[Federal Register Volume 86, Number 231 (Monday, December 6, 2021)]
[Notices]
[Page 69029]
[FR Doc No: 2021-26378]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. AC21-153-000]

Notice of Filing; Pacific Gas and Electric Company

    Take notice that on November 22, 2021, Pacific Gas and Electric
Company (PG&E) submitted a response to the Chief Accountant of the
Federal Energy Regulatory Commission (Commission or FERC) regarding its
Tower Coating Program.
    Any person desiring to intervene or to protest this filing must
file in accordance with Rules 211 and 214 of the Commission's Rules of
Practice and Procedure (18 CFR 385.211 and 385.214). Protests will be
considered by the Commission in determining the appropriate action to
be taken, but will not serve to make protestants parties to the
proceeding. Any person wishing to become a party must file a notice of
intervention or motion to intervene, as appropriate. Such notices,
motions, or protests must be filed on or before the comment date.
Anyone filing a motion to intervene or protest must serve a copy of
that document on the Applicant. On or before the comment date, it is
not necessary to serve motions to intervene or protests on persons
other than the Applicant.
    In addition to publishing the full text of this document in the
Federal Register, the Commission provides all interested persons an
opportunity to view and/or print the contents of this document via the
internet through the Commission's Home Page (http://ferc.gov) using the
``eLibrary'' link. Enter the docket number excluding the last three
digits in the docket number field to access the document. At this time,
the Commission has suspended access to the Commission's Public
Reference Room, due to the proclamation declaring a National Emergency
concerning the Novel Coronavirus Disease (COVID-19), issued by the
President on March 13, 2020. For assistance, contact FERC at
[email protected] or call toll-free,<PHONE_NUMBER> or TYY,
(202) 502-8659.
    The Commission strongly encourages electronic filings of comments,
protests and interventions in lieu of paper using the ``eFiling'' link
at http://www.ferc.gov. Persons unable to file electronically may mail
similar pleadings to the Federal Energy Regulatory Commission, 888
First Street NE, Washington, DC 20426. Hand delivered submissions in
docketed proceedings should be delivered to Health and Human Services,
12225 Wilkins Avenue, Rockville, Maryland 20852.
    Comment Date: 5:00 p.m. Eastern Time on December 13, 2021.

    Dated: November 30, 2021.
Kimberly D. Bose,
Secretary.
[FR Doc. 2021-26378 Filed 12-3-21; 8:45 am]
BILLING CODE 6717-01-P


[Federal Register Volume 76, Number 249 (Wednesday, December 28, 2011)]
[Rules and Regulations]
[Pages 81360-81362]
[FR Doc No: 2011-33281]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

14 CFR Part 25

[Docket No. FAA-2011-1172: Special Conditions No. 25-453-SC]

Special Conditions: Gulfstream Aerospace LP (GALP) Model G280
Airplane, Operation Without Normal Electrical Power

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Final special conditions.

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SUMMARY: These special conditions are issued for the Gulfstream
Aerospace LP (GALP) Model G280 airplane. This airplane will have a
novel or unusual design feature associated with operation without
normal electrical power. The applicable airworthiness regulations do
not contain adequate or appropriate safety standards for this design
feature. These special conditions contain the additional safety
standards that the Administrator considers necessary to establish a
level of safety equivalent to that established by the existing
airworthiness standards.

DATES: Effective Date: The effective date of these special conditions
is December 20, 2011.

FOR FURTHER INFORMATION CONTACT: Nazih Khaouly, Transport Airplane
Directorate, Aircraft Certification Service, 1601 Lind Avenue SW.,
Renton, Washington 98057-3356; telephone<PHONE_NUMBER>; facsimile
(425) 227-1149.

SUPPLEMENTARY INFORMATION:

Background

    On March 30, 2006, GALP applied for a type certificate for their
new Model G280 airplane. The Model G280 will have a novel or unusual
design feature associated with operation without normal electrical
power.

Type Certification Basis

    Under the provisions of Title 14, Code of Federal Regulations (14
CFR) 21.17, GALP must show that the Model G280 airplane meets the
applicable provisions of part 25 as amended by Amendments 25-1 through
25-117.
    If the Administrator finds that the applicable airworthiness
regulations (i.e., 14 CFR part 25) do not contain adequate or
appropriate safety standards for the Model G280 airplane because of a
novel or unusual design feature, special conditions are prescribed
under the provisions of Sec.  21.16.
    Special conditions are initially applicable to the model for which
they

are issued. Should the type certificate for that model be amended later
to include any other model that incorporates the same novel or unusual
design feature, the special conditions would also apply to the other
model.
    In addition to the applicable airworthiness regulations and special
conditions, the Model G280 airplane must comply with the fuel-vent and
exhaust-emission requirements of part 34 and the noise-certification
requirements of part 36; and the FAA must issue a finding of regulatory
adequacy under Sec.  611 of Public Law 92-574, the ``Noise Control Act
of 1972.''
    The FAA issues special conditions, as defined in 14 CFR 11.19, in
accordance with Sec.  11.38, and they become part of the type-
certification basis under Sec.  21.17(a)(2).

Novel or Unusual Design Features

    The Model G280 airplane will incorporate the following novel or
unusual design features:
    The Model G280 airplane is equipped with electrical and electronic
systems that control critical functions and systems. Examples of these
include the electronic displays, rudder, brakes, spoilers, flaps, and
electronic engine controls. The Model G280 electrical-power generation
and distribution architecture is equipped with an auxiliary power unit
(APU) and is not equipped with a Ram Air Turbine (RAT) generator. The
loss of all electrical power to certain functions and systems impacts
the airplane's ability to land safely. Therefore, these special
conditions are issued to retain the level of safety intended by the
current Sec.  25.1351(d).

Discussion

    The Model G280 airplane requires a continuous source of electrical
power for continued safe flight and landing. The current regulation in
Sec.  25.1351(d), ``Operation without normal electrical power,'' states
that the airplane must be operated safely in visual-flight-rules
conditions, for a period of not less than five minutes, with the normal
electrical power (electrical power sources excluding the battery)
inoperative. This rule was structured around a traditional design
utilizing mechanical controls for flight systems while the crew took
time to sort out the electrical failure, start engine(s) if necessary,
and re-establish some of the electrical-power-generation capability.
    To maintain the same level of safety associated with traditional
designs, the Model G280 airplane electrical-system design must not be
time-limited in its operation. It should be noted that service
experience has shown that the loss of all electrical power, which is
generated by the airplane's engine generators or APU is not extremely
improbable. Thus, it must be demonstrated that the airplane can
continue through safe flight and landing (including steering and
braking on ground for airplanes using steer/brake-by-wire) with the use
of its emergency electrical-power systems. These emergency electrical-
power systems must be able to power loads that are required for
continued safe flight and landing.

Discussion of Comments

    Notice of proposed special conditions no. 25-11-17-SC for the GALP
Model G280 airplanes was published in the Federal Register on October
27, 2011 (76 FR 66660). No comments were received, and the special
conditions are adopted as proposed.

Applicability

    As discussed above, these special conditions are applicable to the
GALP Model G280 airplane. Should GALP apply at a later date for a
change to the type certificate to include another model incorporating
the same novel or unusual design feature, the special conditions would
apply to that model as well.
    Under standard practice, the effective date of final special
conditions would be 30 days after the date of publication in the
Federal Register; however, as the certification date for the GALP Model
G280 airplane is imminent, the FAA finds good cause to make these
special conditions effective upon issuance.

Conclusion

    This action affects only certain novel or unusual design features
on the GALP Model G280 airplane. It is not a rule of general
applicability and it affects only the applicant who applied to the FAA
for approval of these features on the airplane.

List of Subjects in 14 CFR Part 25

    Aircraft, Aviation safety, Reporting and recordkeeping
requirements.

    The authority citation for these special conditions is as follows:

    Authority: 49 U.S.C. 106(g), 40113, 44701, 44702, 44704.

The Special Conditions

    Accordingly, pursuant to the authority delegated to me by the
Administrator, the following special conditions are issued as part of
the type-certification basis for GALP Model G280 airplanes. The special
conditions are issued in lieu of 14 CFR 25.1351(d) and are required to
ensure that the airplane has sufficient electrical power for continued
safe flight and landing.
    1. The applicant must show by test or a combination of test and
analysis that the airplane is capable of continued safe flight and
landing with all normal electrical power sources inoperative, as
prescribed by paragraphs (1)(a) and (1)(b) below.
    For purposes of this special condition, normal sources of
electrical-power generation do not include any alternate power sources
such as a battery, ram-air turbine (RAT), or independent power systems
such as the flight-control permanent-magnet generating system.
    In showing capability for continued safe flight and landing,
consideration must be given to systems capability, effects on crew
workload and operating conditions, and the physiological needs of the
flightcrew and passengers for the longest diversion time for which
approval is sought.
    a. Common-cause failures, cascading failures, and zonal physical
threats must be considered in showing compliance with this requirement.
    b. The ability to restore operation of portions of the electrical-
power generation and distribution system may be considered if it can be
shown that unrecoverable loss of those portions of the system is
extremely improbable. An alternative source of electrical power must be
provided for the time required to restore the minimum electrical-power-
generation capability required for safe flight and landing.
Unrecoverable loss of all engines may be excluded when showing that
unrecoverable loss of critical portions of the electrical system is
extremely improbable. Unrecoverable loss of all engines is covered in
special condition 2, below, and thus may be excluded when showing
compliance with this requirement.
    2. Regardless of any electrical-generation and distribution-system
recovery capability shown under special condition 1, above, sufficient
electrical-system capability must be provided to:
    a. Allow time to descend, with all engines inoperative, at the
speed that provides the best glide slope, from the maximum operating
altitude to the altitude at which the soonest possible engine restart
could be accomplished, and
    b. Subsequently allow multiple start attempts of the engines and
APU. This capability must be provided in addition to the electrical
capability required by existing part 25 requirements related to
operation with all engines inoperative.

    3. The airplane emergency electrical-power system must be designed
to supply:
    a. Electrical power required for immediate safety, which must
continue to operate without the need for crew action following the loss
of the normal electrical power, for a duration sufficient to allow
reconfiguration to provide a non-time-limited source of electrical
power.
    b. Electrical power required for continued safe flight and landing
for the maximum diversion time.
    4. If APU-generated electrical power is used in satisfying the
requirements of these special conditions, and if reaching a suitable
runway upon which to land is beyond the capacity of the battery
systems, then the APU must be able to be started under any foreseeable
flight condition prior to the depletion of the battery or the
restoration of normal electrical power, whichever occurs first. Flight
tests must demonstrate this capability at the most critical condition.
    a. It must be shown that the APU will provide adequate electrical
power for continued safe flight and landing.
    b. The Airplane Flight Manual (AFM) must incorporate non-normal
procedures that direct the pilot to take appropriate actions to
activate the APU after loss of normal engine-driven generated
electrical power.
    As a part of showing compliance with these special conditions, the
tests by which loss of all normal electrical power is demonstrated must
also take into account the following:
    1. The failure condition should be assumed to occur during night
instrument meteorological conditions (IMC), at the most critical phase
of the flight, relative to the worst possible electrical-power
distribution and equipment-loads-demand condition.
    2. After the un-restorable loss of normal engine generator power,
the airplane-engine-restart capability must be provided and operations
continued in IMC.
    3. It should be demonstrated that the aircraft is capable of
continued safe flight and landing. The length of time must be computed
based on the maximum diversion-time capability for which the airplane
is being certified. Consideration for airspeed reductions resulting
from the associated failure or failures must be made.
    4. The airplane must provide adequate indication of loss of normal
electrical power to direct the pilot to the non-normal procedures, and
the AFM must incorporate non-normal procedures that will direct the
pilot to take appropriate actions.

    Issued in Renton, Washington, on December 20, 2011.
K.C. Yanamura,
Acting Manager, Transport Airplane Directorate, Aircraft Certification
Service.
[FR Doc. 2011-33281 Filed 12-27-11; 8:45 am]
BILLING CODE 4910-13-P


Arauco North America, Inc.  -  Eugene MDF (Arauco) was called in on February 3, 2020. Their emission inventory was due May 4, 2020. However, the facility announced on February 11, 2020 that the company would begin decommissioning the facility on May 1, 2020. On February 27, 2020 the facility submitted a request to cancel the CAO call-in. LRAPA granted the request on March 2, 2020. Arauco notified LRAPA on April 29, 2020 that the facility was permanently shut down on April 28, 2020.

http://www.lrapa.org/300/Cleaner-Air-Oregon


[Federal Register Volume 79, Number 129 (Monday, July 7, 2014)]
[Notices]
[Page 38287]
[FR Doc No: 2014-15701]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket Nos. EL14-78-000; QF14-91-001]

Notice of Petition for Declaratory Order; Beaver Falls Municipal
Authority

    Take notice that on June 26, 2014, pursuant to Rule 207 of the
Federal Energy Regulatory Commission's (Commission) Rules of Practice
and Procedure, 18 CFR 385.207(a)(2), Beaver Falls Municipal Authority
(BFMA) filed a petition for declaratory order seeking limited waiver of
the Commission's small power production qualifying (QF) filing
regulations set forth in 18 CFR 292.203(a)(3) from March 17, 2006 to
November 15, 2003 when BFMA inadvertently failed to file its QF self-
certification with the Commission.
    Any person desiring to intervene or to protest this filing must
file in accordance with Rules 211 and 214 of the Commission's Rules of
Practice and Procedure (18 CFR 385.211, 385.214). Protests will be
considered by the Commission in determining the appropriate action to
be taken, but will not serve to make protestants parties to the
proceeding. Any person wishing to become a party must file a notice of
intervention or motion to intervene, as appropriate. Such notices,
motions, or protests must be filed on or before the comment date. On or
before the comment date, it is not necessary to serve motions to
intervene or protests on persons other than the Petitioner.
    The Commission encourages electronic submission of protests and
interventions in lieu of paper using the ``eFiling'' link at http://www.ferc.gov. Persons unable to file electronically should submit an
original and 5 copies of the protest or intervention to the Federal
Energy Regulatory Commission, 888 First Street NE., Washington, DC
20426.
    This filing is accessible on-line at http://www.ferc.gov, using the
``eLibrary'' link and is available for review in the Commission's
Public Reference Room in Washington, DC. There is an ``eSubscription''
link on the Web site that enables subscribers to receive email
notification when a document is added to a subscribed docket(s). For
assistance with any FERC Online service, please email
<EMAIL_ADDRESS>or call<PHONE_NUMBER> (toll free). For
TTY, call<PHONE_NUMBER>.
    Comment Date: 5:00 p.m. Eastern Time on July 28, 2014.

    Dated: June 27, 2014.
Kimberly D. Bose,
Secretary.
[FR Doc. 2014-15701 Filed 7-3-14; 8:45 am]
BILLING CODE 6717-01-P


[Federal Register: March 8, 2006 (Volume 71, Number 45)]
[Notices]
[Page 11601]
[DOCID:fr08mr06-58]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. PR06-11-000]

Washington Gas Light Company; Notice of Compliance Filing

March 2, 2006.
    Take notice that on December 9, 2005, Washington Gas Light Company
(Washington Gas) made a filing to comply with FERC Order 103 FERC ]
61,107 (May 1, 2003 Order) and the July 21, 2003 FERC Order approving
Washington Gas' revised Firm Interstate Transportation Service
Operating Statement, regarding the rates charged by Washington Gas for
firm interstate transportation service from its facilities in Virginia
to customer facilities located in West Virginia.
    Any person desiring to participate in this rate proceeding must
file a motion to intervene or to protest this filing must file in
accordance with Rules 211 and 214 of the Commission's Rules of Practice
and Procedure (18 CFR 385.211 and 385.214). Protests will be considered
by the Commission in determining the appropriate action to be taken,
but will not serve to make protestants parties to the proceeding. Any
person wishing to become a party must file a notice of intervention or
motion to intervene, as appropriate. Such notices, motions, or protests
must be filed on or before the date as indicated below. Anyone filing
an intervention or protest must serve a copy of that document on the
Applicant. Anyone filing an intervention or protest on or before the
intervention or protest date need not serve motions to intervene or
protests on persons other than the Applicant.
    The Commission encourages electronic submission of protests and
interventions in lieu of paper using the ``eFiling'' link at http://www.ferc.gov.
 Persons unable to file electronically should submit an

original and 14 copies of the protest or intervention to the Federal
Energy Regulatory Commission, 888 First Street, NE., Washington, DC
20426.
    This filing is accessible on-line at http://www.ferc.gov, using the

``eLibrary'' link and is available for review in the Commission's
Public Reference Room in Washington, DC. There is an ``eSubscription''
link on the Web site that enables subscribers to receive email
notification when a document is added to a subscribed docket(s). For
assistance with any FERC Online service, please e-mail
<EMAIL_ADDRESS>or call<PHONE_NUMBER> (toll free). For

TTY, call<PHONE_NUMBER>.
    Comment Date: March 8, 2006.

Magalie R. Salas,
Secretary.
[FR Doc. E6-3273 Filed 3-7-06; 8:45 am]

BILLING CODE 6717-01-P


[Federal Register Volume 85, Number 108 (Thursday, June 4, 2020)]
[Notices]
[Page 34485]
[FR Doc No: 2020-12092]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

Aviation Rulemaking Advisory Committee; Meeting

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Notice of Aviation Rulemaking Advisory Committee (ARAC)
meeting.

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SUMMARY: This notice announces a meeting of the ARAC.

DATES: The meeting will be held on Thursday, June 18, 2020, from 1:00
p.m. to 4:00 p.m. Eastern Daylight Time.
    Requests to attend the meeting must be received by Monday, June 8,
2020.
    Requests for accommodations to a disability must be received by
Monday, June 8, 2020.
    Requests to submit written materials to be reviewed during the
meeting must be received no later than Monday, June 8, 2020.

ADDRESSES: The meeting will be held virtually. Members of the public
who wish to observe the meeting must RSVP by emailing<EMAIL_ADDRESS>General committee information including copies of the
meeting minutes will be available on the FAA Committee website at
https://www.faa.gov/regulations_policies/rulemaking/committees/documents/.

FOR FURTHER INFORMATION CONTACT: Lakisha Pearson, Federal Aviation
Administration, 800 Independence Avenue SW, Washington, DC 20591,
telephone<PHONE_NUMBER>; fax<PHONE_NUMBER>; email<EMAIL_ADDRESS>
Any committee-related request should be sent to the person listed in
this section.

SUPPLEMENTARY INFORMATION:

I. Background

    The ARAC was created under the Federal Advisory Committee Act
(FACA), in accordance with Title 5 of the United States Code (5 U.S.C.
App. 2) to provide advice and recommendations to the FAA concerning
rulemaking activities, such as aircraft operations, airman and air
agency certification, airworthiness standards and certification,
airports, maintenance, noise, and training.

II. Agenda

    At the meeting, the agenda will cover the following topics:

 Status Report from the FAA
 Status Updates:
    [cir] Active Working Groups
    [cir] Transport Airplane and Engine (TAE) Subcommittee
 Recommendation Reports
 Any Other Business

    Detailed agenda information will be posted on the FAA Committee
website address listed in the ADDRESSES section at least one week in
advance of the meeting.

III. Public Participation

    The meeting will be open to the public on a first-come, first-
served basis, as space is limited. Please confirm your attendance with
the person listed in the FOR FURTHER INFORMATION CONTACT section.
Please provide the following information: Full legal name, country of
citizenship, and name of your industry association, or applicable
affiliation. If you are attending as a public citizen, please indicate
so.
    For persons participating by telephone, please contact the person
listed in the FOR FURTHER INFORMATION CONTACT section by email or phone
for the teleconference call-in number and passcode. Callers are
responsible for paying long-distance charges.
    The U.S. Department of Transportation is committed to providing
equal access to this meeting for all participants. If you need
alternative formats or services because of a disability, such as sign
language, interpretation, or other ancillary aids, please contact the
person listed in the FOR FURTHER INFORMATION CONTACT section.
    The FAA is not accepting oral presentations at this meeting due to
time constraints. Any member of the public may present a written
statement to the committee at any time. The public may present written
statements to the Aviation Rulemaking Advisory Committee by providing a
copy to the Designated Federal Officer via the email listed in the FOR
FURTHER INFORMATION CONTACT section.

    Issued in Washington, DC, on June 1, 2020.
Brandon Roberts,
Acting Executive Director Office of Rulemaking.
[FR Doc. 2020-12092 Filed 6-3-20; 8:45 am]
 BILLING CODE 4910-13-P


[Federal Register Volume 82, Number 153 (Thursday, August 10, 2017)]
[Rules and Regulations]
[Pages 37318-37319]
[FR Doc No: 2017-16901]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 81

[EPA-HQ-OAR-2017-0223; FRL-9965-97-OAR]

Withdrawal of Extension of Deadline for Promulgating Designations
for the 2015 Ozone National Ambient Air Quality Standards

AGENCY: Environmental Protection Agency (EPA).

ACTION: Withdrawal of extension of deadline for promulgating
designations.

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SUMMARY: The Environmental Protection Agency (EPA) is announcing that
it is withdrawing the 1-year extension of the deadline for promulgating
initial area designations for the ozone national ambient air quality
standards (NAAQS) that were promulgated in October 2015. Thus, unless
and until the Administrator takes additional final action, the 2-year
deadline for promulgating designations provided in the Clean Air Act
(CAA) applies.

DATES: The deadline for the EPA to promulgate initial designations for
the 2015 ozone NAAQS is October 1, 2017.

FOR FURTHER INFORMATION CONTACT: For questions regarding this action,
contact

Carla Oldham, Air Quality Planning Division, Office of Air Quality
Planning and Standards, Mail Code C539-04, Environmental Protection
Agency, Research Triangle Park, North Carolina 27711; telephone number:
(919) 541-3347; email address<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

    Entities potentially affected by this action include state, local
and tribal governments that would participate in the initial area
designation process for the 2015 ozone standards.

B. Where can I get a copy of this document and other related
information?

    The EPA has established a docket for designations for the 2015
ozone NAAQS under Docket ID No. EPA-HQ-OAR-2017-0223. All documents in
the docket are listed in the http://www.regulations.gov index. Although
listed in the index, some information is not publicly available, e.g.,
confidential business information or other information whose disclosure
is restricted by statute. Certain other material, such as copyrighted
material, will be publicly available only in hard copy. Publicly
available docket materials are available either electronically in
http://www.regulations.gov or in hard copy at the EPA Docket Center,
WJC West Building, Room 3334, 1301 Constitution Avenue NW., Washington,
DC. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday
through Friday, excluding legal holidays. The telephone number for the
Public Reading Room is<PHONE_NUMBER>, and the telephone number for the
EPA Docket Center is<PHONE_NUMBER>.
    An electronic copy of this notice is also available at http://www.epa.gov/ozone-designations along with other information related to
designations for the 2015 ozone NAAQS.

II. Designations Requirements

    On October 1, 2015, the EPA signed a notice of final rulemaking
that revised the 8-hour primary and secondary ozone NAAQS (80 FR 65292;
October 26, 2015). Both standards were lowered from 0.075 parts per
million (ppm) to a level of 0.070 ppm.
    After the EPA establishes or revises a NAAQS pursuant to CAA
section 109, the CAA directs the EPA and the states to begin taking
steps to ensure that those NAAQS are met. The first step is to identify
areas of the country that meet or do not meet that NAAQS. This step is
known as the initial area designations. Section 107(d)(1)(A) of the CAA
provides that, ``By such date as the Administrator may reasonably
require, but not later than 1 year after promulgation of a new or
revised national ambient air quality standard for any pollutant under
section [109], the Governor of each State shall * * * submit to the
Administrator a list of all areas (or portions thereof) in the State''
that designates those areas as nonattainment, attainment, or
unclassifiable.
    The CAA further provides, ``Upon promulgation or revision of a
national ambient air quality standard, the Administrator shall
promulgate the designations of all areas (or portions thereof) * * * as
expeditiously as practicable, but in no case later than 2 years from
the date of promulgation of the new or revised national ambient air
quality standard. Such period may be extended for up to one year in the
event the Administrator has insufficient information to promulgate the
designations.'' 42 U.S.C. 7407(d)(1)(B)(i).
    In the EPA guidance, ``Area Designations for the 2015 Ozone
National Ambient Air Quality Standards,'' the EPA indicated it expected
to complete the initial area designations by October 1, 2017,
consistent with the statutory requirement that the EPA designate areas
no later than 2 years following promulgation of a revised NAAQS.\1\
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    \1\ Memorandum from Janet G. McCabe, Acting Assistant
Administrator, to Regional Administrators, Regions 1-10. February
25, 2016.
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III. Withdrawal of Extension of Deadline for Promulgating Designations
for the 2015 Ozone NAAQS

    In letters sent to states on June 6, 2017, and in a Federal
Register notice published on June 28, 2017 (82 FR 29246), the EPA
Administrator Scott Pruitt announced that he was using his authority
under section 107(d)(1)(B)(i) of the CAA to extend by 1 year, to
October 1, 2018, the deadline for promulgating initial area
designations for the 2015 ozone NAAQS. At that time (i.e., in early
June), it was not clear that the agency would be in the position to
complete designations for all areas for the 2015 ozone NAAQS in
accordance with the 2-year statutory deadline of October 1, 2017. For a
variety of other NAAQS in the past, previous EPA Administrators have
used the authority under section 107(d)(1)(B)(i) to take additional
time to complete designations.\2\ The Administrator decided to
similarly invoke the extension with regard to designations for the 2015
ozone NAAQS.
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    \2\ For the 2008 ozone NAAQS, see 75 FR 2936 (January 19, 2010);
for the 2008 lead NAAQS, see 75 FR 71033 (November 22, 2010); for
the 2010 sulfur dioxide NAAQS, see 77 FR 46295 (August 3, 2012); and
for the 2012 fine particulate matter NAAQS, see 80 FR 2206 (January
15, 2015).
---------------------------------------------------------------------------

    The EPA has continued to discuss and work with states concerning
designations, and now understands that the information gaps that formed
the basis of the extension may not be as expansive as we previously
believed. The EPA now intends to reassess whether there are areas with
underlying technical issues, whether there are state designation
recommendations that the EPA intends to modify, and whether for any
area there is insufficient information to promulgate the designation.
The EPA believes this reevaluation will help ensure that more Americans
are living and working in areas that meet national air quality
standards. The agency believes that there may be areas of the United
States for which designations could be promulgated in the next few
months. Therefore, the EPA is withdrawing its prior announced 1-year
extension of the deadline for promulgating initial area designations
for the 2015 ozone NAAQS, and the 2-year deadline for promulgating
designations provided in section 107(d)(1)(B) of the CAA applies. The
Administrator may still determine that an extension of time to complete
designations is necessary, but is not making such a determination at
this time.

List of Subjects in 40 CFR Part 81

    Environmental protection, Air pollution control, National parks,
Wilderness areas.

    Dated: August 2, 2017.
E. Scott Pruitt,
Administrator.
[FR Doc. 2017-16901 Filed 8-9-17; 8:45 am]
 BILLING CODE 6560-50-P


[Federal Register Volume 83, Number 31 (Wednesday, February 14, 2018)]
[Notices]
[Pages 6552-6553]
[FR Doc No: 2018-03020]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

Combined Notice of Filings #1

    Take notice that the Commission received the following electric
corporate filings:

    Docket Numbers: EC18-54-000.
    Applicants: Twin Eagle Resource Management, LLC,TERM Holdings, LLC.
    Description: Application under FPA Section 203 of Twin Eagle
Resource Management, LLC, et al.
    Filed Date: 2/7/18.
    Accession Number: 20180207-5153.
    Comments Due: 5 p.m. ET 2/28/18.

    Take notice that the Commission received the following exempt
wholesale generator filings:

    Docket Numbers: EG18-45-000.
    Applicants: ColGreen North Shore, LLC.
    Description: Self-Certification of EWG Status of ColGreen North
Shore, LLC.
    Filed Date: 2/7/18.
    Accession Number: 20180207-5126.
    Comments Due: 5 p.m. ET 2/28/18.

    Take notice that the Commission received the following electric
rate filings:

    Docket Numbers: ER17-1567-002.
    Applicants: PJM Interconnection, L.L.C.
    Description: Compliance filing: Amended Compliance Filing RE:
November 9, 2017 Order in Docket No. ER17-1567-001 to be effective 12/
31/9998.
    Filed Date: 2/8/18.
    Accession Number: 20180208-5047.
    Comments Due: 5 p.m. ET 3/1/18.

    Docket Numbers: ER18-815-001.
    Applicants: PJM Interconnection, L.L.C.
    Description: Tariff Amendment: Errata to Attachment Q re:
Regulation Resource Credit filing-Docket No. ER18-815 to be effective
4/9/2018.
    Filed Date: 2/7/18.
    Accession Number: 20180207-5128.
    Comments Due: 5 p.m. ET 2/28/18.

    Docket Numbers: ER18-828-000.
    Applicants: Pacific Gas and Electric Company.
    Description: Sec.  205(d) Rate Filing: E&P Agreement for Avenal
Solar Holdings LLC to be effective 2/9/2018.
    Filed Date: 2/8/18.
    Accession Number: 20180208-5110.
    Comments Due: 5 p.m. ET 3/1/18.

    Take notice that the Commission received the following PURPA
210(m)(3) filings:

    Docket Numbers: QM18-9-000.
    Applicants: Indiana Municipal Power Agency.

    Description: Application of Indiana Municipal Power Agency to
Terminate Mandatory Purchase Obligation Under the Public Utility
Regulatory Policies Act of 1978.
    Filed Date: 2/8/18.
    Accession Number: 20180208-5088.
    Comments Due: 5 p.m. ET 3/8/18.

    The filings are accessible in the Commission's eLibrary system by
clicking on the links or querying the docket number.
    Any person desiring to intervene or protest in any of the above
proceedings must file in accordance with Rules 211 and 214 of the
Commission's Regulations (18 CFR 385.211 and 385.214) on or before 5:00
p.m. Eastern time on the specified comment date. Protests may be
considered, but intervention is necessary to become a party to the
proceeding.
    eFiling is encouraged. More detailed information relating to filing
requirements, interventions, protests, service, and qualifying
facilities filings can be found at: http://www.ferc.gov/docs-filing/efiling/filing-req.pdf. For other information, call<PHONE_NUMBER>
(toll free). For TTY, call<PHONE_NUMBER>.

    Dated: February 8, 2018.
Nathaniel J. Davis, Sr.,
Deputy Secretary.
[FR Doc. 2018-03020 Filed 2-13-18; 8:45 am]
 BILLING CODE 6717-01-P


Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 1 Final draft Chapter VI. Health Effects in Humans A. Case Reports and Clinical Studies Cyanogen Chloride. Human toxicity data on cyanogen chloride are summarized in Table VIII 1. No studies of short term oral exposure of humans to cyanogen chloride were located.

Data are available on short term exposure in air, which results in both inhalation exposure and dermal/ ocular exposure to the cyanogen chloride vapor. Cyanogen chloride was used as a poison gas by the military in World War I. Its effects were noted to be quick acting, but reversible if exposure was below a critical concentration ( Prentiss, 1937). Death was reported as occurring via rapid paralysis of nerve centers, similarly to hydrogen cyanide; however eye, throat, and lung irritation and coughing were noted following short exposures to low concentrations ( Prentiss,

1937; Flury and Zernik, 1931). The lethal concentration was reported as 400 mg CNCl/ m3 for 10 minutes ( Prentiss, 1937). Exposure to 50 mg CNCl/ m3 for 1 minute was considered " unendurable" ( Flury and Zernick, 1931). By contrast, Aldridge and Evans ( 1946) reported that a concentration of 60 mg CNCl/ m3 was not " unduly irritating." " Copious lacrimation" was reported within a few minutes at 2.5 mg CNCl/ m3 ( Prentiss, 1937). These concentration estimates are subject to the limitations of the technology of that period in measuring and maintaining consistent exposure levels. Longer exposure to lower concentrations that did not cause immediate nervous system effects were reported to result in hoarseness and slight inflammation of the conjunctiva ( Flury and Zernick, 1931). These early data are supported by a more recent report that exposure to approximately 1.8 mg CNCl/ m3 for an unspecified duration Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 2 Final draft ( on the order of minutes) resulted in severe eye and nose irritation ( Michigan Department of Public Health, 1977, as cited by ACGIH, 1991).

Cyanide. Several studies of the short terms effects of cyanide in humans following suicide attempts or accidental poisoning by the oral and inhalation routes were located. However,

many of these studies are limited by inadequate characterization of exposure. Oral toxicity studies for cyanide are summarized in Table VIII 2, and inhalation studies are summarized in Table VIII

3.

Liebowitz and Schwartz ( 1948) report a case of cyanide poisoning following ingestion of potassium cyanide. A 60 year old white male was admitted to the hospital one hour after ingesting an estimated 38 63 mg/ kg of potassium cyanide ( 15 25 mg CN/ kg). On admission, the patient was comatose with muscular rigidity. The pulse was thready with a rate of 140 per minute; heart sounds were inaudible. Respirations were 40 per minute and stertorous. The skin was pink, cold, and clammy, and the pupils were dilated. By eight hours after admission, the patient was alert, and the symptoms had begun to subside ( with the exception of weakness,

nausea, and an enlarged heart). Blood thiocyanate was measured on the first, second, fourth, and fifth days of hospitalization and found to be negative. Urinary thiocyanate peaked on the second day of hospitalization and total thiocyanate excretion was 237 mg over a 72 hour period. ( By comparison, a total of 1050 1750 mg CN was ingested, assuming a 70 kg body weight.) The authors were unable to explain why this patient recovered from exposure to a dose that was about 30 times the estimated lethal dose. However, the authors noted that the patient was a chemist Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 3 Final draft who used thiosulfate daily in his work, " immersing his hands in it frequently." Therefore,

exposure to thiosulfate may have had an antidote effect.

Lasch and El Shawa ( 1981) report the effects of accidental poisoning in children who ate apricot kernels or a sweet made from apricot kernels. In two episodes of poisoning, 24 children developed symptoms of cyanide poisoning within two hours after ingesting apricot kernels. The authors noted that apricot kernels contain the cyanogenic compound amygdalin, and that this compound can be hydrolyzed to cyanide enzymatically or in an alkaline environment. The authors did not estimate the amount of amygdalin consumed or the amount of cyanide produced, although the severity of symptoms appeared to correlate with amount of apricot kernels ingested. Four children died. The remaining children recovered after developing symptoms of vomiting, nausea,

weakness, confusion, lethargy, cyanosis, and coma with respiratory depression.

Saincher et al. ( 1994) report the acute effects of cyanide ingestion in a 23 year old man who had ingested 1.4 mg/ kg potassium cyanide ( 0.56 mg CN/ kg) in a suicide attempt. The patient was found unconscious. Following administration of oxygen, the patient recovered consciousness and reported numbness in thighs, shortness of breath, and weakness in hip flexors and hamstrings. The patient's blood cyanide concentration was 4.65 mg/ L at 3 hours following ingestion. Blood concentrations greater than 2.5 3.0 mg/ L are considered fatal, but the patient recovered without antidote therapy.

Several authors ( Uitti et al., 1985; Carella et al., 1988; Rosenberg et al., 1989; and Grandas et al., 1989) report the development of symptoms of parkinsonism in patients who Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 4 Final draft recovered from ingestion of a single dose of cyanide. The four cases included an 18 year old male who ingested 5.6 7.6 mg/ kg cyanide in a suicide attempt ( Uitti et al., 1985), a 46 year old woman who ingested an unreported amount of cyanide by accidental poisoning ( Carella et al.,

1988), a 46 year old man who ingested 8.6 mg/ kg cyanide in a suicide attempt ( Rosenberg et al.,

1989), and a 39 year old man who ingested an unknown amount of cyanide in a suicide attempt ( Grandas et al., 1989). In all cases, the patients recovered from the acute symptoms of cyanide poisoning with treatment, and a neurologic examination immediately following the poisoning was normal. Follow up neurologic examination at times of 3 weeks ( Rosenberg et al., 1989), 4 months ( Uitti et al., 1985), or 1 year ( Grandas et al., 1989; Carella et al., 1988), revealed that the patients had developed symptoms of parkinsonism, including generalized rigidity, bradykinesia,

tremors of tongue and eyelids, slow shuffling gait, and a weak dysphonic voice. A computerized tomography ( CT) scan or magnetic resonance imaging ( MRI) showed lesions in the putamen and globus pallidus regions of the brain in three of the cases ( Uitti et al., 1985; Rosenberg et al.,

1989; and Grandas et al., 1989).

Potter ( 1950) reported a case study of a worker accidentally exposed via inhalation to an undetermined concentration of hydrogen cyanide. Early symptoms were dizziness, dyspnea, and weakness of legs. This was followed by deep unconsciousness, accompanied by absent reflexes,

stertorous respiration, rapid pulse, fixed and unreactive pupils, and convulsions. The subject recovered with treatment, and no after effects were reported. In another case report, a worker was found unconscious lying in tank sludge after working without protective gear in a plating tank containing silver cyanide sludge ( Singh et al., 1989). The duration of exposure was unknown, but the tank air was later measured to contain 200 ppm hydrogen cyanide ( 213 mg Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 5 Final draft CN/ m3). He had dermal evidence of chemical burns, and was apnoeic, with a rapid pulse, fixed and dilated pupils, and no recorded blood pressure or response to pain. Blood cyanide was 804

mol/ L within ½ hour of arrival, and decreased to 15

mol/ L at 18 hours after arrival and following detoxification efforts. The patient died within 3 days despite extensive treatment.

A case report of a worker accidentally exposed to a brief stream of liquid hydrogen cyanide on his hand ( amount not specified) reported that the worker became deeply unconscious within 5 minutes of exposure ( Potter, 1950). Breathing was stertorous, and his face was flushed and reflexes were absent. The subject recovered with treatment. Dizziness, weakness, and a throbbing pulse were reported when three workers wearing gas masks providing " excellent respiratory protection" entered an atmosphere containing 2% hydrogen cyanide gas ( Drinker,

1932). These toxic effects were attributed to the dermal absorption of the gas.

One early case study reports acute effects of hydrogen cyanide following dermal exposure ( Drinker, 1932). Three men using hydrocyanic acid gas as a fumigant were working in an atmosphere containing 2% HCN. The men were wearing gas masks that appeared to be giving adequate respiratory protection. After about 10 minutes, the men developed symptoms of dizziness, weakness and throbbing pulse before they lost consciousness. The symptoms persisted several hours following exposure. The authors concluded that the symptoms were due to dermal absorption of the HCN.

Thiocyanate. No relevant inhalation or dermal toxicity studies were identified. There is a large amount of data on the toxicity of thiocyanate in humans, as summarized in Table VIII 4. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites 1This text expands on the summary of thiocyanate toxicity found in an Issue Paper prepared by U. S. EPA's Superfund Health Risk Technical Support Center in June 1996.

EPA/ OW/ OST/ HECD VI 6 Final draft However, most of these data involve the short term use of thiocyanates to decrease blood pressure in hypertensive patients. Data on the toxicity of thiocyanate in normotensive humans are limited to an acute exposure study conducted by Smith and Rudolf ( 1928), a 12 week study conducted by Dalhberg et al. ( 1984), and a study on women in India who ingested thiocyanate in milk for 5 years ( Banerjee et al., 1997). The latter two studies are addressed in the section on epidemiology studies of thiocyanate.

Smith and Rudolf ( 1928) administered oral doses of 325 mg sodium thiocyanate ( 233 mg SCN; 10 mg SCN/ kg day, assuming a reference body weight of 70 kg) to 6 healthy adults ( sex not specified) for 1 week. A 15 30 mm Hg decrease in systolic blood pressure was observed.

Blood pressure was the only endpoint measured; the authors noted that the subjects did not complain of any symptoms.

In the first half of the 1900s, thiocyanate ( in particular, sodium thiocyanate and potassium thiocyanate) was used to treat hypertension. 1 A number of papers have been published that report the effectiveness of thiocyanate in reducing blood pressure; some also discuss the adverse effects associated with this treatment. However, in general, these studies mainly focused on blood pressure and did not examine other endpoints. The reported effectiveness of thiocyanate in reducing blood pressure varies greatly from study to study. Andersen and Chen ( 1940) reviewed a number of human studies, and found that decreases in blood pressure have been observed in 12

100% of patients treated with thiocyanate. This large inter study variation in the effectiveness of Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 7 Final draft Table VI 1. Serum Thiocyanate and Thyroid Hormone Levels in Women Exposed for > 5 Years to Thiocyanate in Milk.

Endpoint Thiocyanate exposed women1 Mean SE Non exposed controls Mean SE SCN (

mol/ l) 230.0** 10.0 90.8 9.0 T 4 ( nmol/ l) 87.8** 6.6 125.4 11.5 T 3 ( nmol/ l) 2.39 0.32 1.71 0.16 TSH (

U/ ml) 2.49** 0.20 1.09 0.28 1Mean values with their standard errors for thirty five nonsmoking subjects. ** Mean values were significantly different from those for the control group, P < 0.01. Adapted from Banerjee et al. ( 1997)

thiocyanate in decreasing blood pressure is partly due to differences in the criteria used to determine a significant decrease in systolic blood pressure and in the underlying cause of the hypertension ( i. e., essential hypertension versus hypertension secondary to renal failure). The magnitude of the decrease in blood pressure typically ranged from 10 to 50 mm Hg, although decreases of 100 mm Hg have been reported. The decrease in blood pressure was often seen within several weeks of treatment initiation. Typically, blood pressure would return to pretreatment levels shortly after termination of the thiocyanate treatment. Ayman ( 1931) noted that the magnitude of the decrease in blood pressure, as well as the onset of the decrease were doserelated The large individual variations in blood pressure, however, make a determination of the dose dependency of the magnitude of change and the duration of onset difficult to independently evaluate. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 8 Final draft The most commonly reported adverse effects in hypertensive patients treated with thiocyanate were weakness, fatigue, and nausea/ vomiting. Other observed effects include thyroid toxicity ( enlarged thyroid, myxedema, decreased basal metabolic rate), dermatitis ( pruritus,

exfoliative dermatitis, and maculopapular eruption), neurotoxicity, and angina. Some of these effects may have been secondary to the rapid decrease in blood pressure. As noted earlier, most of these studies were not designed to adequately assess toxicity.

When thiocyanate treatment was first introduced in the early 1900s, high doses of thiocyanates were used, resulting in " toxic psychosis" deaths ( Domzalski et al., 1953). In all cases but one ( which involved co administration of bromide), blood thiocyanate levels were 14 mg SCN/ 100 mL or higher. When thiocyanate treatment was reintroduced in 1925, lower doses were used, and many physicians followed similar treatment regimes, administering 97.2 324 mg potassium thiocyanate or sodium thiocyanate one to five times per day. In the papers reviewed during the preparation of this criteria document, the lowest dose tested was 97.2 mg potassium thiocyanate ( 58.1 mg thiocyanate) administered three times per day for the first week, two times per day for the second week, and one time per day for 1 2 weeks ( time weighted average [ TWA]

dose of 1.5 1.7 mg SCN/ kg day, assuming a reference body weight of 70 kg) ( Palmer and Sprague, 1929; Palmer et al., 1929). In this study, 42.4% of the 59 hypertensive subjects had a decrease in systolic blood pressure of 30 mm Hg or more. Adverse effects ( weakness, angina,

and precordial distress) were observed in six subjects.

Several studies used moderate dose levels ( 1.7 2.8 mg SCN/ kg day). Ayman ( 1931)

reported on the toxicity and therapeutic effect of thiocyanate in 26 patients administered Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 9 Final draft potassium thiocyanate using a variety of treatment protocols. The individual doses ranged from 100 to 400 mg potassium thiocyanate, one to four times per day. The total daily dose of potassium thiocyanate ranged from 200 to 1200 mg potassium thiocyanate, corresponding to 1.7 to 10 mg SCN/ kg day, with the most common low dose being 3 x 100 mg potassium thiocyanate ( 2.6 mg SCN/ kg day). The duration of dosing at the lower doses was for 42 109 days, and resulted in decreases in blood pressure in only 3/ 13 subjects. These decreases were considered slight to moderate, and occurred only after prolonged treatment. By contrast, mild toxic effects ( weakness, fatigue, and diarrhea) were reported in 5/ 14 of these subjects. Treatment at the higher doses was for 4 89 days. Decreases of 30 40 mm Hg systolic and 10 30 mm Hg diastolic were observed in 12/ 14 patients. The author noted that the marked toxic symptoms precluded continuation of the treatment. Adverse effects ( weakness, fatigue, " laziness", drowsiness,

diarrhea, abdominal cramps, tremors, numbness in upper body) were observed in 12/ 14 patients.

Barker et al. ( 1941) administered 300 mg/ day potassium thiocyanate ( 180 mg SCN/ day;

2.6 mg SCN/ kg day) for 2 10 years. ( Although it is not clearly reported, there may have been interruptions in the dosing schedule.) Goldring and Chasis ( 1931) used 326 mg/ day potassium thiocyanate or sodium thiocyanate ( 190 mg SCN/ day, assuming all was in the form of potassium thiocyanate; 2.8 mg SCN/ kg day) for 14 78 days. In the Barker et al. ( 1941) study, the dose was increased or decreased as needed, based on comparison to the target blood concentration and signs of toxicity, respectively. The doses at which symptoms were observed were not reported,

but the most severe effects were seen at blood concentrations of 20 mg SCN/ 100 mL blood and higher. Decreases in systolic blood pressure ( magnitude of response not reported) were observed in 67% of the subjects in the Barker et al. ( 1941) study, and 32.4% of the subjects in the Goldring Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites 2The study author reported the concentrations as amounts of " cyanates," but discussed using thiocyanate standards. Therefore, it appears that the concentrations in blood are actually of thiocyanate. Therefore, discussion of the results of this study uses the term ( thio) cyanate where the authors referred to " cyanate" levels.

EPA/ OW/ OST/ HECD VI 10 Final draft and Chasis ( 1931) study had a decrease in blood pressure of at least 45 mm Hg systolic and 31 mm Hg diastolic. In the Barker et al. ( 1941) and Goldring and Chasis ( 1931) studies,

neurological effects ( depression, aphasia, slurring speech, mental confusion, disorientation,

hallucinations of sight and hearing, and unsteady gait) were observed. Signs of thyroid toxicity ( enlarged thyroid and myxedematous facies with decreased basal metabolic rate) were also observed in some of subjects in the Barker et al. ( 1941) study. Barker et al. ( 1941) noted that " it is not unusual to see fatigue, secondary anemia, and a dry scaling skin appear after many months of continuous ingestion of cyanates." It is not known if this statement is referring to results of the study or general observations in patients being treated with thiocyanate. The incidence of adverse effects was 18/ 246 in Barker et al. ( 1941) and 13/ 50 in Goldring and Chasis ( 1931). Two subjects in the Goldring and Chasis ( 1931) study died. Russell and Stahl ( 1942) reported deaths in several patients receiving potassium thiocyanate, one receiving only 400 mg/ day ( 3.4 mg SCN/ kg day) for approximately one week. Markedly decreased renal clearance may, however,

have led to increased blood thiocyanate levels, and contributed to the death.

Barker ( 1936) treated 45 patients ( with systolic blood pressure well over 200 mm) with sodium or potassium thiocyanate. After a basal level of thiocyanate in blood was attained,

increasing doses were administered, until sharp falls in blood pressure or toxicity were observed.

The concentration of thiocyanate in the blood was followed, with reduction of blood pressure seen in 35 of 45 patients. The author noted that the optimum therapeutic level was in the range of 8 12 mg thiocyanate/ 100 mL blood2, with significant toxicity beginning to appear at blood Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 11 Final draft ( thio) cyanate levels of 15 30 mg. Dosages were adjusted for each individual to maintain a blood ( thio) cyanate level of 10 mg, because clearance increased with repeated dosing. Slight toxicity was noted in many patients at blood ( thio) cyanate levels above 5 or 10 mg/ 100 mL, and included weakness, disease, and fatiguing more easily. These toxic symptoms were not considered disturbing until above blood ( thio) cyanate levels of 10 15 mg/ 100 mL. Above 20 mg ( thio) cyanate/ 100 mL in blood, toxicity increased rapidly; serious manifestations were noted at levels of 35 50 mg ( thio) cyanate/ 100 mL. There was high variability among individuals, with different blood ( thio) cyanate levels obtained with widely varying doses.

As reviewed by Gorman et al. ( 1949), the large within study variability in the effectiveness of thiocyanate in decreasing blood pressure and the incidence of adverse effects may be due to individual differences in the excretion of thiocyanate. The differences in individual average daily excretion rates of thiocyanate can vary as much as 500% ( Goldring and Chasis, 1931, as cited by Gorman et al., 1949). Because of the large potential differences in thiocyanate excretion, a number of physicians advocated monitoring blood thiocyanate levels, and adjusting dosages to maintain therapeutic blood levels. Blood levels between 5 and 14 mg/ 100 mL were considered optimal for reduction of blood pressure ( Barker, 1936; Domzalski et al., 1953; Gorman et al.,

1949), with toxicity ( muscular fatigue, nausea and vomiting, dermatitis, disorientation, mental confusion, motor aphasia, hallucinations, delirium, convulsions, and death) believed to occur at blood levels above 14 20 mg/ 100 mL. Although maintenance of a blood level of 5 14 mg/ 100 mL is advocated as a " safe" blood level, Beamish et al. ( 1954) observed thyroid toxicity ( decreases in protein bound plasma iodine concentration and thyroid uptake of iodine) in subjects with blood Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 12 Final draft thiocyanate levels ( 1.3 5 mg/ 100 mL) below the therapeutic range. Normal blood thiocyanate levels are 0.2 0.7 mg/ 100 mL ( Wood, 1975).

There are many limitations to the human database on the effects of thiocyanate on blood pressure. With the exception of the Smith and Rudolf ( 1928) study, hypertensive subjects were used, and no control group was used. All of these studies ( Palmer et al., 1929; Goldring and Chasis, 1931; Barker et al., 1941; Ayman, 1931) showed decreases in blood pressure, and the magnitude of the change ( where reported) was 10 50 mm Hg. The decrease in blood pressure observed in the human studies was considered a beneficial effect of oral exposure to thiocyanate because the subjects were hypertensive. If oral exposure to thiocyanate resulted in a 30 mm Hg or greater decrease in systolic blood pressure in normotensive as well as hypertensive individuals,

the effect would be considered adverse. In the Palmer et al. ( 1929) study, over 40% of the subjects had a decrease in systolic blood pressure of 30 mm Hg or greater; the subjects were orally exposed to a TWA dose of 1.5 1.8 mg/ kg day for 3 4 weeks. It is not known whether the magnitude of the decrease in systolic blood pressure would be the same if normotensive subjects were exposed to similar doses. Smith and Rudolf ( 1928) demonstrated a 15 30 mm Hg drop in systolic blood pressure in normotensive subjects treated with 3.3 mg SCN/ kg day for 1 week. If the assumption is made that a similar magnitude decrease in blood pressure would be observed in normotensive as was observed in hypertensive individuals, then the TWA dose of 1.5 1.7 mg/

kgday used in the Palmer et al. ( 1929) study is a LOAEL.

Only one study evaluated thyroid function in patients administered thiocyanate for treatment of hypertension. Blackburn et al. ( 1951) reported on 15 patients ( 4 men and 11 Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 13 Final draft women) who had received KSCN for hypertension for an unspecified duration, and developed myxedematous symptoms. Blackburn et al. ( 1951) also reported that two additional patients who developed thyroid enlargement without clinical symptoms. Thiocyanate treatment was terminated, and the extrarenal disposal rate ( a measure of thyroidal accumulation of radioiodine)

was measured. In all but one case, the extrarenal disposal rate increased as blood thiocyanate levels dropped.

Two studies reported on the effects of thiocyanate on thyroid function in normotensive subjects; one of these is addressed in the section on epidemiological studies. Dahlberg et al.

( 1984) tested the effects of sodium thiocyanate supplemented milk on thyroid function in 37 volunteers in Sweden ( 9 men and 28 women) aged 16 to 54 years. The subjects were given the milk, which provided 8 mg/ day thiocyanate ( 0.11 mg SCN/ kg day, assuming a 70 kg body weight), for 12 weeks. No significant differences from pretest levels were observed for serum T3,

T4, or thyrotropic hormone, or the T3: T4 ratio. Average serum thiocyanate levels increased from 0.4 mg/ 100 mL to 0.78 mg/ 100 mL in non smokers at 4 weeks, and from 0.84 mg/ 100 mL to 1.07 mg/ 100 mL in smokers after 12 weeks of exposure; thiocyanate levels at 12 weeks in the nonsmokers were somewhat lower than at 4 weeks. This study only assessed the effect of thiocyanate on thyroid toxicity and did not measure blood pressure.

B. Epidemiological Studies Cyanogen chloride. Only one report on the effects of longer term exposure to cyanogen chloride in humans is available. Fourteen men who worked at a plant that manufactured cyanogen Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 14 Final draft chloride were evaluated ( Reed, 1920). The men were exposed daily to cyanogen chloride in the air for eight months. The air concentration of cyanogen chloride was not measured, but was characterized as having a continuous presence of small amounts of gas with occasional instances of severe exposure. During the periods of severe exposure, men reported symptoms such as dizziness, nausea, tearing, blurring of vision, gasping, coughing, staggering, and prostration that lasted several hours. Chronic symptoms included muscular weakness; lassitude; lung congestion;

irritation of eyes, skin, and throat; decreased appetite; and severe weight loss. The authors noted that the symptoms observed are very similar to the symptoms observed in cases of chronic cyanide poisoning, except that with cyanogen chloride the weight loss is greater and there is severe congestion of the lungs. The authors attributed these latter effects to the presence of " chlorine."

In light of the irritative effects reported for short term exposures to cyanogen chloride ( Flury and Zernick, 1931; Prentiss, 1937), it is plausible that the observed irritation was due to the chlorine moiety in cyanogen chloride.

Cyanide. No longer term studies of exposure in humans by the oral or dermal routes were located.

El Ghawabi et al. ( 1975) evaluated the effects of long term occupational exposure to cyanide in workers in the electroplating industry. Thirty six male workers from three electroplating factories in Egypt were evaluated for occupational and medical history.

Iodineuptake tests were performed to assess thyroid function. Blood was drawn for hematological analysis and urine was collected for thiocyanate determination. Twenty males who had never been exposed to chemicals and who did not smoke were used as the control population. Cyanide Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 15 Final draft concentration in the workplace air was also measured. The mean cyanide air concentrations for the three plants were 10.4, 6.4, and 8.3 ppm ( 11.7, 7.2, and 9.3 mg/ m3, respectively). Of the 36 workers, 14 were exposed for 5 years, 14 were exposed for 5 10 years, 7 were exposed for 10 15 years, and only one was exposed for greater than 15 years. Approximately 80% of the workers reported symptoms of headache, weakness, and alterations of taste; only 30%, 20%, or 0% of the controls, respectively, reported these symptoms. Other symptoms reported by workers included giddiness, throat irritation, vomiting, and tearing. Finally, a small percentage of workers, who worked in the factory with the highest air concentration, reported symptoms of neurological disorders, such as salivation, disturbances of accommodation, and psychosis. Twenty workers ( 56%) had mild to moderate thyroid enlargement, although none of the workers showed clinical symptoms of either hypo or hyper thyroidism. In a thyroid iodine uptake study, the workers had a statistically significant increase in iodine concentration in the thyroid gland compared with the controls. This finding is the opposite from the expected result for workers exposed to an antithyroid agent. However, the authors noted that the test was conducted immediately after the workers had been away from work for two days, and they concluded that the sudden cessation of cyanide exposure caused the iodine depleted gland to rapidly accumulate iodine. Workers had significantly higher hemoglobin and lymphocyte counts than did controls. Finally, the authors noted that the urinary concentration of thiocyanate was linearly related to cyanide concentration in air. This study is limited by the small sample size and the possibility that workers were also exposed to other chemicals in the work place. However, the study does indicate that the thyroid is a target organ in humans following chronic exposure to cyanide. An air concentration of 7.2 mg CN/ m3 can be considered to be a LOAEL. After adjusting for intermittent exposure and the occupational minute volume, the LOAEL( HEC) was 2.6 mg CN/ m3. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 16 Final draft Blanc et al. ( 1985) reported on health effects in a group of 36 male silver reclaiming workers. The workers had been employed at the facility for an average of 11 ± 10.4 months when the facility was cited for safety violations and shut down. Environmental monitoring, after the plant was shut down, found that the 24 hour time weighted average ( TWA) exposure was 15 ppm HCN ( 16 mg CN/ m3). After adjusting for intermittent exposure and the occupational minute volume, the human equivalent concentration was 5.7 mg CN/ m3. Workers were classified into low, moderate, or high exposure categories based on their primary job activity. However, no information was provided on the actual exposure of the workers in each exposure category. In addition, no information was provided on how the TWA concentration related to personal exposure of workers. A thorough medical examination was conducted, including analysis for serum biochemistry, thyroid hormones, and neurological effects. A number of subjective symptoms, including nausea, dizziness, syncope, and vomiting, exhibited a relationship to the exposure index. There were no workers with palpable thyroid gland abnormalities, mucosal erosion, or neurological deficits. All individual values for T3, T4, and TSH were normal,

although the average TSH value was higher than the mean laboratory control value. The difference was statistically significant for the high exposure workers. However, since it is not possible to correlate the TWA concentration of 5.7 mg CN/ m3 with the actual exposure of highexposure workers, it is not possible to designate this concentration as an adverse effect level.

Thiocyanate. Banerjee et al. ( 1997) evaluated thyroid hormone levels in 35 women in India who ingested thiocyanate from a commercial milk product supplemented with bacteriocide known as the LP system ( lactoperioxidase thiocyanate hydrogen peroxide system). The LP system produces OSCN ( the actual bacteriostat) from the reaction of peroxide with thiocyanate. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites 3EPA's standard body weight default value is 70 kg for adults, including both men and women, and the default average body weight for women in the U. S. is 65.4 kg ( U. S. EPA, 1997b). However, since women in India are smaller than American women, a lower average body weight of 60 kg was used, taking into account the uncertainty in the overall estimate; no information was located on average body weight of adult Indian women.

EPA/ OW/ OST/ HECD VI 17 Final draft In these systems, thiocyanate is typically present in the milk at 30 50 mg/ L ( 45 mg/ L average).

These 35 women who had regularly consumed 250 mL/ day of the LP milk for more than five consecutive years were matched for age, dietary habits, and socioeconomic status to an equal number of women who consumed a similar amount of untreated raw milk. Assuming a body weight of 60 kg for these women3, and that all of the thiocyanate was ingested as SCN, rather than as OSCN, the exposed women ingested approximately 0.19 mg SCN/ kg day. All subjects had no prior history of thyroid disease. Both the thiocyanate exposed and non exposed control groups were analyzed for urinary and serum SCN and for serum T 3, T 4 and TSH. The average serum level of thiocyanate was 230

mol/ L ( 1.3 mg/ 100 mL) in the exposed group, and 91

mol/ L ( 0.53 mg/ 100 mL) in the controls ( Table VI 1). The thiocyanate exposed group had significantly lower levels of serum T 4 and higher levels of TSH than the non exposed group. T 3 levels were slightly elevated in the thiocyanate exposed group, but the change was not statistically significant. This study identifies 0.19 mg SCN/ kg day as a LOAEL for thyroid effects in humans.

However, it is unclear if the presence of OSCN ( rather than only SCN) exacerbated the effects of thiocyanate on the thyroid. In addition, the study authors did not address whether the study population might constitute a sensitive population. For example, one may hypothesize that the study subjects may have had protein deficient diets, since much of the population of India is malnourished. An iodine deficiency appears less likely, since the study population was from Calcutta, a coastal city, and seafood is a major source of iodine. People who are protein deficient or iodine deficient would be more susceptible to effects of thiocyanate on T 4 levels. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 18 Final draft C. Summary of Human Studies Cyanogen Chloride. Cyanogen chloride was used as a nerve agent during World War I,

with rapid lethality resulting from sufficiently high exposures. Acute exposure to lower concentrations resulted in irritation of the eyes, throat, and lungs ( Flury and Zernick, 1931;

Prentiss, 1937; Michigan Department of Public Health, 1977). Only one epidemiology study of the human health effects of cyanogen chloride exposure was located. Reed ( 1920) reported on symptoms in a group of 14 men at a plant that manufactured cyanogen chloride. No exposure levels were available, but the symptoms reported during periods of high exposure included dizziness, nausea, and prostration that lasted several hours. Chronic symptoms included weakness, lassitude, and eye, nose and throat irritation. The observed symptoms are consistent with those seen following cyanide exposure. The irritative effects and lung congestion were attributed to co exposure to chlorine.

Cyanide. Case reports of accidental exposure to cyanide and hydrogen cyanide indicate that exposure via the oral, inhalation, and dermal routes are of concern. The reported symptoms include dizziness, weakness, nausea, and a rapid pulse; these symptoms can progress to convulsions, unconsciousness, and death ( Saincher et al., 1994; Liebowitz and Schwartz, 1948;

Potter, 1950; Drinker, 1932). Similar symptoms were reported for all three routes of exposure.

Symptoms characteristic of parkinsonism have been reported among subjects who recover from acute cyanide poisoning ( Uitti et al., 1985; Carella et al., 1988; Rosenberg et al., 1989; and Grandas et al., 1989). Studies of long term exposure to cyanide were conducted in Egypt with 36 workers exposed to cyanide in the electroplating industry ( El Ghawabi et al., 1975) and in the U. S. with 36 workers in the silver reclaiming industry ( Blanc et al., 1985). In El Ghawabi et al. Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 19 Final draft ( 1975), air concentrations were monitored. Reported symptoms included headache, weakness,

throat irritation, and vomiting. A small percentage, who were exposed to the highest concentrations, reported neurological disorders. Mild to moderate thyroid enlargement was reported in 56% of the workers, although none of the workers had clinical evidence of hypo or hyper thyroidism. This study identified a LOAEL of 7.2 mg CN/ m3, corresponding to a LOAEL( HEC) of 2.6 mg CN/ m3. In Blanc et al. ( 1985), a single 24 hour TWA measurement found a concentration of 16 mg CN/ m3 ( corresponding to a HEC of 5.7 mg CN/ m3), but this TWA was not correlated with the actual exposure of any of the three worker exposure categories ( high, medium, or low exposure). Several subjective symptoms exhibited a relationship to the exposure index; no thyroid effects or neurological deficits were observed. Both studies are limited by small sample size and the possibility of co exposure to other chemicals. In addition,

Blanc et al. ( 1985) is limited by an incomplete characterization of exposure for each of the exposure categories.

Thiocyanate. No relevant inhalation or dermal toxicity studies of thiocyanate exposure of humans were identified. There is a significant amount of data on thiocyanate orally administered to humans, because thiocyanate was used for many years to treat hypertension. However, data on the effects in normotensive humans is limited. Adverse effects observed included weakness,

nervous system effects ( including slurred speech, disorientation, and hallucinations), and enlarged thyroid. Some of the observed effects may have been due to a rapid decrease in blood pressure.

While the decreased blood pressure was a beneficial effect for the hypertensive subjects, the same change could be adverse in normotensive subjects, although it is unclear if the drop in blood Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites 4 OSCN is not reported as one of the ions which are known to inhibit iodine transport in the thyroid ( Wolff, 1998).

EPA/ OW/ OST/ HECD VI 20 Final draft pressure would be as large in normotensive subjects. Doses were reported inconsistently, but doses of 1.7 2.8 mg SCN/ kg day had a relatively low incidence of adverse effects.

Two studies evaluated thyroid effects of thiocyanate in normotensive populations.

Dahlberg et al. ( 1984) found no effect on serum T 3, T 4, or thyrotropic hormone, or the T 3: T 4 ratio in 37 volunteers administered 8 mg/ day thiocyanate in milk ( 0.11 mg SCN/ kg day) for 12 weeks.

Maximum serum thiocyanate levels were 0.78 mg/ 100 mL in non smokers and 1.07 mg/ 100 mL in smokers. Banerjee et al. ( 1997) evaluated thyroid hormone levels in 35 women in India who ingested thiocyanate and hydrogen peroxide as a bacteriocide in milk for at least 5 years,

compared with matched women ingesting raw milk. The exposed women ingested approximately 0.19 mg SCN/ kg day. The average serum level of thiocyanate was 230

mol/ L ( 1.3 mg/ 100 mL)

in the exposed group, and 91

mol/ L ( 0.53 mg/ 100 mL) for matched women. The thiocyanateexposed group had significantly lower levels of serum T 4 and higher levels of TSH than the nonexposed group. Together, these two studies identify an apparent NOAEL/ LOAEL pair. The primary uncertainty in that identification is whether the Indian population was more susceptible to the effects of thiocyanate, due to such potential factors as low protein intake or low iodide intake.

Another uncertainty is whether OSCN ( to which the Indian women were exposed) is more toxic than the equivalent amount of SCN. 4 Since the thyroid responds rapidly to changes in iodine or related ions, progression of the effect with increased exposure duration from 12 weeks to 5 years would not be expected. Beamish et al. ( 1954) observed thyroid toxicity ( decreases in proteinbound plasma iodine concentration and thyroid uptake of iodine) in subjects with blood Drinking Water Criteria Document for Cyanogen Chloride and Potential Metabolites EPA/ OW/ OST/ HECD VI 21 Final draft thiocyanate levels ( 1.3 5 mg/ 100 mL) comparable to those reported by Banerjee et al. ( 1997), but no information on intake ( in mg/ kg day) was reported.


[Federal Register Volume 85, Number 19 (Wednesday, January 29, 2020)]
[Notices]
[Pages 5274-5275]
[FR Doc No: 2020-01551]

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DEPARTMENT OF TRANSPORTATION

Federal Motor Carrier Safety Administration

[Docket No. FMCSA-2015-0118]

Qualification of Drivers; Exemption Applications; Epilepsy and
Seizure Disorders

AGENCY: Federal Motor Carrier Safety Administration (FMCSA), DOT.

ACTION: Notice of final disposition.

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SUMMARY: FMCSA announces its decision to renew an exemption for one
individual from the requirement in the Federal Motor Carrier Safety
Regulations (FMCSRs) that interstate commercial motor vehicle (CMV)
drivers have ``no established medical history or clinical diagnosis of
epilepsy or any other condition which is likely to cause loss of
consciousness or any loss of ability to control a CMV.'' The exemption
enables this individual who has had one or more seizures and is taking
anti-seizure medication to continue to operate CMVs in interstate
commerce.

DATES: The exemption was applicable on October 22, 2019. The exemption
expires on October 22, 2021.

FOR FURTHER INFORMATION CONTACT: Ms. Christine A. Hydock, Chief,
Medical Programs Division,<PHONE_NUMBER><EMAIL_ADDRESS>FMCSA,
Department of Transportation, 1200 New Jersey Avenue SE, Room W64-224,
Washington, DC 20590-0001. Office hours are from 8:30 a.m. to 5 p.m.,
ET, Monday through Friday, except Federal holidays. If you have
questions regarding viewing or submitting material to the docket,
contact Docket Operations,<PHONE_NUMBER>.

SUPPLEMENTARY INFORMATION:

I. Public Participation

A. Viewing Documents and Comments

    To view comments, as well as any documents mentioned in this notice
as being available in the docket, go to or http://www.regulations.gov/docket?D=FMCSA-2015-0118 and choose the document to review. If you do
not have access to the internet, you may view the docket online by
visiting Docket Operations in Room W12-140 on the ground floor of the
DOT West Building, 1200 New Jersey Avenue SE, Washington, DC 20590,
between 9 a.m. and 5 p.m., ET, Monday through Friday, except Federal
holidays.

B. Privacy Act

    In accordance with 5 U.S.C. 553(c), DOT solicits comments from the
public to better inform its rulemaking process. DOT posts these
comments, without edit, including any personal information the
commenter provides, to www.regulations.gov, as described in the system
of records notice (DOT/ALL-14 FDMS), which can be reviewed at
www.transportation.gov/privacy.

II. Background

    On December 4, 2019, FMCSA published a notice announcing its
decision to renew an exemption for one individual from the epilepsy and
seizure disorders prohibition in 49 CFR 391.41(b)(8) to operate a CMV
in interstate commerce and requested comments from the public (84 FR
66454). The public comment period ended on January 3, 2020, and no
comments were received.
    FMCSA has evaluated the eligibility of this applicant and
determined that renewing the exemption would achieve a level of safety
equivalent to, or greater than, the level that would be achieved by
complying with Sec.  391.41(b)(8).
    The physical qualification standard for drivers regarding epilepsy
found in Sec.  391.41(b)(8) states that a person is physically
qualified to drive a CMV if that person has no established medical
history or clinical diagnosis of epilepsy or any other condition which
is likely

to cause the loss of consciousness or any loss of ability to control a
CMV.
    In addition to the regulations, FMCSA has published advisory
criteria \1\ to assist medical examiners in determining whether drivers
with certain medical conditions are qualified to operate a CMV in
interstate commerce.
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    \1\ These criteria may be found in APPENDIX A TO PART 391--
MEDICAL ADVISORY CRITERIA, section H. Epilepsy: Sec.  391.41(b)(8),
paragraphs 3, 4, and 5, which is available on the internet at
https://www.gpo.gov/fdsys/pkg/CFR-2015-title49-vol5/pdf/CFR-2015-title49-vol5-part391-appA.pdf.
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III. Discussion of Comments

    FMCSA received no comments in this proceeding.

IV. Conclusion

    Based on its evaluation of the one renewal exemption application,
FMCSA announces its decision to exempt the following driver from the
epilepsy and seizure disorders prohibition in Sec.  391.41(b)(8).
    As of October 22, 2019, and in accordance with 49 U.S.C. 31136(e)
and 31315(b), Anthony Martens (SD) has satisfied the renewal conditions
for obtaining an exemption from the epilepsy and seizure disorders
prohibition in the FMCSRs for interstate CMV drivers (84 FR 66454).
    This driver was included in docket number FMCSA-2015-0118. The
exemption is applicable as of October 22, 2019, and will expire on
October 22, 2021.
    In accordance with 49 U.S.C. 31315(b), the exemption will be valid
for 2 years from the effective date unless revoked earlier by FMCSA.
The exemption will be revoked if the following occurs: (1) The person
fails to comply with the terms and conditions of the exemption; (2) the
exemption has resulted in a lower level of safety than was maintained
prior to being granted; or (3) continuation of the exemption would not
be consistent with the goals and objectives of 49 U.S.C. 31136(e) and
31315(b).

     Issued on: January 23, 2020.
Larry W. Minor,
Associate Administrator for Policy.
[FR Doc. 2020-01551 Filed 1-28-20; 8:45 am]
BILLING CODE 4910-EX-P