biological 
Interactions 97:175-184.
Lag, M; Omichinski, J; Dybing, E; Nelson, S; Soderlund, E. 1994. 
Mutagenic activity of halogenated propanes and propenes: effect of 
bromine and chlorine positioning. Chemico-Biological Interactions 
93:73-84.
Lag, M; Soderlund, E; Omichinski, J; Brunborg, G; Holme, J; Dahl, J; 
Nelson, S; Dybing, E. 1991. Effect of bromine and chlorine 
positioning in the induction of renal and testicular toxicity by 
halogenated propanes. Chem Res Toxicol 4:528-534.
Lee, Y; Buchanan, B; Klopman, G; Dimayuga, M; Rosenkranz, H. 1996. 
The potential of organ specific toxicity for predicting rodent 
carcinogenicity. Mutation Research 358:37-62.
Linhart, I; Gescher, A; Goodwin, B. 1991. Investigation of the 
chemical basis of nitroalkane toxicity: tautomerism and 
decomposition of propane 1-and 2-nitronate under physiological 
conditions. Chemico-Biological Interactions 80:187-201.
Loveday, K; Lugo, M; Resnick, M; Anderson, B; Zeiger, E. 1989. 
Chromosome aberration and sister chromatid exchange tests in Chinese 
hamster ovary cells in vitro: II. results with 20 chemicals. 
Environmental and Molecular Mutagenesis 13:60-94.
Maeng, SH; Yu, IJ. 1997. Mutagenicity of 2-bromopropane. Industrial 
Health 35:87-95.
Oh B, Kaneko H, Sato A. 1998. Effects of 1-BP to the translation of 
beta-amyloid protein in mouse brain comparison between young mouse 
and adult mouse. Translated by Albemarle Corporation.
Ong, J; Kerr, D; Lacey, G; Curtis, D; Hughes, R; Prager, R. 1994. 
Differing actions of nitropropane analogs of GABA and baclofen in 
central and peripheral preparations. European Journal of 
Pharmacology 264:49-54.
Perocco, P; Bolognesi, S; Alberghini, W. 1983. Toxic activity of 
seventeen industrial solvents and halogenated compounds on human 
lymphocytes cultured in vitro. Toxicology Letters 16:69-75.
Ratpan, F; Plaumann, H. 1988. Mutagenicity of halogenated propanes 
and their methylated derivatives. Environmental and Molecular 
Mutagenesis 12:253-259.
Roscher, E; Kyriakoula Z-S; Andrae, U. 1990. Involvement of 
different pathways in the genotoxicity of nitropropanes in cultured 
mammalian cells. Mutagenesis 5(4):375-380.
Rosenkranz, H; Klopman, G. 1990. Prediction of the carcinogenicity 
in rodents of chemicals currently being tested by the US National 
Toxicology Program: structure-activity correlations. Mutagenesis 
5(5):425-432.
Rosenkranz, H; Klopman, G. 1993. Structural evidence for a dichotomy 
in rodent carcinogenesis: Involvement of genetic and cellular 
toxicity. Mutation Research 303:83-89.
Saito-Suzuki, R; Teramoto, S; Shirasu, Y. 1982. Dominant lethal 
studies in rats with 1,2-dibromo-3-chloropropane and its 
structurally related compounds. Mutation Research 101:321-327.
Smith, R.L. 1997. ``Significance of the Japanese presentation on 1-
BP and 2-BP.'' Fax transmission from Robert Smith, Albemarle 
Corporation to EPA, December 29, 1997.
Smith, R.L. 1998. Assessments of occupational exposure to nPB in 
adhesive spray and metal cleaning applications. Written 
communications from Robert Smith, Albemarle Corporation to EPA, 
March 19 through June 26, 1998.
Sodum, R; Soon Shon, O; Nie, G; Fiala, E. 1994. Activation of the 
liver carcinogen 2-nitropropane by aryl sulfotransferase. Chemical 
Research in Toxicology 7:344-351.
Takeuchi, Y; Ichihara, G.; Kamijima, M. 1997. A review of toxicity 
of 2-bromopropane: mainly on its reproductive toxicity. J. Occup 
Health 39:179-191.
World Meteorological Organization. 1994. Scientific Assessment of 
Ozone Depletion: 1994. Global Ozone Research and Monitoring Project, 
Report No. 37. Geneva, Switzerland; World Meteorological 
Organization.
Wuebbles, D.J., A.K. Jain, K.O. Patten, and P.S. Connell. 1997. 
``Evaluation of Ozone Depletion Potentials for chlorobromomethane 
(CH2ClBr) and 1-bromo-propane 
(CH2BrCH2CH2),'' Atmos. Environ., 
32, 107-113.
Wuebbles, D.J., R. Kotamarthi, and K.O. Patten. 1998. ``Updated 
Evaluation of Ozone Depletion Potentials for Chlorobromomethane 
(CH2ClBr) and 1-bromo-propane 
(CH2BrCH2CH2),'' Atmos. Environ., 
in press.


[[Page 8048]]


    Dated: February 10, 1999.
Carol M. Browner,
Administrator.
[FR Doc. 99-3993 Filed 2-17-99; 8:45 am]
BILLING CODE 6560-50-P