[Federal Register Volume 65, Number 51 (Wednesday, March 15, 2000)]
[Notices]
[Pages 14186-14197]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-6397]



[[Page 14185]]

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Part VIII





Environmental Protection Agency





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National Advisory Committee for Acute Exposure Guideline Levels (AEGLs) 
for Hazardous Substances, Proposed AEGL Values; Notice

  Federal Register / Vol. 65, No. 51 / Wednesday, March 15, 2000 / 
Notices  

[[Page 14186]]


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ENVIRONMENTAL PROTECTION AGENCY

[OPPTS-00289; FRL-6492-4]


National Advisory Committee for Acute Exposure Guideline Levels 
(AEGLs) for Hazardous Substances; Proposed AEGL Values

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice and request for comments.

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SUMMARY: The National Advisory Committee for Acute Exposure Guideline 
Levels for Hazardous Substances (NAC/AEGL Committee) is developing AEGL 
values on an ongoing basis to provide Federal, State, and local 
agencies with information on short-term exposures to hazardous 
chemicals. This notice provides ``Proposed'' AEGL values and Executive 
Summaries for 10 chemicals for public review and comment. Comments are 
welcome on both the ``Proposed'' AEGL values in this notice and the 
Technical Support Documents placed in the public version of the 
official record in the TSCA Docket for these 10 chemicals.

DATES: Comments, identified by the docket control number OPPTS-00289, 
must be received by EPA on or before April 14, 2000.

ADDRESSES: Comments may be submitted by mail, electronically, or in 
person. Please follow the detailed instructions for each method as 
provided in Unit I. of the ``SUPPLEMENTARY INFORMATION.'' To ensure 
proper receipt by EPA, it is imperative that you identify docket 
control number OPPTS-00289 in the subject line on the first page of 
your response.

FOR FURTHER INFORMATION CONTACT: For general information contact: 
Joseph S. Carra, Deputy Director, Office of Pollution Prevention and 
Toxics (7401), Environmental Protection Agency, Ariel Rios Bldg., 1200 
Pennsylvania Ave., NW., Washington, DC 20460; telephone numbers: (202) 
554-1404 and TDD: (202) 554-055; e-mail address: [email protected].
    For technical information contact: Paul S. Tobin, Designated 
Federal Officer (DFO), Office of Pollution Prevention and Toxics 
(7406), Environmental Protection Agency, Ariel Rios Bldg., 1200 
Pennsylvania Ave., NW., Washington, DC 20460; telephone number: (202) 
260-1736; e-mail address: [email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    This action is directed to the general public to provide an 
opportunity for review and comment on ``Proposed'' AEGL values and 
their supporting scientific rationale. This action may be of particular 
interest to anyone who may be affected if the AEGL values are adopted 
by government agencies for emergency planning, prevention, or response 
programs, such as EPA's Risk Management Program under the Clean Air Act 
and Amendments Section 112r. It is possible that other Federal agencies 
besides EPA, as well as State and local agencies and private 
organizations, may adopt the AEGL values for their programs. As such, 
the Agency has not attempted to describe all the specific entities that 
may be affected by this action. If you have any questions regarding the 
applicability of this action to a particular entity, consult the DFO 
listed under ``FOR FURTHER INFORMATION CONTACT.''

B. How Can I Get Additional Information, Including Copies of this 
Document or Other Related Documents?

    1. Electronically. You may obtain electronic copies of this 
document, and certain other related documents that might be available 
electronically, from the EPA Internet Home Page at http://www.epa.gov/. 
To access this document, on the Home Page select ``Laws and 
Regulations'' and then look up the entry for this document under the 
``Federal Register--Environmental Documents.'' You can also go directly 
to the Federal Register listings at http://www.epa.gov/fedrgstr/.
    2. In person. The Agency has established an official record for 
this action under docket control number OPPTS-00289. The official 
record consists of the documents specifically referenced in this 
action, any public comments received during an applicable comment 
period, and other information related to this action, including any 
information claimed as Confidential Business Information (CBI). This 
official record includes the documents that are physically located in 
the docket, as well as the documents that are referenced in those 
documents. The public version of the official record does not include 
any information claimed as CBI. The public version of the official 
record, which includes printed, paper versions of any electronic 
comments submitted during an applicable comment period, is available 
for inspection in the TSCA Nonconfidential Information Center, North 
East Mall Rm. B-607, Waterside Mall, 401 M St., SW., Washington, DC. 
The Center is open from noon to 4 p.m., Monday through Friday, 
excluding legal holidays. The telephone number of the Center is (202) 
260-7099.
    3. Fax-on-Demand. Using a faxphone call (202) 401-0527 and select 
item 4800 for an index of items in this category. For a more specific 
item number, see the table in Unit III.

C. How and to Whom Do I Submit Comments?

    You may submit comments through the mail, in person, or 
electronically. To ensure proper receipt by EPA, it is imperative that 
you identify docket control number OPPTS-00289 in the subject line on 
the first page of your response.
    1. By mail. Submit your comments to: Document Control Office 
(7407), Office of Pollution Prevention and Toxics (OPPT), Environmental 
Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., 
Washington, DC 20460.
    2. In person or by courier. Deliver your comments to: OPPT Document 
Control Office (DCO) in East Tower Rm. G-099, Waterside Mall, 401 M 
St., SW., Washington, DC. The DCO is open from 8 a.m. to 4 p.m., Monday 
through Friday, excluding legal holidays. The telephone number for the 
DCO is (202) 260-7093.
    3. Electronically. You may submit your comments electronically by 
e-mail to: ``[email protected],'' or mail your computer disk to the 
address identified above. Do not submit any information electronically 
that you consider to be CBI. Electronic comments must be submitted as 
an ASCII file avoiding the use of special characters and any form of 
encryption. Comments and data will also be accepted on standard disks 
in WordPerfect 6.1/8.1 or ASCII file format. All comments in electronic 
form must be identified by docket control number OPPTS-00289. 
Electronic comments may also be filed online at many Federal Depository 
Libraries

D. How Should I Handle CBI That I Want to Submit to the Agency?

    Do not submit any information electronically that you consider to 
be CBI. You may claim information that you submit to EPA in response to 
this document as CBI by marking any part or all of that information as 
CBI. Information so marked will not be disclosed except in accordance 
with procedures set forth in 40 CFR part 2. In addition to one complete 
version of the comment that includes any information claimed as CBI, a 
copy of the comment that does not contain the information claimed as 
CBI must be

[[Page 14187]]

submitted for inclusion in the public version of the official record. 
Information not marked confidential will be included in the public 
version of the official record without prior notice. If you have any 
questions about CBI or the procedures for claiming CBI, please consult 
the technical person identified under ``FOR FURTHER INFORMATION 
CONTACT.''

E. What Should I Consider as I Prepare My Comments for EPA?

    You may find the following suggestions helpful for preparing your 
comments:
    1. Explain your views as clearly as possible.
    2. Describe any assumptions that you used.
    3. Provide copies of any technical information and/or data you used 
that support your views.
    4. If you estimate potential burden or costs, explain how you 
arrived at the estimate that you provide.
    5. Provide specific examples to illustrate your concerns.
    6. Offer alternative ways to improve the proposed rule or 
collection activity.
    7. Make sure to submit your comments by the deadline in this 
document.
    8. To ensure proper receipt by EPA, be sure to identify the docket 
control number assigned to this action in the subject line on the first 
page of your response. You may also provide the name, date, and Federal 
Register citation.

II. Background

    Since its first meeting on June 19-21, 1996, the NAC/AEGL Committee 
has been evaluating scientific data and developing ``Proposed'' AEGLs 
for 76 of the first 85 priority chemicals initially scheduled for 
development of AEGL values. This first list of 85 chemicals was 
published in the Federal Register of May 21, 1997 (62 FR 27733-27734) 
(FRL-5718-9). EPA published the first ``Proposed'' AEGL values for 12 
chemicals from the initial priority list in the Federal Register of 
October 30, 1997 (62 FR 58839-58851) (FRL-5737-3) in order to provide 
an opportunity for public review and comment. That Federal Register 
notice also provides the AEGL Program's history and development 
process. Since then, the NAC/AEGL Committee continues to develop AEGL 
values for other chemicals from the initial priority list and continues 
to establish greater consistency in the procedures and methodologies 
used in their development. Additionally, the NAC/AEGL Committee has 
expanded the number of exposure periods to include AEGL values for 10 
minute exposure periods to cover a wider range of potential exposures 
to hazarous chemicals. The NAC/AEGL Committee plans to publish 
``Proposed'' AEGL values for 10 minute exposure periods for other 
chemicals on the priority list of 85 in groups of approximately 10 to 
20 chemicals in future Federal Register notices.
    The NAC/AEGL Committee will review and consider all public comments 
received on this notice, with revisions to the ``Proposed'' AEGL 
values, as appropriate. The resulting AEGL values will be established 
as ``Interim'' AEGL values and will be forwarded to the National 
Research Council, National Academy of Sciences (NRC/NAS), for review 
and comment. The ``Final'' AEGL values will be published under the 
auspices of the NRC/NAS following concurrence on the values and the 
scientific rationale used in their development.

III. 10 Chemicals for Public Notice and Comment

A. Fax-On-Demand Table

 
----------------------------------------------------------------------------------------------------------------
                 CAS No.                                 Chemical name                  Fax-On-Demand item no.
----------------------------------------------------------------------------------------------------------------
71-55-6                                    1,1,1-Trichloroethane                       4937
74-90-8                                    Hydrogen cyanide                            4858
156-59-2                                  Cis-1,2-Dichloroethylene                     4895
156-60-5                                  Trans-1,2-Dichloroethylene                   4895
505-60-2                                   Agent HD (sulfur mustard)                   4936
811-97-2                                   HFC-134a (1,1,1,2-tetrafluoroethane)        4899
1717-00-6                                  HCFC-141b (1,1-dichloro-1-fluoroethane)     4902
7664-39-3                                  Hydrogen fluoride                           4909
7783-06-4                                  Hydrogen sulfide                           4917
106602-80-6                               Otto Fuel II (main component propylene       4935
                                           glycol dinitrate; CAS No. 6423-43-4)
----------------------------------------------------------------------------------------------------------------

B. Executive Summaries

    1. Cis-1,2-Dichloroethylene and 2. Trans-1,2-Dichloroethylene--i. 
Description. 1,2-Dichloroethylene is a flammable, colorless liquid 
existing in both cis- and trans-forms and as a mixture of these two 
isomers. It has been used as an intermediate in the production of 
chlorinated solvents and as a low-temperature extraction solvent for 
decaffeinated coffee, dyes, perfumes, lacquers, and thermoplastics. The 
compound is a narcotic. Data on narcosis in humans, cats, rats, and 
mice, and systemic effects in cats, rats, and mice were available for 
development of AEGLs. The data were considered adequate for derivation 
of the three AEGL classifications.
    The AEGL-1 was based on a human exposure concentration of 825 parts 
per million (ppm) trans-1,2-dichloroethene for 5 minutes (Lehmann and 
Schmidt-Kehl 1936). This concentration is a no-effect-level for eye 
irritation. Because the mechanism of irritation is not expected to 
differ greatly among individuals (including sensitive individuals), 
this value was divided by an uncertainty factor (UF) of 3 to protect 
sensitive individuals. This UF of 3 was applied for AEGL-1 values for 
both the cis- and trans-isomers. Since animal data suggest that the 
cis-isomer is approximately twice as toxic as the trans-isomer, a 
modifying factor of 2 was applied in the derivation of the cis-isomer 
values only. The same value was applied across the 10- and 30-minute 
and 1-, 4-, and 8-hour exposure time points since mild irritantancy is 
a threshold effect and generally does not vary greatly over time. Thus, 
prolonged exposure will not result in an enhanced effect.
    The AEGL-2 for the 4- and 8-hour time points was based on narcosis 
observed in pregnant rats exposed to 6,000 ppm of the trans-isomer for 
6 hours (Hurtt et al., 1993). Uncertainty factors of 3 each (total UF = 
10) were applied for both inter- and intraspecies differences because 
the endpoint,

[[Page 14188]]

narcosis, is unlikely to vary greatly among individuals or species. 
This total UF of 10 was applied for AEGL-2 values for both the cis- and 
trans-isomers. The concentration-exposure time relationship for many 
irritant and systemically acting vapors and gases may be described by 
Cn x t = k, where the exponent, n, ranges from 0.8 to 3.5 
(ten Berge et al., 1986). To obtain protective AEGL values in the 
absence of an empirically derived chemical-specific scaling exponent, a 
conservative approach to temporal scaling was performed using n = 3 
when extrapolating to shorter time points and n = 1 when extrapolating 
to longer time points using the Cn x t = k equation. The 
AEGL-2 for the 10- and 30-minute and 1-hour time points was set as a 
ceiling based on a plateau for anesthetic effects in humans (Lehman and 
Schmidt-Kehl, 1936). Since data suggest that the cis-isomer is 
approximately twice as toxic as the trans-isomer, a modifying factor of 
2 was applied in the derivation of the cis-isomer values only.
    The AEGL-3 for the 4- and 8-hour time points was based on a 4-hour 
no-effect-level for death in rats of 12,300 ppm trans-1,2-
dichloroethene (Kelly, 1999). Uncertainty factors of 3 each (total UF = 
10) were applied for both inter- and intraspecies differences. Rat and 
mouse lethality data indicate little species variability with regard to 
death. This total UF of 10 was applied for AEGL-3 values for both the 
cis- and trans-isomers. The concentration-exposure time relationship 
for many irritant and systemically acting vapors and gases may be 
described by Cn x t = k, where the exponent, n, ranges from 
0.8 to 3.5 (ten Berge et al., 1986). To obtain protective AEGL values 
in the absence of an empirically derived chemical-specific scaling 
exponent, a conservative approach to temporal scaling was performed 
using n = 3 when extrapolating to shorter time points and n = 1 when 
extrapolating to longer time points using the Cn x t = k 
equation. The AEGL-3 for the 10- and 30-minute and 1-hour time points 
was set as a ceiling based on a plateau for intracranial pressure, 
nausea, and severe dizziness in humans (Lehman and Schmidt-Kehl, 1936). 
Since data suggest that the cis-isomer is approximately twice as toxic 
as the trans-isomer, a modifying factor of 2 was applied in the 
derivation of the cis-isomer values only.
    The calculated values are listed in the tables below.

                              Summary of Proposed AEGL Values for Trans-1,2-Dichloroethene [ppm (mg/m3 (milligram/meter3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
AEGL-1 (Nondisabling)             280 (1,109)         280 (1,109]         280 (1,109)         280 (1,109)         280 (1,109)         Ocular irritation
                                                                                                                                      in humans (Lehman
                                                                                                                                      and Schmidt-Kehl,
                                                                                                                                      1936)
AEGL-2 (Disabling)                1,000 (3,960)       1,000 (3,960)       1,000 (3,960)       690 (2,724)         450 (1,782)        Narcosis in rats: 4-
                                                                                                                                       and 8-hour (Hurtt
                                                                                                                                      et al., 1993);
                                                                                                                                      Anesthetic effects
                                                                                                                                      in humans (Lehman
                                                                                                                                      and Schmidt-Kehl,
                                                                                                                                      1936)
AEG L-3 (Lethality)               1,700 (6,732)       1,700 (6,732)       1,700 (6,732)       1,200 (4,752)       620 (2,455)         No-effect-level
                                                                                                                                      for death in rats:
                                                                                                                                      4- and 8-hour
                                                                                                                                      (Kelly, 1999);
                                                                                                                                      Nausea,
                                                                                                                                      intracranial
                                                                                                                                      pressure, and
                                                                                                                                      dizziness in
                                                                                                                                      humans (Lehman and
                                                                                                                                      Schmidt-Kehl,
                                                                                                                                      1936)
--------------------------------------------------------------------------------------------------------------------------------------------------------


                                        Summary of Proposed AEGL Values for Cis-1,2-Dichloroethene [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
AEGL-1 (Nondisabling)             140 (554)           140 (554)           140 (554)           140 (554)           140 (554)           Ocular irritation
                                                                                                                                      in humans (Lehman
                                                                                                                                      and Schmidt-Kehl,
                                                                                                                                      1936)
AEGL-2 (Disabling)                500 (1,980)         500 (1,980)         500 (1,980)         340 (1,346)         230 (911)           Narcosis in rats:
                                                                                                                                      4- and 8-hour
                                                                                                                                      (Hurtt et al.,
                                                                                                                                      1993); Anesthetic
                                                                                                                                      effects in humans
                                                                                                                                      (Lehman and
                                                                                                                                      Schmidt-Kehl,
                                                                                                                                      1936)
AEGL-3 (Lethality)                850 (3,366)         850 (3,366)         850 (3,366)         620 (2,455)         310 (1,228)         No-effect-level
                                                                                                                                      for death in rats:
                                                                                                                                      4- and 8-hour
                                                                                                                                      (Kelly, 1999);
                                                                                                                                      Nausea,
                                                                                                                                      intracranial
                                                                                                                                      pressure, and
                                                                                                                                      dizziness in
                                                                                                                                      humans (Lehman and
                                                                                                                                      Schmidt-Kehl,
                                                                                                                                      1936)
--------------------------------------------------------------------------------------------------------------------------------------------------------

    ii. References.
    Hurtt, M.E., Valentine, R., and Alvarez, L. 1993. Developmental 
toxicity of inhaled trans-1,2-dichloroethylene in the rat. Fundamental 
and Applied Toxicology. 20:225-230.
    Kelly, D. P. 1999. Trans-1,2-dichloroethylene and cis-1,2-
dichloroethylene: Inhalation median lethal concentration 
(LC50) study in rats. E.I. du Pont de Nemours and Company, 
Haskell Laboratory for Toxicology and Industrial Medicine, Newark, DE. 
Laboratory Project ID: DuPont-2806.
    Lehman, K.B. and Schmidt-Kehl, L. 1936. The thirteen most important 
chlorinated aliphatic hydrocarbons from the standpoint of industrial 
hygiene. Archiv Fuer Hygiene und Bakteriologie. 116:9-268.
    ten Berge, W.F., Zwart, A., and Appelman, L.M. 1986. Concentration-
time mortality response relationship of irritant and systemically 
acting vapours and gases. Journal of Hazardous Materials. 13:301-309.
    3. Agent HD (sulfur mustard)--i. Description. Sulfur mustard (Agent 
HD) is an alkylating chemical vesicant developed as a warfare agent 
that affects any epithelial surface it contacts. The active component 
is bis(2-chloroethyl)sulfide (CAS No. 505-60-2). Although the chemical 
is a liquid at ordinary ambient temperatures, its volatility results in 
rapid generation of vapors with a garlic-like odor. Due to its low 
aqueous solubility, it is persistent in the environment. Odor 
thresholds of 1 mg-min/m3 (milligram-minute/meter) and 0.6 
mg/m3 have been reported.
    Exposure to sulfur mustard vapor may result in irritation and 
damage to the eyes, respiratory tract, and skin. The toxic effects of 
sulfur mustard are temperature and humidity dependent; for a given 
exposure, the effects may be greater with increasing temperature and 
humidity. An exposure-dependent latency period of hours to days is 
documented for the toxic effects of sulfur mustard and is relevant for 
all routes of exposure but may be less for

[[Page 14189]]

ocular and upper respiratory tract effects than for dermal and systemic 
responses. Both human and animal data indicate that the eyes are the 
most sensitive organ/tissue although deaths resulting from sulfur 
mustard exposure are likely the result of respiratory tract 
involvement. Because the toxic effects of sulfur mustard (at least for 
short-time periods) appear to be a linear function of exposure duration 
and exposure concentration, most of the available exposure-response 
data are expressed as cumulative exposures (Ct).
    Minor ocular irritation (conjunctival injection in the absence of 
irritation) is reported to occur in humans following exposures to 12-30 
mg-min/m3 and more severe effects at 60-75 mg-min/
m3 (conjunctivitis, irritation, photophobia) and 100 mg-min/
m3 (severe ocular irritation). Exposure estimates for human 
lethality range from 900-1,500 mg-min/m3.
    Animal lethality following acute exposure to sulfur mustard occurs 
at cumulative exposures ranging from approximately 600-1,500 mg-min/
m3. Nonlethal effects were similar to those observed in 
humans and included effects on the eyes, respiratory tract, and skin. 
Long-term exposure of dogs, rats, and guinea pigs to concentrations of 
0.03 mg/m3 produced only minor signs of ocular and 
respiratory tract irritation. 1-hour exposure of mice to concentrations 
up to 16.9 mg/m3 resulted in notable but not serious effects 
on respiratory parameters and acute exposures of rabbits (20 minutes to 
12 hours) to concentrations ranging from 58-389 mg/m3 (Ct 
2,300 mg-min/m3) resulted in severe respiratory 
tract damage.
    Because exposure-response data were unavailable for all of the 
AEGL-specific exposure durations, temporal extrapolation was used in 
the development of AEGL values for the AEGL-specific time periods. The 
concentration-exposure time relationship for many irritant and 
systemically acting vapors and gases may be described by Cn 
x t = k, where the exponent n ranges from 0.8 to 3.5 (ten Berge, 1986). 
Analysis of available data regarding AEGL-1 type effects reported by 
Reed (1918), Reed et al. (1918), Guild et al. (1941), and Anderson 
(1942) indicate that, for exposure periods up to several hours, the 
concentration-exposure time relationship is a near-linear function 
(i.e., Haber's Law where n = 1 for Cn x t = k) as shown by n 
values of 1.11 and 0.96 for various data sets analyzed that were 
consistent with AEGL-1 effects. Therefore, an empirically derived, 
chemical-specific estimate of n = 1 was used for derivation of most of 
the AEGL values rather than a default value based upon the ten Berge 
(1986) analysis. Due to uncertainty regarding linear extrapolation to a 
time duration notably shorter than that for which empirically derived 
lethality data were available, the 10-minute AEGL-3 values utilized 
exponential time scaling where n was 3.
    The AEGL-1 values were based upon data from Anderson (1942) who 
found that an exposure concentration-time product of 12 mg-min/
m3 represented a threshold for ocular effects (conjunctival 
injection and minor discomfort with no functional decrement) in human 
volunteers acutely exposed to sulfur mustard. An UF adjustment was 
limited to a factor of 3 for protection of sensitive individuals. This 
adjustment was considered appropriate for acute exposures to chemicals 
whose mechanism of action primarily involves surface contact irritation 
of ocular and/or respiratory tract tissue rather than systemic activity 
that involves absorption and distribution of the parent chemical or a 
biotransformation product to a target tissue. Anderson (1942) noted 
that there was little variability in the ocular responses among the 
subjects in his study, thereby providing additional justification for 
the intraspecies UF of 3.
    The AEGL-2 values for sulfur mustard were also developed using the 
data from Anderson (1942). Anderson reported that a Ct value of 
approximately 60 mg-min/m3 represented the lowest 
concentration-time product for which ocular effects could be 
characterized as military casualties. The 60 mg-min/m3 
exposure was used as the basis for developing the AEGL-2 values because 
it represented an acute exposure causing an effect severe enough to 
impair escape and, although not irreversible, would certainly result in 
potential for additional injury. Anderson (1942) characterized the 60 
mg-min/m3 Ct as representing the lower margin of the 
concentration-effect zone that would result in ineffective military 
performance (necessary to complete a mission), and that may require 
treatment for up to 1 week. The ocular irritation and damage were also 
considered appropriate as a threshold estimate for AEGL-2 effects 
because the eyes are generally considered the most sensitive indicator 
of sulfur mustard exposure and would likely occur in the absence of 
vesication effects and severe pulmonary effects. The fact that the 
AEGL-2 is based upon human data precludes the use of an interspecies 
UF. A factor of 3 was applied for intraspecies variability (protection 
of sensitive populations). This factor was limited to three under the 
assumption that the primary mechanism of action of sulfur mustard 
involves a direct effect on the ocular surface and that this response 
will not vary greatly among individuals. Anderson also noted little 
variability in the ocular responses among the subjects in his study. A 
modifying factor of 3 was applied to accommodate potential onset of 
long-term ocular or respiratory effects. This was justified by the fact 
that there was no long-term follow-up reported by Anderson with which 
to confirm or deny the development of permanent ocular or respiratory 
tract damage. The total uncertainty/modifying factor adjustment was 10 
[The total adjustment is 10 because the factors of 3 each represent a 
logarithmic mean (3.16) of 10, therefore 3.16 x 3.16 = 10].
    For development of the AEGL-3, a 1-hour exposure of mice to 21.2 
mg/m3 was used as an estimated lethality threshold (Kumar 
and Vijayaraghavan, 1998). This value is also near the lower bound of 
the 95% confidence interval for the 1-hour mouse LC50 of 
42.5 mg/m3 reported by Vijayaraghavan (1997). An UF for 
intraspecies variability of 3 was used because the lethality resulting 
from acute inhalation exposure to sulfur mustard appears to be a 
function of pulmonary damage resulting from direct contact of the agent 
with epithelial surfaces and would not likely exhibit an order-of-
magnitude variability among individuals. An UF of 3 was also applied to 
account for possible interspecies variability in the lethal response to 
sulfur mustard. The resulting total UF adjustment was 10. The modifying 
factor of 3 utilized for AEGL-2 development to account for 
uncertainties regarding the latency and persistence of the irritant 
effects of low-level exposure to sulfur mustard was not applied for 
AEGL-3 because lethality of the mice was assessed at 14 days post 
exposure in a study by Vijayaraghavan (1997). Application of any 
additional UFs or modifying factors was not warranted because the 
proposed AEGL-3 values are equivalent to exposures in humans that are 
known to produce only ocular and respiratory tract irritation.
    The AEGL values for sulfur mustard are based upon noncancer 
endpoints. Sulfur mustard is genotoxic and has induced carcinogenic 
responses in humans following single high exposures and following 
multiple exposures that were sufficient to produce adverse effects. 
Carcinogenic responses, however, are not known to occur with 
asymptomatic exposures. Limitations on the currently available data do 
not allow for a definitive quantitative cancer risk

[[Page 14190]]

assessment, especially for an acute, once-in-a-lifetime, exposure.
    The AEGL-1 and AEGL-2 values are based upon human exposure data and 
are considered to be defensible estimates for exposures representing 
thresholds for the respective AEGL effect levels. The ocular irritation 
upon which the AEGL-1 and AEGL-2 values are based is the most sensitive 
response to sulfur mustard vapor. The AEGL-3 values provide Ct products 
(approximately 60-130 mg-min/m3) that are known to cause 
only moderate to severe ocular irritation and possible respiratory 
tract irritation in human subjects but not life- threatening health 
effects or death. Although, the overall database for acute inhalation 
exposure to sulfur mustard is not extensive, the AEGL values appear to 
be supported by the available data and in some cases, similar values 
obtained using somewhat differing approaches.

                                            Summary of Proposed AEGL Values for Sulfur Mustard [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
AEGL-1 (Nondisabling)            0.06 (0.40)         0.02 (0.13)         0.01 (0.067)        0.003 (0.017)       0.001 (0.008)       Conjunctival
                                                                                                                                      injection and
                                                                                                                                      minor discomfort
                                                                                                                                      with no functional
                                                                                                                                      decrement in human
                                                                                                                                      volunteers
                                                                                                                                      (Anderson, 1942)
AEGL-2 (Disabling)               0.09 (0.60)          0.03 (0.20)        0.02 (0.10)         0.004 (0.025)       0.002 (0.013)       Well marked,
                                                                                                                                      generalized
                                                                                                                                      conjunctivitis,
                                                                                                                                      edema,
                                                                                                                                      photophobia, and
                                                                                                                                      eye irritation in
                                                                                                                                      human volunteers
                                                                                                                                      (Anderson, 1942)
AEGL-3 (Lethality)               0.91 (6.1)          0.63 (4.2)          0.32 (2.1)          0.08 (0.53)         0.04 (0.27)         Lethality estimate
                                                                                                                                      in mice (Kumar and
                                                                                                                                      Vijayaraghavan,
                                                                                                                                      1998)
--------------------------------------------------------------------------------------------------------------------------------------------------------

    ii. References.
    Anderson, J.S. 1942. The effect of mustard gas vapour on eyes under 
Indian hot weather conditions. CDRE Report No. 241. Chemical Defense 
Research Establishment (India).
    Guild, W.J., Harrison, K.P., Fairly, A., and Childs, A.E. 1941. The 
effect of mustard gas vapour on the eyes. Porton Report No. 2297, 
Serial No. 12. November 8, 1941.
    Kumar, O. and Vjayaraghavan, R. 1998. Effect of sulphur mustard 
inhalation exposure on some urinary variables in mice. Journal of 
Applied Toxicology. 18:257-259.
    Reed, C.I. 1918. The minimum concentration of mustard gas effective 
for man. Preliminary Report. Report 318. War Department, Medical 
Division, Chemical Warfare Section, Pharmacological Research Section, 
American University Experiment Station. October 26, 1918.
    Reed, C.I., Hopkins, E.F., and Weyand, C.F. 1918. The minimum 
concentration of mustard gas effective for man. Final Report. Report 
329. War Department, Medical Division, Chemical Warfare Section, 
Pharmacological Research Section, American University Experiment 
Station. December 2, 1918.
    ten Berge, W.F. 1986. Concentration-time mortality response 
relationship of irritant and systemically acting vapours and gases. 
Journal of Hazardous Materials. 13:301-309.
    Vijayaraghavan, R. 1997. Modifications of breathing pattern induced 
by inhaled sulphur mustard in mice. Archives of Toxicology. 71:157-164.
    4. HCFC-141b (1,1-dichloro-1-fluoroethane) or 
hydrochlorofluorocarbon-141b--i. Description. 1,1-Dichloro-1-
fluoroethane has been developed as a replacement for fully halogenated 
chlorofluorocarbons as its residence time in the atmosphere is shorter 
and its ozone depleting potential is lower than that of presently used 
chlorofluorocarbons. HCFC-141b may be used in the production of rigid 
polyurethane and polyisocyanurate or phenolic insulation foams for 
residential and commercial buildings. It may also be used as a solvent 
in electronic and other precision cleaning applications.
    HCFC-141b is of low inhalation toxicity. Its effects have been 
studied with human subjects and several animal species including the 
monkey, dog, rat, mouse, and rabbit. In addition, studies addressing 
repeated and chronic exposures, genotoxicity, carcinogenicity, 
neurotoxicity, and cardiac sensitization were also available. At high 
concentrations, halogenated hydrocarbons may produce cardiac 
arrhythmias; this sensitive endpoint was considered in development of 
AEGL values.
    Adequate data were available for development of the three AEGL 
classifications. Inadequate data were available for determination of 
the relationship between concentration and exposure duration for a 
fixed effect. However, based on the rapidity with which blood 
concentrations in humans approached equilibrium, the similarity in 
lethality values in rats exposed for 4 or 6 hours, and the fact that 
the cardiac sensitization effect is based on a concentration threshold 
rather than exposure duration, all AEGL values were flat-lined across 
time. The fact that some experimental exposure durations in both human 
and animal studies were generally long, 4 to 6 hours, lends confidence 
to flat-lining the values for the shorter exposure durations.
    The AEGL-1 value was based on the observation that exercising human 
subjects could tolerate exposure to concentrations of 500 or 1,000 ppm 
for 4 hours with no effects on lung functions, respiratory symptoms, 
irritation of the eyes, or cardiac symptoms (Utell et al., 1997). 
Results of exposures of two subjects for an additional 2 hours to the 
500 ppm concentration and one of the subjects to the 1,000 ppm 
concentration for an additional 2 hours did not indicate a clear effect 
on neurobehavioral parameters. Because the 4- or 6-hour 1,000 ppm 
concentration is a no-observed-effect-level (NOEL), there were no 
indications of response differences among tested subjects, and animal 
studies indicate that adverse effects occur only at considerably higher 
concentrations, the value was not adjusted by an UF to protect 
sensitive individuals. Because blood concentrations of HCFC-141b 
rapidly approached equilibrium and did not greatly increase after 55 
minutes of exposure, the value of 1,000 ppm was used for all time 
periods.
    The AEGL-2 value was based on the lowest concentration that caused 
cardiac sensitization in dogs exposed to HCFC-141b for 10 minutes 
(Mullin, 1977). This value of 5,200 ppm is far below the lowest 
concentrations that caused death from cardiac fibrillation (10,000 ppm 
in this study and 20,000 ppm in a similar study [Hardy et al., 1989a]). 
Because the cardiac sensitization test is supersensitive as the 
response to epinephrine is optimized (the epinephrine dose is greater 
than the physiological level in stressed animals by up to a factor of 
10), a single

[[Page 14191]]

intraspecies UF of 3 was applied to protect sensitive individuals. 
Cardiac sensitization is concentration dependent; duration of exposure 
did not influence the concentration at which this effect occurred. 
Using the reasoning that the concentration is the determining factor in 
cardiac sensitization and exposure duration is of lesser importance, 
the resulting value of 1,700 ppm is proposed for all time periods.
    The AEGL-3 values were based on the concentration of 9,000 ppm, the 
highest value that resulted in mild to marked cardiac responses but did 
not cause death in a cardiac sensitization study with the dog (Hardy et 
al., 1989a). Because the cardiac sensitization test is supersensitive 
as the response to epinephrine is optimized, a single intraspecies UF 
of 3 was applied to protect sensitive individuals. Using the reasoning 
that the concentration is the determining factor in cardiac 
sensitization and exposure duration is of lesser importance, the 
resulting value of 3,000 ppm is proposed for all time periods.
    Based on the extensive database involving both human and animal 
exposures and use of the most sensitive endpoint in the studies, 
confidence in the AEGL values is high. Values are summarized in the 
table below.

                             Summary Table of Proposed AEGL Values for HCFC-141b (1,1-Dichloro-1-fluoroethane) [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
AEGL-1 (Nondisabling)            1,000 (4,850)       1,000 (4,850)       1,000 (4,850)       1,000 (4,850)       1,000 (4,850)       No effect-humans
                                                                                                                                      (Utell et al.,
                                                                                                                                      1997)
AEGL-2 (Disabling)               1,700 (8,245)       1,700 (8,245)       1,700 (8,245)       1,700 (8,245)       1,700 (8,245)       Threshold for
                                                                                                                                      cardiac
                                                                                                                                      arrhythmia--dog\1\
                                                                                                                                      (Mullin, 1977)
AEGL-3 (Lethality)               3,000 (14,550)      3,000 (14,550)      3,000 (14,550)      3,000 (14,550)      3,000 (14,550)      Threshold for
                                                                                                                                      severe cardiac
                                                                                                                                      response--dog\1\
                                                                                                                                      (Hardy et al.,
                                                                                                                                      1989a)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Response to challenge dose of epinephrine (cardiac sensitization test).

    ii. References.
    Hardy, J.C., Sharman, I.J., and Chanter, D.O. 1989a. Assessment of 
cardiac sensitization potential in dogs and monkeys. Comparison of I-
141b and F11. PWT 86/89437, Huntingdon Research Centre Ltd., 
Huntingdon, Cambridgeshire, England.
    Mullin, L.S. 1977. Cardiac sensitisation. Haskell Laboratory Report 
957-77, E.I. du Pont de Nemours and Co., Newark, DE.
    Utell, M.J., Anders, M.W., and Morrow, P.E. 1997. Clinical 
inhalation studies with HCFC-141b. Final Report: December 4, 1997. MA-
RR-97-2406, Departments of Medicine, Environmental Medicine, and 
Pharmacology and Physiology, University of Rochester Medical Center, 
Rochester, NY.
    5. HFC-134a (1,1,1,2-tetrafluoroethane) or hydrofluorocarbon-134a--
i. Description. 1,1,1,2-Tetrafluoroethane has been developed as a 
replacement for fully halogenated chlorofluorocarbons because its 
residence time in the atmosphere is shorter and its ozone depleting 
potential is insignificant. HFC-134a may be used in refrigeration and 
air conditioning systems, as a blowing agent for polyurethane foams, 
and as a propellant for medical aerosols. Yearly production is 
estimated at 175,000 tons.
    HFC-134a has a very low acute inhalation toxicity. Its acute 
inhalation effects have been studied with human subjects and several 
animal species including the monkey, dog, rat, and mouse. In addition, 
studies addressing repeated and chronic exposures, genotoxicity, 
carcinogenicity, neurotoxicity, and cardiac sensitization were also 
available. At high concentrations, halogenated hydrocarbons may produce 
cardiac arrhythmias; this sensitive endpoint was considered in 
development of AEGL values.
    Adequate data were available for development of the three AEGL 
classifications. Inadequate data were available for determination of 
the relationship between concentration and time for a fixed effect. 
Based on the observations that:
    a. Blood concentrations in humans rapidly approach equilibrium with 
negligible metabolism and tissue uptake.
    b. The endpoint of cardiac sensitization is a blood concentration-
related threshold phenomenon, derived values for each AEGL 
classification were flat-lined across time.
    The AEGL-1 concentration was based on a 1-hour no-effect 
concentration of 8,000 ppm in human subjects (Emmen and Hoogendijk, 
1998). This concentration was without effects on lung functions, 
respiratory parameters, the eyes (irritation), or the heart (cardiac 
symptoms). Because this concentration is considerably below that 
causing any effect in animal studies, no intraspecies UF was applied. 
Based on the fact that blood concentrations in this study appeared to 
be approaching equilibrium following 55 minutes of exposure and effects 
are determined by blood concentrations, the value of 8,000 ppm was used 
across all time periods.
    The AEGL-2 concentration was based on the no-effect concentration 
of 40,000 ppm for cardiac sensitization in dogs (Hardy et al., 1991). 
Because the cardiac sensitization test is supersensitive as the 
response to epinephrine is optimized (the epinephrine dose is greater 
than the physiological level in stressed animals by up to a factor of 
10), a single intraspecies UF of 3 was applied to protect sensitive 
individuals. Cardiac sensitization is concentration dependent; duration 
of exposure does not influence the concentration at which this effect 
occurs. Using the reasoning that the concentration is the determining 
factor in cardiac sensitization and exposure duration is of lesser 
importance, the resulting value of 13,000 ppm is proposed for all time 
periods.
    The AEGL-3 concentration was based on the concentration of 80,000 
which caused marked cardiac effects but no deaths in dogs (Hardy et 
al., 1991). Because the cardiac sensitization test is supersensitive as 
the response to epinephrine is optimized (the epinephrine dose is 
greater than the physiological level in stressed animals by up to a 
factor of 10), a single intraspecies UF of 3 was applied to protect 
sensitive individuals. Cardiac sensitization is concentration 
dependent; duration of exposure does not influence the concentration at 
which this effect occurs. Using the reasoning that the concentration is 
the determining factor in cardiac sensitization and exposure duration 
is of lesser importance, the resulting value of 27,000 ppm is proposed 
for all time periods.
    Based on the extensive database involving both human and animal

[[Page 14192]]

exposures and use of the most sensitive endpoint in the studies, 
confidence in the AEGL values is high. Values are summarized in the 
table below.

                              Summary Table of Proposed AEGL Values for HFC-134a (1,1,1,2-Tetrafluoroethane) [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1 (Nondisabling)            8,000 (34,000)      8,000 (34,000)      8,000 (34,000)      8,000 (34,000)      8,000 (34,000)      No effects--humans
                                                                                                                                      (Emmen and
                                                                                                                                      Hoogendijk, 1998)
 AEGL-2 (Disabling)               13,000 (55,250)     13,000 (55,250)     13,000 (55,250)     13,000 (55,250)     13,000 (55,250)     No effect, cardiac
                                                                                                                                      sensitization--dog
                                                                                                                                      s (Hardy et al.,
                                                                                                                                      1991)
 AEGL-3 (Lethality)               27,000 (114,750)    27,000 (114,750)    27,000 (114,750)    27,000 (114,750)    27,000 (114,750)    Marked effect,
                                                                                                                                      cardiac
                                                                                                                                      sensitization--dog
                                                                                                                                      s (Hardy et al.,
                                                                                                                                      1991)
--------------------------------------------------------------------------------------------------------------------------------------------------------

    ii. References.
    Emmen, H.H. and Hoogendijk, E.M.G. 1998. Report on an ascending 
dose safety study comparing HFA-134a with CFC-12 and air, administered 
by whole-body exposure to healthy volunteers. MA-250B-82-306, TNO 
Report V98.754, The Netherlands Organization Nutrition and Food 
Research Institute, Zeist, The Netherlands.
    Hardy, C.J., Sharman, I.J., and Clark, G.C. 1991. Assessment of 
cardiac sensitisation potential in dogs: Comparison of HFA 134a and 
A12. Report No. CTL/C/2521. Huntingdon Research Centre, Huntingdon, 
Cambridgeshire, U.K.
    6. Hydrogen cyanide (HCN)--i. Description. Hydrogen cyanide is a 
colorless, rapidly acting, highly poisonous gas or liquid having an 
odor of bitter almonds. Most HCN is used as an intermediate at the site 
of production. Major uses include the manufacture of nylons, plastics, 
and fumigants; it is also used in electroplating and mining. Exposures 
to HCN may occur in industrial situations as well as from cigarette 
smoke, combustion products, and naturally occurring cyanide compounds 
in foods.
    HCN is a systemic poison; toxicity is due to inhibition of 
cytochrome oxidase which prevents cellular utilization of oxygen. Lack 
of oxygen supply to the brain results in loss of consciousness, 
respiratory arrest, and, ultimately, death. Stimulation of the 
chemoreceptors of the carotid and aortic bodies produces a brief period 
of hyperpnea; cardiac irregularities may also occur. These mechanisms 
of action are the same for all species.
    Inhalation studies resulting in sublethal effects such as 
incapacitation and changes in respiratory and cardiac parameters were 
described for the monkey, rat, and mouse; lethality studies were 
available for the rat, mouse, and rabbit. Exposure durations ranged 
from a few seconds to 24 hours. Regression analyses of the exposure 
duration-concentration relationships for both incapacitation and 
lethality for the monkey determined that the relationship is 
C2 x t = k and that the relationship for lethality (based on 
rat data) is C2.6 x t = k. Although human exposures have 
occurred, no reliable data on exposure concentrations were available.
    The AEGL-1 was not determined because serious effects may occur at 
concentrations below those causing irritation or notable discomfort. In 
addition, the onset of serious effects is very rapid.
    The AEGL-2 was based on a concentration of 60 ppm for 30 minutes 
which resulted in a slight depressive effect on the central nervous 
system of monkeys as evidenced by changes in electroencephalograms; 
there was no physiological response (Purser, 1984; Purser et al., 
1984). The mechanism of action of HCN is the same for all mammalian 
species, but the rapidity of the toxic effect may be related to 
relative respiration rates as well as pharmacokinetic considerations. 
The monkey is an appropriate model for extrapolation to humans as the 
respiratory systems of monkeys and humans are similar. Because the 
monkey is an appropriate model and the mechanism of action of HCN is 
the same for all species, an interspecies UF of 2 was applied. Humans 
may differ in their sensitivity to HCN but no data regarding specific 
differences were located in the available literature. Therefore, an 
intraspecies UF of 3 was applied. The 30-minute concentration of 60 ppm 
was divided by a combined interspecies and intraspecies UF of 6 and 
scaled across time for the AEGL specified exposure periods using the 
relationship C2 x t = k. The safety of the 10- and 30-minute 
values are supported by monitoring studies in which concentrations of 
10-15 ppm produced central nervous system effects in some workers.
    The rat provided the only data set for calculation of 
LC01 values for different time periods (E.I. du Pont de 
Nemours and Company, 1981). The LC01 values were considered 
the threshold for lethality and were used as the basis for deriving 
AEGL-3 values. The mouse, rat, and rabbit were equally sensitive to the 
lethal effects of HCN as determined by similar LC50 values 
for the same time periods. In an earlier study, times to death for 
several animal species showed that mice and rats may be slightly more 
sensitive to HCN than monkeys (and presumably humans). The differences 
in sensitivity were attributed, at least partially, to the more rapid 
respiratory rate of the rodent species. Because LC50 values 
for several species were within a factor of 1.5 of each other, an 
interspecies UF of 2 was applied. Humans may differ in their 
sensitivity to HCN but no data regarding specific differences were 
located in the available literature. Therefore, an intraspecies UF of 3 
was applied to protect sensitive individuals. The 15- and 30-minute and 
1-hour LC01 values, 138, 127, and 88 ppm, respectively, were 
divided by a total UF of 6. The 15-minute value was time scaled to 10 
minutes to derive the 10-minute AEGL-3, the 30-minute LC01 
was used for the 30-minute AEGL-3 value, and the 60-minute 
LC01 was used to calculate the 1-, 4-, and 8-hour AEGL-3 
concentrations. For the AEGL-3 values, scaling across time utilized the 
lethal concentration-exposure duration relationship for the rat, 
C2.6 x t = k.
    The proposed values appear in the table below.

[[Page 14193]]



                                           Summary of Proposed AEGL Values for Hydrogen Cyanide [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour               8-hour           (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1 (Nondisabling)            NA\1\               NA                  NA                  NA                  NA                  Serious effects
                                                                                                                                      may occur below
                                                                                                                                      detectable
                                                                                                                                      concentrations or
                                                                                                                                      concentrations
                                                                                                                                      causing discomfort
 AEGL-2 (Disabling)               17 (19)             10 (11)             7.1 (7.8)           3.5 (3.9)           2.5 (2.8)           Slight central
                                                                                                                                      nervous system
                                                                                                                                      depression--monkey
                                                                                                                                      (Purser, 1984)
 AEGL-3 (Lethality)               27 (30)             21 (23)             15 (17)             8.6 (9.7)           6.6 (7.3)           Lethality (LC01)--
                                                                                                                                      rat (E.I. du Pont
                                                                                                                                      de Nemours, 1981)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Not appropriate.

    ii. References.
    E.I. du Pont de Nemours and Company. 1981. Inhalation Toxicity of 
Common Combustion Gases. Haskell Laboratory Report No. 238-81. Haskell 
Laboratory, Newark, DE.
    Purser, D.A. 1984. A bioassay model for testing the incapacitating 
effects of exposure to combustion product atmospheres using cynomolgus 
monkeys. Journal of Fire Sciences. 2:20-36.
    Purser, D.A., Grimshaw, P., and Berrill, K.R. 1984. Intoxication by 
cyanide in fires: A study in monkeys using polyacrylonitrile. Archives 
of Environmental Health. 39:394-400.
    7. Hydrogen fluoride (HF)--i. Description. Hydrogen fluoride is a 
colorless, highly irritating and corrosive gas. Reaction with water is 
rapid, producing heat and hydrofluoric acid. Hydrogen fluoride is used 
in the manufacture of artificial cryolite; in the production of 
aluminum, fluorocarbons, and uranium hexafluoride; as a catalyst in 
alkylation processes in petroleum refining; in the manufacture of 
fluoride salts; and in stainless steel pickling operations. It is also 
used to etch glass and as a cleaner in metal finishing processes.
    Hydrogen fluoride is a severe irritant to the eyes, skin, and nasal 
passages; high concentrations may penetrate to the lungs resulting in 
edema and hemorrhage. Data on irritant effects in humans and lethal and 
sublethal effects in six species of mammals (monkey, dog, rat, mouse, 
guinea pig, and rabbit) were available for development of AEGLs. The 
data were considered adequate for derivation of the three AEGL 
classifications for five exposure periods. Regression analyses of the 
reported concentration-exposure durations for lethality for the animal 
species determined that the relationship between concentration and time 
is C2 x t = k.
    The AEGL-1 values were based on the observation that human 
volunteers could tolerate exposure to a concentration of 2 ppm for 6 
hours with only mild irritation of the eyes, skin, and upper 
respiratory tract (Largent, 1960, 1961). This concentration was 
adjusted by an UF of 3 to protect sensitive individuals and scaled to 
the 30-minute and 1-, 4-, and 8-hour exposure durations using 
C2 x t = k. The factor of 3 was selected because hydrogen 
fluoride reacts chemically with the tissues of the respiratory tract; 
the adverse effects are unlikely to differ among individuals. The 
resulting derived values, 2.3, 1.6, 0.82, and 0.58 ppm, were rounded to 
the nearest whole integers of 2.0, 2.0, 1.0, and 1.0, respectively, by 
the NAC/AEGL Committee. Because irritant properties would not change 
greatly between the 10-minute and 30-minute time frames, the 10-minute 
AEGL-1 was set at the same value of 2.0 ppm as the 30-minute AEGL-1.
    The 10-minute AEGL-2 value was based on an absence of serious 
pulmonary or other adverse effects in rats during direct delivery of HF 
to the trachea for an exposure period of 10 minutes (Dalbey, 1996; 
Dalbey et al., 1998). This reported concentration-exposure value of 950 
ppm for 10 minutes was adjusted by a combined UF of 10: 3 for 
interspecies variation since the rat was not the most sensitive species 
in other studies (but direct delivery to the trachea is a sensitive 
model) and an intraspecies UF of 3 since HF reacts chemically and 
indiscriminately with the tissues of the respiratory tract and adverse 
effects are unlikely to differ among individuals.
    The 30-minute and the 1-, 4- and 8-hour AEGL-2 values were based on 
a study in which dogs exposed to 243 ppm for 1 hour showed signs of 
more than mild irritation, including blinking, sneezing, and coughing 
(Rosenholtz et al., 1963). The 1-hour value of 243 ppm was adjusted by 
a total UF of 10: 3 for intraspecies variation since the dog is a 
sensitive species for sensory irritation and 3 for intraspecies 
variation since HF reacts chemically and indiscriminately with the 
tissues of the respiratory tract and effects are unlikely to differ 
among individuals. The values were scaled across time using 
C2 x t = k where the value of n = 2 was derived from 
concentration: Exposure duration relationships based on lethality.
    The 10-minute AEGL-3 value was based on the reported 10-minute 
lethal threshold in orally cannulated rats of 1,764 ppm (Dalbey, 1996; 
Dalbey et al., 1998). This value was rounded down to 1,700 ppm and 
adjusted by UFs of 3 for interspecies differences (LC50 
values differ by a factor of approximately 2-4 between the mouse and 
rat) and 3 for intraspecies differences since HF reacts chemically and 
indiscriminately with tissues of the respiratory tract and effects are 
unlikely to differ among individuals. The total adjustment for UFs for 
the 10-minute AEGL-3 value was 10.
    The 30-minute and the 1-, 4-, and 8-hour AEGL-3 values were derived 
from a reported 1-hour exposure resulting in no deaths in mice 
(Wohlslagel et al., 1976). The data indicated that the value of 263 ppm 
was the threshold for lethality. A comparison of LC50 values 
among species in several studies determined that the mouse was the most 
sensitive species in lethality studies. The 1-hour value of 263 ppm was 
adjusted by an interspecies UF of 1 since the mouse was the most 
sensitive species and intraspecies UF of 3 since HF reacts chemically 
and indiscriminately with tissues of the respiratory tract and effects 
are unlikely to differ among individuals. A modifying factor of 2 was 
applied to account for the steepness of the lethal dose-response curve 
and the value was scaled to the other AEGL-specified exposure periods 
using a value of n = 2.
    Based on the extensive database involving both human and animal 
exposures (six species of mammals) for various exposure durations, 
confidence in the AEGL values is high. Values are summarized in the 
table below.

[[Page 14194]]



                                        Summary of Proposed AEGL Values for Hydrogen Fluoride (HF) [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1 (Nondisabling)            2 (1.6)             2 (1.6)             2 (1.6)             1 (0.8)             1 (0.8)             Irritation in
                                                                                                                                      humans (Largent,
                                                                                                                                      1960; 1961)
 AEGL-2 (Disabling)               95 (78)             34 (28)             24 (20)             12 (9.8)            8.6 (7.0)           NOAEL for lung
                                                                                                                                      effects in
                                                                                                                                      cannulated rats
                                                                                                                                      (Dalbey, 1996;
                                                                                                                                      Dalbey et al.,
                                                                                                                                      1998);\1\ sensory
                                                                                                                                      irritation in dogs
                                                                                                                                      (Rosenholtz et
                                                                                                                                      al., 1963)\2\
 AEGL-3 (Lethality)               170 (139)           62 (51)             44 (36)             22 (18)             15 (12)             Lethality
                                                                                                                                      threshold in
                                                                                                                                      cannulated rats
                                                                                                                                      (Dalbey, 1996;
                                                                                                                                      Dalbey et al.,
                                                                                                                                      1998);\3\
                                                                                                                                     Lethality threshold
                                                                                                                                      in mice
                                                                                                                                      (Wohlslagel et
                                                                                                                                      al., 1976)\4\
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ 10-minute AEGL-2 value.
\2\ 30-minute and 1-, 4-, and 8-hour AEGL-2 values.
\3\ 10-minute AEGL-3 value.
\4\ 30-minute and 1-, 4-, and 8-hour AEGL-3 values.

    ii. References.
    Dalbey, W. 1996. Evaluation of the toxicity of hydrogen fluoride at 
short exposure times. Petroleum Environmental Research Forum Project 
92-09, performed at Stonybrook Laboratories Inc., Pennington, NJ.
    Dalbey, W., Dunn, B., Bannister, R., Daughtrey, W., Kirwin, C., 
Reitman, F., Steiner, A., and Bruce, J. 1998. Acute effects of 10-
minute exposure to hydrogen fluoride in rats and derivation of a short-
term exposure limit for humans. Regulatory Toxicology and Pharmacology. 
27:207-216.
    Largent, E.J. 1960. The metabolism of fluorides in man. American 
Medical Association Archives of Industrial Health. 21:318-323.
    Largent, E.J. 1961. Fluorosis: The Health Aspects of Fluorine 
Compounds. Ohio State University Press, Columbus, OH.
    Rosenholtz, M.J., Carson, T.R., Weeks, M.H., Wilinski, F., Ford, 
D.F., and Oberst, F.W. 1963. A toxicopathologic study in animals after 
brief single exposures to hydrogen fluoride. American Industrial 
Hygiene Association Journal. 24:253-261.
    Wohlslagel, J., DiPasquale, L.C., and Vernot, E.H. 1976. Toxicity 
of solid rocket motor exhaust: Effects of HCl, HF, and alumina on 
rodents. Journal of Combustion Toxicology. 3:61-69.
    8. Hydrogen sulfide (H2S)--i. Description. The AEGL-1 
was based on persistent odors, eye and throat irritation, headache, and 
nausea in six workers exposed to a mean concentration of 0.09 ppm 
H2S for approximately 5 hours in a monitoring van downwind 
from an oil refinery (TNRCC, 1998). An UF of 3 was applied to account 
for intraspecies variability since minor irritation is not likely to 
vary greatly between individuals. The value was flat-lined across the 
10- and 30-minute and 1-, 4-, and 8-hour exposure time points. The 
flat-lining approach was considered appropriate since mild irritant 
effects generally do not vary greatly over time.
    The AEGL-2 was based on focal areas of perivascular edema and an 
increase in protein and lactic acid dehydrogenase (LDH) in 
bronchioalveolar lavage fluid in rats exposed to 200 ppm hydrogen 
sulfide for 4 hours (Green et al., 1991; Khan et al., 1991). An UF of 3 
was used to extrapolate from animals to humans since rat and mouse data 
suggest little interspecies variability. An UF of 3 was also applied to 
account for sensitive individuals since data suggest little strain 
variability of hydrogen sulfide toxicity among rats (total UF = 10). 
The 4-hour experimental value was then scaled to the 10- and 30-minutes 
and 1- and 8-hour time points, using C4.36 x t = k. The 
exponent of 4.36 was derived from rat lethality data ranging from 10-
minutes to 6-hour exposure duration.
    The AEGL-3 was based on a 1-hour no-effect-level for death in rats 
(504 ppm) (MacEwen and Vernot, 1972). An UF of 3 was used to 
extrapolate from animals to humans since rat and mouse data suggest 
little interspecies variability. An UF of 3 was also applied to account 
for sensitive individuals since data suggest little strain variability 
of hydrogen sulfide toxicity among rats (total UF = 10). The value was 
then scaled to the 10- and 30-minutes and 1-, 4-, and 8-hour time 
points, using C4.36 x t = k. The exponent of 4.36 was 
derived from rat lethality data ranging from 10 minutes to 6 hours 
exposure duration.
    The calculated values are listed in the table below.

                                           Summary of Proposed AEGL Values for Hydrogen Sulfide [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1 (Nondisabling)            0.03 (0.04)         0.03 (0.04)         0.03 (0.04)         0.03 (0.04)         0.03 (0.04)         Persistent odor,
                                                                                                                                      eye, and throat
                                                                                                                                      irritation,
                                                                                                                                      headache, nausea
                                                                                                                                      (TNRCC, 1998)
 AEGL-2 (Disabling)               42 (59)             32 (45)             28 (39)             20 (28)             17 (24)             Perivascular
                                                                                                                                      edema, increased
                                                                                                                                      protein, and LDH
                                                                                                                                      in lavage fluid in
                                                                                                                                      rats (Green et
                                                                                                                                      al., 1991; Khan et
                                                                                                                                      al., 1991)
 AEGL-3 (Lethality)               76 (106)            60 (85)             50 (71)             37 (52)             31 (44)            1 hour no-effect-
                                                                                                                                      level for death in
                                                                                                                                      rats (MacEwen and
                                                                                                                                      Vernot, 1972)
--------------------------------------------------------------------------------------------------------------------------------------------------------

    ii. References.
    Green, F. H. Y., Schurch, S., and DeSanctis, G. T., et al. 1991. 
Effects of hydrogen sulfide exposure on surface properties of lung 
surfactant. Journal of Applied Physiology. 70:1943-1949.
    Khan, A. A., Yong, S., and Prior, M. G., et al. 1991. Cytotoxic 
effects of hydrogen sulfide on pulmonary alveolar macrophages in rats. 
Journal of Toxicology and Environmental Health. 33:57-64.
    MacEwen, J. D. and Vernot, E. H. 1972. Toxic Hazards Research Unit 
Annual Report. Aerospace Medical Research Laboratory, Air Force Systems 
Command, Wright-Patterson Air Force Base, Ohio. Report No. ARML-TR-72-
62. pp. 66-69.

[[Page 14195]]

    TNRCC (Texas Natural Resources Conservation Commission). 1998. Memo 
from Tim Doty to JoAnn Wiersma. Corpus Christi Mobile Laboratory Trip, 
January 31-February 6, 1998; Real-Time Gas Chromatography and Composite 
Sampling, Sulfur Dioxide, Hydrogen Sulfide, and Impinger Sampling. 
April 20, 1998.
    9. Otto Fuel II (main component propylene glycol dinitrate; CAS No. 
6423-43-4)--i. Description. Otto Fuel II, a liquid propellant used 
exclusively by the U.S. Navy in torpedoes and other weapon systems, is 
a mixture of three synthetic compounds: 1,2-Propylene glycol dinitrate 
(PGDN), which is a nitrate ester explosive, dibutyl sebacate (a 
desensitizer), and 2-nitrodiphenylamine (a stabilizer). The primary 
component and the one responsible for the toxicity of Otto Fuel II is 
PGDN, a volatile liquid with a disagreeable odor. Because PGDN is the 
primary and most toxic component of Otto Fuel II and because only PGDN 
is relatively volatile compared with the other components, AEGLs have 
been derived in terms of PGDN with the notation that the values are 
appropriate for Otto Fuel II.
    PGDN is a systemic toxicant with effects on the cardiovascular and 
central nervous systems. Its vasodilatory action results in headaches 
during human exposures. Symptoms of dizziness, loss of balance, nasal 
congestion, eye irritation, palpitations, and chest pains have also 
been reported. Methemoglobinemia has been reported at the high 
concentrations used in studies with animals.
    Few data were available that met the definitions of AEGL endpoints. 
One inhalation study with 20 human subjects described effects of 
headaches and slight loss of balance at exposure concentrations of 0.1 
to 1.5 ppm for exposure durations up to 8 hours (Stewart et al., 1974). 
Acute exposure of monkeys to concentrations of 70-100 ppm for 6 hours 
resulted in severe signs of toxicity including convulsions but no 
deaths (Jones et al., 1972). In the same study, exposure of rats to a 
higher concentration (#199 ppm for 4 hours) resulted in no toxic signs. 
Examination of the relationship between exposure duration and 
concentration for both mild and severe headaches in humans over periods 
of time of 1 to 8 hours determined that the relationship is 
C1 x t = k.
    The AEGL-1 values were based on concentrations of 0.5 ppm and 0.1 
ppm which were the thresholds for mild headaches at exposure durations 
of 1 and 6 hours, respectively (Stewart et al., 1974). This effect can 
be considered the threshold for mild discomfort (only one subject was 
affected at each exposure) which falls within the definition of an 
AEGL-1. The 0.5 ppm concentration was used to derive the 30-minutes and 
1-hour AEGL-1 values and the 0.1 ppm concentration was used for the 4- 
and 8-hour values. Because the time and concentration values were based 
on the most sensitive subject, these concentrations were adjusted by an 
UF of 3 to account for additional differences in human sensitivity and 
scaled to the appropriate time periods using the C1 x t = k 
relationship. An UF of 3 was considered sufficient as no susceptible 
populations were identified (the headache effect is the same as that 
experienced by heart patients medicated with nitroglycerin for angina 
and these concentrations are far below those inducing methemoglobinemia 
in infants); the vasodilatory effects of PGDN, responsible for the 
headaches, are not expected to vary greatly among individuals. The 10-
minute AEGL-1 value was made equal to the 30-minute value.
    The AEGL-2 values were based on a concentration of 0.5 ppm which 
caused severe headaches accompanied by dizziness in one subject and 
slight loss of equilibrium in two subjects in one of several sensitive 
equilibrium tests after 6 hours of exposure (Stewart et al., 1974). 
This concentration-exposure duration was considered the threshold for 
impaired inability to escape as defined by the AEGL-2. The 0.5 ppm 
concentration was adjusted by an intraspecies UF of 3 to protect 
sensitive individuals and scaled across time using the C1 x 
t = k relationship as for the AEGL-1 in Unit III.B.9.
    The AEGL-3 values were based on the exposure of squirrel monkeys to 
concentrations of 70-100 ppm for 6 hours which resulted in vomiting, 
pallor, cold extremities, semiconscousness, and clonic convulsions; 
these signs disappeared upon removal from the exposure chamber (Jones 
et al., 1972). The lower concentration, 70 ppm, was adjusted by a total 
UF of 10. An interspecies UF of 3 was chosen because both the monkey 
and human subjects showed changes in electrical activity of the brain 
at similar PGDN concentrations, the threshold for central nervous 
system depressants does not vary widely among mammalian species, and 
the monkey is an appropriate model for extrapolation to humans. An 
intraspecies UF of 3 was chosen because the threshold for central 
nervous system depression also does not vary greatly among individuals. 
Because the endpoint for the AEGL-3 values is different than the 
endpoint for the AEGLs-1 and -2 and no data on the relationship between 
concentration and exposure duration is available for the endpoint of 
central nervous system depression, the more conservative values of n = 
3 and n = 1 were used to scale from 6 hours to the shorter- and longer-
time periods, respectively.
    The proposed values appear in the table below.

                                             Summary of Proposed AEGL Values for Otto Fuel II [ppm (mg/m3)]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1\a\ (Nondisabling)         0.33 (2.3)          0.33 (2.3)          0.17 (1.1)          0.05 (0.34)         0.03 (0.17)         Mild headaches in
                                                                                                                                      humans (Stewart et
                                                                                                                                      al., 1974)
 AEGL-2 (Disabling)               6.0 (43)            2.0 (14)            1.0 (6.8)           0.25 (1.7)          0.13 (0.8)          Severe headaches
                                                                                                                                      and slight
                                                                                                                                      imbalance in
                                                                                                                                      humans (Stewart et
                                                                                                                                      al., 1974)
 AEGL-3 (Lethality)               23 (165)            16 (114)            13 (93)             8.0 (57)            5.3 (38)            Convulsions in
                                                                                                                                      monkeys (Jones et
                                                                                                                                      al., 1972)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\a\ The distinctive odor of PGDN will be noticeable to most individuals at the 0.33 and 0.17 ppm concentrations.

    ii. References.
    Jones, R.A., Strickland, J.A., and Siegel, J. 1972. Toxicity of 
propylene glycol 1,2-dinitrate in experimental animals. Toxicology and 
Applied Pharmacology. 22:128-137.
    Stewart, R.D., Peterson, J.E., Newton, P.E., Hake, C.L., Hosko, 
M.J., Lebrun, A. J., and Lawton, G.M. 1974. Experimental human exposure 
to propylene glycol dinitrate. Toxicology and Applied Pharmacology. 
30:377-395.
    10. 1,1,1-Trichloroethane--i. Description. 1,1,1-Trichloroethane is 
a colorless, nonflammable liquid used primarily as an industrial metal 
degreasing agent. It is also used as a solvent for adhesives, inks, and 
coatings

[[Page 14196]]

and as an aerosol propellant (Nolan et al., 1984). Solvent vapor is 
readily absorbed from the respiratory tract and distributed throughout 
the body, accumulating in tissues with high lipid content. In both 
humans and animals, the primary response to acute inhalation exposures 
involve effects on the central nervous system (CNS). This chemical is 
arrhythmogenic and there is some evidence that it produces transient 
hepatotoxicity (Mcleod et al., 1987; Stahl et al., 1969; Hodgson et 
al., 1989). It has little effect on other organs and does not seem to 
be a developmental toxin although reliable epidemiological data for 
humans are unavailable. 1,1,1-Trichloroethane does not seem to have 
carcinogenic activity based on the available animal studies. A 
considerable amount of human and animal data are available for 
derivation of AEGLs. Rat ataxia and lethality data were used for the 
regression analyses of the concentration-exposure durations. The 
relationship between time and concentration was Cn x t = k, 
where n = 3.3 or 3.
    The AEGL-1 was based on consistent complaints of eye irritation and 
slight dizziness experienced by humans in an atmosphere controlled 
setting with exposures of 450 ppm for two 4-hour sessions separated by 
a 1.5-hour interval (Salvini et al., 1971). Stewart et al., 1969, 
exposed human subjects to time-weighted average (TWA) concentration of 
500 ppm for 7 hour repeatedly for 5 days, the only consistent complaint 
was mild sleepiness and failure of the Romberg test by two of the 
subjects which had trouble with this test initially. Torkelson et al. 
(1958) reported a NOAEL for the Romberg test in humans after exposure 
to a TWA of 506 ppm for 7.5 hour. For derivation of the AEGL-1, the 
observations of Salvini et al. (1971) were used as the starting point 
for the threshold of eye irritation and very subtle CNS effects in 
humans at a concentration of 450 ppm for 4 hour. An UF of 2 was chosen 
based on the observation that the severity of the eye irritation did 
not increase with time and the threshold for mild CNS effects does not 
vary by more than two-three fold which should be protective of 
sensitive individuals. The resulting figure of 230 ppm was used at all 
time points based on the information reported by Salvini et al. (1971) 
indicating that this exposure represented a threshold for these effects 
and the severity did not increase with duration of exposure.
    The AEGL-2 was based on more serious CNS effects which might impede 
escape. Mullin and Krivanek (1982) calculated EC50 values 
for ataxia in rats at 30-minute and 1-, 2-, and 4-hour exposures to be 
6,740; 6,000; 4,240; and 3,780 ppm. These values were used as the basis 
for AEGL-2 derivation using an UF of 10 and extrapolations were made to 
the 10-minute and 8-hour time points using the equation Cn x 
t = k, where n = 3.3 based on the data presented by Mullin and Krivanek 
(1982). An UF of 10 was applied which includes a factor of 3 to account 
for sensitive individuals and a factor of 3 for interspecies 
extrapolation. These UFs were based on the two-three fold variation of 
minimum alveolar concentration for anesthesia (MAC) values among humans 
and the similarities in toxicity, metabolism, and excretion of 1,1,1-
trichloroethane in rats compared to humans. The resulting 
concentrations are similar to the concentration exposure durations 
applied in experimental human studies which resulting in effects that 
could impede escape, i.e., CNS intoxication.
    The AEGL-3 values were derived from a lethality concentration-
effect curve in the rat for a 6-hour exposure duration (Bonnet et al., 
1980). The LC0 was conservatively estimated from this curve 
as a concentration of about 7,000 ppm for a 6-hour exposure duration. 
An extrapolation was made to the 30-minute and 1-, 4-, and 8-hour time 
points using the equation Cn x t = k, where n = 3 based on 
the rat lethality data. An UF of 10 was applied. An intraspecies factor 
of 3 was used to account for sensitive individuals based on the two-
three fold variation of MAC values observed among humans and an 
interspecies factor of 3 was used because of the similarities in 
toxicity, metabolism, and excretion of 1,1,1-trichloroethane in rats 
compared to humans. The resulting concentrations were multiplied by a 
modifying factor of 3 in order to achieve a reasonable concentration at 
which humans might experience life-threatening toxic effects. This 
factor is justified by the existence of a higher blood: Air partition 
coefficient for rats compared to humans. This principle determines the 
relative blood concentration for a vapor and because it is higher for 
rats, a higher blood concentration is achieved.
    The proposed values appear in the table below.

                                        Summary of Proposed AEGL Values for 1,1,1-Trichloroethane [ppm (mg/m3 )]
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                                                                           Endpoint
         Classification                10-min.             30-min.             1-hour              4-hour              8-hour            (Reference)
--------------------------------------------------------------------------------------------------------------------------------------------------------
 AEGL-1 (Nondisabling)            230 (1,252)         230 (1,252)         230 (1,252)         230 (1,252)         230 (1,252)         Eye irritation and
                                                                                                                                      slight dizziness
                                                                                                                                      in humans observed
                                                                                                                                      (Salvini et al.,
                                                                                                                                      1971)
 AEGL-2 (Disabling)               930 (5,064)         670 (3,650)         600 (3,270)         380 (2,070)         310 (1,688)         EC50 for ataxia in
                                                                                                                                      rats (Mullin and
                                                                                                                                      Krivanek, 1982)
 AEGL-3 (Lethality)               4,800\1\ (26,135)   4,800 (26,135)      3,800 (20,690)      2,400 (13,067)      1,900 (10,345)      LC0 extrapolated
                                                                                                                                      (Bonnet et al.,
                                                                                                                                      1980)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\The 30-minute value was used as the 10-minute value so as not to exceed the threshold for cardiac sensitization observed in dogs (Reinhardt et al.,
  1973).

    ii. References.
    Bonnet, P., Francin, J.M., Gradiski, D., Raoult, G., and Zissu, D. 
1980. Determination of the median lethal concentration of principle 
chlorinated aliphatic hydrocarbons in the rat Archives des Maladies 
Professionelles. 41:317-321.
    Mullin, L.S. and Krivanek, N.D. 1982. Comparison of unconditioned 
avoidance tests in rats exposed by inhalation to carbon monoxide, 
1,1,1-trichloroethane, and toluene or ethanol. Neurotoxicology. 1:126-
137.
    Reinhardt, C.F., Mullin, L.S., and Maxfield, M.E. 1973. 
Epinephrine-induced cardiac arrhythmia potential of some common 
industrial solvents. Journal of Occupational Medicine. 15(12):953-955.
    Salvini, M. S. and Binaschi, M. Riva. 1971. Evaluation of the 
psychophysiological functions in humans exposed to the threshold limit 
value of 1,1,1-trichloroethane. British Journal of Industrial Medicine. 
28(3):286-292.

List of Subjects

    Environmental protection, Hazardous substances.


[[Page 14197]]


    Dated: March 8, 2000.
Susan H. Wayland,
Deputy Assistant Administrator for Prevention, Pesticides and Toxic 
Substances.
[FR Doc. 00-6397 Filed 3-14-00; 8:45 am]
BILLING CODE 6560-50-F