[Federal Register Volume 78, Number 44 (Wednesday, March 6, 2013)]
[Notices]
[Pages 14533-14536]
[FR Doc No: 2013-05245]

=======================================================================
-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

[EPA-R09-OAR-2013-0126; FRL-9788-3]

Official Release of EMFAC2011 Motor Vehicle Emission Factor Model
for Use in the State of California

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice of Availability.

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

SUMMARY: EPA is approving and announcing the availability of the latest
version of the California EMFAC model (short for EMission FACtor) for
use in state implementation plan (SIP) development and transportation
conformity in California. EMFAC2011 is the latest update to the EMFAC
model for use by California state and local governments to meet Clean
Air Act (CAA) requirements. The new model, which is based on new and
improved data, calculates air pollution emissions factors for passenger
cars, trucks, motorcycles, motor homes and buses. Today's notice also
sets the date after which EMFAC2011 is required to be used statewide in
all new regional emissions analyses and carbon monoxide (CO),
particulate matter of ten microns or less (PM10) and fine
particulate matter (PM2.5) hot-spot analyses for
transportation conformity determinations in California. Since the EMFAC
model is used only in California, EPA's approval of the model does not
affect MOVES model users in other states.

DATES: EPA's approval of the EMFAC2011 emissions model for SIP and
conformity purposes is effective March 6, 2013. EMFAC2011 must be used
for all new regional emissions analyses and CO, PM10 and
PM2.5 hot-spot analyses that are started on or after
September 6, 2013.

FOR FURTHER INFORMATION CONTACT: Karina O'Connor,
<EMAIL_ADDRESS>(775) 433-8176, Air Planning Office (AIR-2),
Air Division, U.S. EPA, Region 9, 75 Hawthorne Street, San Francisco,
California, 94105-3901.

SUPPLEMENTARY INFORMATION: Copies of the official version of the
EMFAC2011 model are available on the California Air Resources Board
(CARB) Web site: http://www.arb.ca.gov/msei/modeling.htm (model,
technical support documents, etc.).

I. Background

A. What is the EMFAC model?

    The EMFAC model is a computer model that can estimate emission
rates for on-road mobile sources (``motor vehicles'') for calendar
years from 1990 to 2035 operating in California. Pollutant emissions
for hydrocarbons (HC), CO, nitrogen oxides (NOX),
PM10, PM2.5, lead, carbon dioxide
(CO2), and sulfur oxides are output from the model.
Emissions are calculated for forty-two different vehicle classes
composed of passenger cars, various types of trucks and buses,
motorcycles, and motor homes.
    EMFAC is used to calculate current and future inventories of motor
vehicle emissions at the state, air district, air basin, or county
level. EMFAC contains default vehicle activity data, and the option of
modifying that data, so it can be used to estimate a motor vehicle
emissions inventory in tons/day for a specific year, month, or season,
and as a function of ambient temperature, relative humidity, vehicle
population, mileage accrual, miles of travel and speeds. Thus the model
can be used to make decisions about air pollution policies and programs
at the local or state level. Inventories based on EMFAC are also used
to meet the federal CAA's SIP and transportation conformity
requirements. Transportation conformity is required under CAA section
176(c) to ensure that federally supported transportation plans,
transportation improvement programs (TIPs), and highway and transit
projects are consistent with (``conform to'') the purpose of the SIP.
Conformity to a SIP means that a transportation activity will not cause
or contribute to new air quality violations, worsen existing
violations, or delay timely attainment of the national ambient air
quality standards (NAAQS) or interim milestones. EPA's transportation
conformity regulations (40 CFR Parts 51.390 and 93) describe how
federally funded and approved highway and transit projects meet these
statutory requirements.

B. What versions of EMFAC are currently in use in California?

    Most SIPs in California were developed using EMFAC2007 (released by
CARB in October 2007) or EMFAC2002 (released by CARB in October 2002).
EPA approved EMFAC2007 on January 18, 2008 (73 FR 3464) and approved
EMFAC2002 on April 1, 2003 (68 FR 15720) for all areas in California.
    EMFAC2007 was considered a major update to previous versions of
EMFAC and most SIPs in California were updated with EMFAC2007 in the
2007-2008 timeframe. EMFAC2007 included new data and methodologies
regarding calculation of motor vehicle emissions, and revisions to
implementation data for control measures.

C. Why is EPA announcing its approval of the EMFAC model?

    CAA section 172(c)(3) and 40 CFR 51.112(a)(1) require that SIP
inventories be based on the most current, accurate, and applicable
models that are available at the time the SIP is developed. CAA section
176(c)(1) requires that the latest emissions estimates be used in
conformity analyses. EPA approves models that fulfill these
requirements.
    Under 40 CFR 93.111(a), EPA must approve new versions of EMFAC for
SIP purposes before they can be used in transportation conformity
analyses. In an April 6, 2012 letter, CARB requested that EPA approve
EMFAC2011 for use in developing SIPs and in determining conformity in
California.\1\ EMFAC2011 is a significant change from previous EMFAC
models with a new model user interface and is capable of calculating
motor vehicle emissions for all California areas. EMFAC2011 is being
approved as the latest emissions model for statewide use in SIP
development and emissions analyses for conformity purposes. Since the
EMFAC model is only used in California, EPA's statewide approval of the
model does not affect MOVES emissions factor model users in other
states.
---------------------------------------------------------------------------

    \1\ The EMFAC2011 model and supporting information is available
for downloading at http://www.arb.ca.gov/msei/modeling.htm.
Technical documentation explaining the changes to the model and the
technical foundations for the model is available at http://www.arb.ca.gov/msei/emfac2011-documentation-final.pdf.
---------------------------------------------------------------------------

II. EPA Action

A. What version of EMFAC is EPA approving?

    In this notice, EPA is approving and announcing that EMFAC2011 is
available to use in statewide California SIP development and for
regional emissions analyses and CO, PM10 and
PM2.5 hot-spot analyses for transportation conformity.
EMFAC2011 was developed by CARB and transmitted for approval to EPA on
April 6, 2012.
    The EMFAC2011 model is composed of a new modular structure that
will facilitate future model updates and allow CARB to incorporate
updated information about truck and bus activity and emissions data
into the model. The three major modules of EMFAC include EMFAC-LDV,
EMFAC-HD and EMFAC-SG. EMFAC-LDV can be used to estimate emissions for
gasoline powered on-road vehicles and smaller on-road diesel vehicles
and urban transit buses. EMFAC-HD provides

emissions factors for heavy-duty diesel trucks and buses. EMFAC-SG
allows users to run one tool for SIP inventories and regional emissions
analyses to combine the emissions factors from both EMFAC-LDV and
EMFAC-HD with user defined vehicle miles of travel and speeds, combine
emissions from multiple model-defined subareas and incorporate
reductions associated with CARB's Pavley and Low Carbon Fuel standard
regulations.
    CARB developed the EMFAC-SG module to provide users, including
transportation planners, with a simplified method to generate emissions
with different future growth scenarios for specific geographic areas
needed for transportation conformity and SIP development. CARB also
developed the EMFAC-PL tool for use for doing multiple model runs to
extract emissions factors for project-level analyses needed for hot-
spot analyses.\2\ Due to the modular structure of the EMFAC2011 model,
to obtain emissions factors for project-level analyses, an EMFAC2011
user would have to run multiple modules to generate emission factors.
Therefore ARB has developed the EMFAC-PL tool to produce emissions
factors for projects that are consistent with the default assumptions
in EMFAC2011. For projects that have site-specific ambient temperature
and relative humidity profiles, project-specific vehicle age
distributions and/or project-specific rest and soak time data, the user
will have to use a more detailed approach other than EMFAC-PL that
requires getting emissions factors from EMFAC-LDV and EMFAC-HD. As
discussed later in this notice, EPA is consulting with CARB to provide
updated EMFAC guidance for how to apply the EMFAC2011 emissions model
through either the EMFAC-PL tool or the more detailed approach that
would not use EMFAC-PL.
---------------------------------------------------------------------------

    \2\ The EMFAC-PL tool is available at: http://www.arb.ca.gov/msei/modeling.htm. In an email to EPA dated 2/08/2013, CARB
clarified that the EMFAC-PL tool is available for use in project-
level assessments.
---------------------------------------------------------------------------

B. What analyses can EMFAC2011 be used for?

    EPA is approving the model to estimate regional emissions of HC,
CO, NOX, PM10, PM2.5, lead, and sulfur
oxides.\3\ However, EMFAC2011 will only be used in transportation
conformity for pollutants and precursors that affect transportation-
related emissions, e.g., HC, NOX, CO, PM10 and
PM2.5.
---------------------------------------------------------------------------

    \3\ EPA notes that EMFAC2011 can be used for CO2
emissions analyses as well, but there are no SIP or transportation
conformity requirements for greenhouse gases (GHGs).
---------------------------------------------------------------------------

    EPA is also approving EMFAC2011 to estimate CO, PM10 and
PM2.5 emissions for conformity hot-spot analyses involving
individual transportation projects. A hot-spot analysis is defined in
40 CFR 93.101 as an estimation of likely future localized pollutant
concentrations and a comparison of those concentrations to the relevant
NAAQS. This analysis is conducted on a smaller scale than a
nonattainment or maintenance area, e.g., for a congested roadway
intersection.
    EPA also notes that today's approval action does not impact what
methodology is required for calculating re-entrained road dust for
regional PM10 and PM2.5 SIPs and transportation
conformity analyses. EMFAC2011's PM10 and PM2.5
estimates do not include such emissions. When applicable,
PM10 and PM2.5 nonattainment and maintenance
areas are required to use EPA's AP-42 road dust method for calculating
road dust emissions, unless a local method is approved in advance by
EPA.\4\ In addition, EMFAC2011 does not estimate ammonia emissions; air
quality and transportation agencies should contact the EPA Regional
Office if ammonia emissions estimates are needed for SIPs or regional
conformity emissions analyses.
---------------------------------------------------------------------------

    \4\ For further information, see EPA's February 4, 2011 Notice
of Availability for the January 2011 AP-42 Method for Estimating Re-
entrained Road Dust from Paved Roads (76 FR 6328). Also, for using
AP-42 for unpaved roads, see EPA's August 2, 2007 memorandum,
``Policy Guidance on the Use of the November 1, 2006, Update to AP-
42 for Re-entrained Road Dust for SIP Development and Transportation
Conformity.''
---------------------------------------------------------------------------

C. Why is EMFAC2011 being approved for PM10 and PM2.5 hot-spot analyses
at this time?

    On December 20, 2010, EPA published a notice which announced the
availability of EPA guidance documents for completing quantitative hot-
spot analyses and approved the use of the MOVES and the EMFAC2007
models for use in quantitative PM10 and PM2.5
hot-spot analyses (75 FR 79370). That notice started a two-year grace
period requiring project sponsors to use EMFAC2007 for new quantitative
PM10 and PM2.5 hot-spot analyses in California,
for conformity determinations involving projects of local air quality
concern.
    As with EMFAC2007, EMFAC2011 is capable of assessing project-level
emissions for PM10 and PM2.5 hot-spot analyses,
therefore EPA is approving EMFAC2011 for use in quantitative PM hot-
spot analyses for transportation conformity purposes within California.
As mentioned earlier, CARB has developed the EMFAC-PL tool, as a
simplified method to extract the appropriate emissions factors for
alternative vehicle data and speeds from EMFAC2011 for appropriate
projects. In today's notice, EPA recognizes the importance of this tool
for ensuring that project-level conformity analyses are done in a
consistent and accurate matter. To that end, we are also approving the
EMFAC-PL tool for project-level conformity analyses, and allowing other
tools to be approved by EPA, if such alternate project-level tools
provide for similar performance in applying EMFAC2011 emissions factors
for appropriate projects.\5\ EPA is updating Section 5 and related
appendices of our PM hot-spot quantitative guidance to describe how to
use the EMFAC2011 model for PM hot-spot analyses.\6\ EPA's revised
guidance will include details on what PM hot-spot analyses can rely on
the EMFAC-PL tool and which projects will require a different approach
to obtain the appropriate project-level EMFAC2011 emission factors. EPA
intends to complete its PM hot-spot guidance revision in the near
future. When completed, the updated guidance will be made available on
EPA's Web site: www.epa.gov/otaq/stateresources/transconf/projectlevel-hotspot.htm.
---------------------------------------------------------------------------

    \5\ EPA would approve any alternate project-level tool through a
letter, after completion of its review of model documentation
showing consistency with the EMFAC-PL approach.
    \6\ ``Transportation Conformity Guidance for Quantitative Hot-
Spot Analyses in PM2.5 and PM10 Nonattainment
and Maintenance Areas'' [EPA-420-B-10-040]. See www.epa.gov/otaq/stateresources/transconf/projectlevel-hotspot.htm.
---------------------------------------------------------------------------

D. Why does EPA consider EMFAC2011 as a major update to EMFAC?

    EMFAC2011 includes significant changes to its model interface, new
data and methodologies regarding calculation of motor vehicle emissions
and revisions to implementation data for control measures. EMFAC2011
includes updated data on truck activity, and emissions reductions
associated with the 2010 Truck and Bus rule, supporting new estimates
of emissions from heavy-heavy duty diesel trucks and buses. Motor
vehicle fleet age, vehicle types and vehicle population have also been
updated based on 2009 California Department of Motor Vehicle (DMV)
data. EMFAC2011 incorporates new temperature and humidity profiles.
Each of these changes impact emission factors for each area in
California. In addition to changes to truck activity, EMFAC
incorporates updated vehicle

miles traveled (VMT) for all vehicle classes. The new model interface
EMFAC-SG module will allow users to update the default VMT data and
speed profiles by vehicle class for different future scenarios. CARB's
web site describes these and other model changes at: http://www.arb.ca.gov/msei/emfac2011-documentation-final.pdf.

E. How were stakeholders and the public involved in the EMFAC
development process?

    Since 2010, CARB has held a series of public workshops to discuss
emissions inventory updates related to California's In-Use Heavy-Duty
Diesel Fueled Truck and Bus regulation (``Truck and Bus Regulation''),
and to receive comments on the regulations and the resulting changes in
the emissions inventory. Since the major changes to the EMFAC model are
associated with incorporation of the Truck and Bus Regulation into the
model, the technical foundations of these changes were presented to the
public in these workshops. CARB also conducted extensive beta testing
of interim versions of the model with air districts and Metropolitan
Planning Organizations (MPOs). These stakeholders had the opportunity
to request briefings with CARB staff and provide them with comments and
suggestions to improve the model. EPA was included in those discussions
and our suggestions were incorporated into the material available on
the CARB EMFAC2011 public web site. CARB also developed and posted
training modules for EMFAC2011 and supports a mobile source emissions
inventory email listserv to announce updates and changes to the EMFAC
supporting material.\7\
---------------------------------------------------------------------------

    \7\ To subscribe to CARB's listserv for Mobile Source Emission
Inventory development, see ``Join our MSEI listserv'' at
www.arb.ca.gov/msei/msei.htm.
---------------------------------------------------------------------------

    CARB also released a series of technical memos that describe each
update to the model and public presentations that summarize the changes
from earlier versions of the model. The technical memos are available
on CARB's Web site at: http://www.arb.ca.gov/msei/supportdocs.htm and
at http://www.arb.ca.gov/msei/categories.htm#onroad_motor_vehicles
Specific changes incorporated into the EMFAC2011 model are also
discussed in http://www.arb.ca.gov/msei/emfac2011-documentation-final.pdf. All presentations from the public workshops are available on
the CARB Web site at: http://www.arb.ca.gov/msprog/onrdiesel/workshops.htm.

F. Will a transportation conformity grace period be set by this
approval?

    Yes. The transportation conformity rule (40 CFR 93.111) requires
that conformity analyses be based on the latest motor vehicle emissions
model approved by EPA for SIP purposes for a state or area. Section
176(c)(1) of the CAA states that

    `` * * * [t]he determination of conformity shall be based on the
most recent estimates of emissions, and such estimates shall be
determined from the most recent population, employment, travel, and
congestion estimates. * * *''

    When EPA approves a new emissions model such as EMFAC2011, EPA will
consult with the U.S. Department of Transportation (DOT) to establish a
grace period before the model is required for conformity analyses (40
CFR 93.111(b)). However, areas have the option of using the new model
prior to the end of the grace period. The conformity rule provides for
a grace period for new emissions models of between 3 to 24 months. In
consultation with the Federal Highway Administration (FHWA) and the
Federal Transit Administration (FTA), EPA considers many factors in
establishing the length of the grace period, including the degree of
change in emissions models and the effects of the new model on
transportation planning in order to assure conformity (40 CFR 93.111).
    Upon consideration of all of these factors, EPA is establishing a
6-month grace period before EMFAC2011 is required for the following
conformity analyses:
     All new HC, NOX, PM10,
PM2.5 and CO regional emissions analyses (e.g., supporting
transportation plan and TIP conformity determinations); and
     All new CO, PM10 and PM2.5 hot-spot
analyses supporting project-level conformity determinations.
    The grace period begins on March 6, 2013 and ends on September 6,
2013. As discussed earlier in the notice, EMFAC2011 incorporates
significant changes to the model interface and procedures used to
estimate both emissions for regional emissions analysis and emissions
factors for hot-spot analyses for CO and PM. While these changes are
significant, the model has been available for review by air quality and
transportation agencies, consultants and the public since September
2011.
    For application of EMFAC2011 at the project level, CARB's EMFAC-PL
tool for appropriate projects has just recently been released,
therefore project sponsors developing project-level analysis may need
some time to familiarize themselves with this tool. EPA is also
updating our PM hot-spot quantitative guidance to include the new
EMFAC2011 procedures.
    Therefore, it is appropriate to set a 6-month grace period to allow
all areas in California to incorporate these new procedures in
conformity hot-spot analysis \8\ and apply the changes to the model
structure and updated planning assumptions incorporated in EMFAC2011 in
a timely manner. In the interim, new quantitative PM hot-spot analyses
that are started prior to the end of the EMFAC2011 grace period can be
based on EMFAC2007 and EPA's existing PM hot-spot guidance and
subsequently completed.
---------------------------------------------------------------------------

    \8\ EMFAC-PL or an alternative method or tool must be used for
new EMFAC2011 analyses of appropriate projects after the 6-month
grace period. If EPA approves alternative tools to the EMFAC-PL
tool, EPA does not intend to establish a new 6-month grace period.
---------------------------------------------------------------------------

    When the grace period ends on September 6, 2013, EMFAC2011 will
become the only approved motor vehicle emissions model for all new
regional and CO, PM10 and PM2.5 hot-spot
transportation conformity analyses across California. In general, this
means that all new HC, NOX, PM10,
PM2.5, and CO regional conformity analyses and CO,
PM10 and PM2.5 hot-spot analyses started after
the end of the 6-month grace period must be based on EMFAC2011, even if
the SIP is based on an earlier version of the EMFAC model.

G. Can areas use any other models during the grace period?

    Yes, the conformity rule provides some flexibility for regional
emissions analyses that are started before the end of the grace period.
Analyses that begin before or during the grace period may continue to
rely on EMFAC2007. The interagency consultation process should be used
if it is unclear if an EMFAC2007-based analysis was begun before the
end of the grace period. When the grace period ends on September 6,
2013, EMFAC2011 will become the only approved motor vehicle emissions
model for regional emissions analyses for transportation conformity in
California.
    CO, PM10 and PM2.5 hot-spot analyses for
project-level conformity determinations can be based on EMFAC2007 if
the analysis was begun before the end of the grace period, and if the
final environmental document for the project is issued no more than
three years after the issuance of the draft environmental document (see
40 CFR 93.111(c)). Therefore new quantitative and qualitative analysis
already underway that were started before the

end of the grace period using EMFAC2007 can be completed as long as
93.111(c) is satisfied. The interagency consultation process should be
used if it is unclear whether an EMFAC2007-based analysis is covered by
the circumstances described above.

H. Future Updates to EMFAC

    On January 31, 2006, CARB submitted a letter to EPA and to the
California Division of the FHWA indicating the State's intention to
make future revisions to update EMFAC. These EMFAC updates would
reflect, among other new information, updated vehicle fleet data every
three years. In California, MPOs and Air Districts have not been able
to update vehicle fleet data embedded into EMFAC. The EPA/USDOT
December 2008 guidance on latest planning assumptions and EPA's July
2004 final rule indicate that new vehicle registration data must be
used when it is available prior to the start of new conformity analyses
and that states and MPOs are strongly encouraged to update the data at
least every five years. CARB reaffirmed their commitment to keeping the
latest planning assumptions included in EMFAC updated on a three-year
cycle in the April 18, 2007 EMFAC submittal letter. The next update to
the planning assumptions in EMFAC is expected in 2014 or 2015 which
would most likely also include updates to the emissions factors of the
model as well.

III. Summary of EPA Actions

    As described in this notice, EPA is approving EMFAC2011 as
submitted by CARB on April 6, 2012 with the following limitations and
conditions:
    (1) The approval is limited to California.
    (2) The approval is Statewide and applies to estimation of
emissions of HC, CO, NOX, PM10, PM2.5,
lead, and sulfur oxides. However, EMFAC2011 will be used in
transportation conformity regional emissions analyses for pollutants
and precursors that are applicable in a given nonattainment or
maintenance area. EPA is approving all components of EMFAC2011,
specifically EMFAC-SG, EMFAC-LDV and EMFAC-HD. EPA is also approving
EMFAC2011 and the EMFAC-PL tool to estimate project-level emissions for
CO, PM10 and PM2.5 conformity hot-spot analyses.
    (3) A 6-month statewide transportation conformity grace period will
be established beginning March 6, 2013 and ending September 6, 2013 for
the transportation conformity uses described in (2) above.

    Dated: February 22, 2013.
Jared Blumenfeld,
Regional Administrator, Region IX.
[FR Doc. 2013-05245 Filed 3-5-13; 8:45 am]
BILLING CODE 6560-50-P


3. Baseline inhalation = no respirator (open mixing/loading or open cab
or enclosed cockpit).

4. 80% R inhalation = quarter-face dust/mist respirator resulting in 80%
reduction (open mixing/loading).

5. Acres treated values are from EPA estimates of acreage that could be
treated in a single day for each exposure scenario of concern, based on
the application method, and formulation/packaging type.

6. Daily dose (mg/kg/day) = [unit exposure (mg/lb ai)] x [absorption
(100%)] x [application rate (lb ai/acre)] x [amount treated (acres/day)]
/ [body weight (70 kg)].

7. Dermal MOE (with UF = 100) = [dermal NOAEL (10 mg/kg/day)] / [daily
dermal dose].

8. Inhalation MOE (with UF = 100) = [inhalation NOAEL (0.08 mg/kg/day)]
/ [daily inhalation dose].

9. Total MOE = 1/ [1/dermal MOE] + [1/inhalation MOE].

10. NA = Not Applicable (because MOEs do not exceed HED’s LOC at the
next lowest mitigation level).

11. Engineering control data for enclosed cockpits used for pilots.

	9.2	Short- and Intermediate-Term Post-Application Risk  TC \l2 "9.2
Short-/Intermediate-/Long-Term/Cancer (if needed) Postapplication Risk

	It is possible for agricultural workers to have post-application
exposures to pesticide residues during the course of typical
agricultural activities.  HED, in conjunction with the Agricultural
Re-entry Task Force (ARTF), has identified a number of post-application
agricultural activities that may occur, and which may result in
post-application exposures to pesticide residues.  HED has also
identified Transfer Coefficients (TCs), having units of cm²/hr,
relative to the various activities, which express the amount of foliar
contact over time during each of the activities identified.  For the
proposed new uses, the highest TC (1,500 cm²/hr) occurs during
"scouting" by crop advisors in flax, leafy green vegetables, legume
vegetables, and safflower.  Therefore, as a screening-level assessment,
HED herein uses a TC of 1,500 cm²/hr.

	The TCs used in this assessment are from an interim TC Standard
Operating Procedure (SOP) developed by HED’s ExpoSAC, using
proprietary data from the ARTF database (SOP #3.1).  It is the intended
by HED’s ExpoSAC that this SOP will be periodically updated to
incorporate additional information about agricultural practices in
crops, and new data on TCs.  Much of this information will originate
from exposure studies currently being conducted by the ARTF, from
further analysis of studies already submitted to the Agency, and from
studies in the published scientific literature.

	Lacking compound specific dislodgeable foliar residue (DFR) data, HED
assumes 20% of the application rate is available as DFR on day zero
after application.  This is adapted from the ExpoSAC SOP #003 of
5/7/1998 (revised 8/7/2000).

Daily dermal doset = DFRt (µg/cm2) x 1E-3 mg/µg x TC (cm2/hr) x DA x
ET (hrs)

						  BW (kg)

Where: 		t	=	number of days after application day (days),

	DFRt	=	dislodgeable foliar residue on day “t” (µg/cm2),

	TC	=	transfer coefficient (cm2/hr),

	DA	=	dermal absorption factor (unitless),

	ET	=	exposure time (hr/day), and

	BW	=	body weight (kg).

DFRt (µg/cm2) = AR (lb ai/acre) x F x (1-D)t x 4.54E8 µg/lb x 24.7E-9
acre/cm2

Where: 		AR	=	application rate (lb ai/acre),

             	F	=	fraction of ai retained on foliage or 20% (unitless),
and

              	D	=	fraction of residue that dissipates daily or 10%
(unitless).

See Table 9.2 (below) for a summary of post-application exposures and
risks.  An MOE of 100 or more is adequate to protect persons from
post-application exposures to lambda-cyhalothrin, as described in the
proposed use patterns.  Because the estimated MOEs are all greater than
100 (ranging from 520 to 13,000), post-application exposures arising
from the proposed uses do not exceed HED’s LOC.

Table 9.2	Exposure and Risk Assessment for Occupational Post-Application
1 Activities.

Proposed Crops	Use Rate

(lb ai/A)	Policy Crop Group Category	Exposure Potential	Transfer
Coefficient 2 (cm2/hour)	Activities

	DFR 3

(µg/cm2)	Daily Dose 4 (mg/kg/day)	MOE 5

Wild Rice	0.04	Field & Row Crops: Low to Medium	Low	100	Scouting	0.090
0.0010	9,700

	Medium	1,500	Scouting	0.090	0.015	650

Barley, Oats, Rye, Buckwheat	0.03	Field & Row Crops: Low to Medium	Low
100	Scouting	0.067	0.00077	13,000

	Medium	1,500	Scouting	0.067	0.012	870

Cucurbit Vegetables

	0.03	Vegetable: Cucurbit	Low	500	Irrigating, scouting, hand-weeding for
immature crops	0.067	0.0038	2600

	Medium	1,500	Irrigating, scouting, hand-weeding	0.067	0.012	870

	High	2,500	Hand-harvesting, hand-pruning, thinning	0.067	0.019	520

Tuberous and Corm Vegetables

[Potato]	0.03	Vegetable: Root & Tuber	Low

	300	Irrigating, scouting, hand-weeding for immature crops, thinning
0.067	0.0023	4,300

	Medium	1,500	Irrigation, scouting	0.067	0.012	870

Tuberous and Corm Vegetables

[All Others]	0.03	Vegetable: Root & Tuber	Low	300	Irrigating, scouting,
hand-weeding for immature crops, thinning	0.067	0.0023	4,300

	Medium	1,500	Irrigation, scouting	0.067	0.012	870

	High	2,500	Hand-harvesting	0.067	0.019	520

1. Post-application day is taken to be Day 0 for all activities (day
after treatment represents approximately 12 hours following application,
when sprays have dried).

2. Transfer coefficient from ExpoSAC Policy Memo #003.1 "Agricultural
Transfer Coefficients" of 8/7/2000.

3. DFR = [application rate (lb ai/acre)] x [fraction of active
ingredient that remains on the foliage when sprays have dried] x [4.54E8
µg/lb] x [24.7E-9 acre/cm2].

4. Daily dose = [DFR (µg/cm2)] x [TC (cm2/hr)] x [conversion factor (1
mg/1,000 µg)] x [exposure time (8 hrs/day)] / [body weight (70 kg)].

5. MOE = [NOAEL (10 mg/kg/day)] / [daily dose (mg/kg/day)].

10.0	Data Needs and Label Recommendations  TC \l1 "10.0	Data Needs and
Label Recommendations

	10.1	Toxicology  TC \l2 "10.1	Toxicology

	None

	10.2	Residue Chemistry  TC \l2 "10.2	Residue Chemistry

	No major deficiencies were noted in the subject petitions that would
preclude the establishment of permanent tolerances for
lambda-cyhalothrin on the proposed commodities.  Only minor deficiencies
were noted pertaining to the proposed label directions and recommended
tolerance levels (listed below).  HED  SEQ CHAPTER \h \r 1  recommends
in favor of establishing permanent tolerances for lambda-cyhalothrin
residues at the levels listed in Table 1.0.

	(1) Use directions for grasses should be clarified to specify that the
restriction of 0.03 lb ai/A per cutting includes pastures and rangeland
in addition to grasses grown for seed.  A minimum re-treatment interval
(RTI) of 30 days should be specified for pastures and rangeland which
are not cut between applications.  In addition, the PHI for forage
should be changed to 0 days, as PHIs for forage are not practical for
rangeland applications.

	(2) A tolerance was not proposed in rye bran.  Based on the available
wheat residue data, a separate tolerance is required at 0.2 ppm in rye,
bran.

	(3) Based on the calculated TDBs for livestock, and the available
livestock residue studies, the current tolerance for lambda-cyhalothrin
in milk fat is too low.  An increased tolerance should be proposed in
milk fat at 10 ppm (reflecting 0.4 ppm in whole milk).  The data also
indicate that the current tolerances in hog commodities could be lowered
to 0.2 ppm in fat, 0.01 ppm in meat, and 0.02 ppm in meat byproducts.

	10.3	Occupational and Residential Exposure  TC \l2 "10.3	Occupational
and Residential Exposure

	The labels for Warrior® Insecticide (EPA Registration #100-1112) and
Karate® Insecticide (EPA Registration #100-1097) should state that
mixer/loaders supporting aerial applications to wild rice at a rate of
0.04 lb ai/A, and treating 1200 acres (or more) per day, are required to
use a dust-mist respirator.

References:  TC \l1 "References:

Carcinogenicity Determination

	GAMMA CYHALOTHRIN - 1ST Report of the Hazard Identification Assessment
Review Committee.; TXR #0052388; Jess Rowland; 3/1/2004.

Dietary Exposure Memorandum

	Lambda-cyhalothrin:  Acute and Chronic Dietary (Food and Drinking
Water) Exposure and Risk Assessment for Section 3 Uses on Barley, Oat,
Rye, Wild Rice, Buckwheat, Pistachio, Cucurbit Vegetables (crop group
9), Grass Forage & Hay (crop group 17), and Tuberous & Corm vegetables
(crop group 1-C).; D324223; Anant Parmar; 3/12/07

Drinking Water Memorandum

	Tier I Estimated Environmental Concentrations of Lambda-Cyhalothrin and
It’s Transformation Product of Concern XV for the Use in the Human
Health Risk Assessment.; D324222, D330149; Jose Melendez; 10/26/2006.

Occupational and Residential Exposure Memorandum

	LAMBDA-CYHALOTHRIN - Human, Nondietary Exposure/Risk Assessment for the
Proposed New Uses of Lambda-Cyhalothrin on Barley, Buckwheat, Oat, Rye,
Wild Rice, Cucurbit and Tuberous and Corm Vegetables.; D334896; Mark I.
Dow; 12/26/2006.

	Lambda Cyhalothrin: Occupational and Residential Risk Assessment for
the use on Cereal Grains, Corn, Soybeans, Sunflowers, Sorghum, Lettuce,
Cole Crops, Onions, Garlic, Legumes, Fruiting Vegetables, Stone and Pome
Fruits, Tree Nuts, Sugar Cane, Cotton, Rice, Tobacco, Canola for Seed
and as a Termiticide.; D280103; Margarita Collantes; 8/14/2002.

Residue Chemistry Data Review Memorandum

	Lambda-Cyhalothrin.  Petitions Requesting Permanent Tolerances
(Associated with Section 3 Registration) for Food/Feed Use of the
Insecticide on Cucurbit Vegetables (Group 9), Tuberous and Corm
Vegetables (Subgroup 1C), Grass Forage, Fodder, and Hay (Group 17),
Barley, Buckwheat, Oat, Rye, Wild Rice, and Pistachios.  Summary of
Analytical Chemistry and Residue Data.  Petition Numbers 5F6994, 3E6593,
and 6E7077; D313315, D324219, D330542; William T. Drew; 12/27/2006.

Risk Assessment Document

	PP#0F6092.  Request for the Use of Lambda-Cyhalothrin in/on Canola,
Pome Fruits, Stone Fruits, Tree Nuts, Almond Hulls, and Tobacco.
PP#9F4875.  Request for the Use of Lambda-Cyhalothrin on Imported
Avocados; Cereal Grains (except Rice); Fruiting Vegetables (except
Cucurbits); Peanut Hay; Peas and Beans, Dried and Succulent Shelled, and
Edible Podded; Sorghum Forage and Fodder; and Sugarcane.  New Use:
IMPASSE Barrier Termiticide End-use Product.; D284860; Kit Farwell;
8/15/2002.

	Risk Assessment for Extension of Tolerances for Synthetic Pyrethroids;
D238737; Pamela Hurley, John Whalan, Jeff Evans, George Herndon, Steve
Knizner; 11/14/1997.

AppendiX A:  Toxicology Assessment

A.1	Toxicology Data Requirements TC \l2 "A.1  Toxicology Data
Requirements

	The requirements (40 CFR §158.340) for food-use of lambda-cyhalothrin
are in Table 1, below.  Use of the new guideline numbers does not imply
that the new (1998) guideline protocols were used.

Table A.1	Toxicology Data Requirements.

Test

	Technical

	Required	Satisfied

870.1100    Acute Oral Toxicity

870.1200    Acute Dermal Toxicity

870.1300    Acute Inhalation Toxicity

870.2400    Primary Eye Irritation

870.2500    Primary Dermal Irritation

870.2600    Dermal Sensitization		yes

yes

yes

yes

yes

yes	yes

yes

yes

yes

yes

yes

870.3100    Oral Subchronic (rodent)

870.3150    Oral Subchronic (non-rodent)

870.3200    21-Day Dermal

870.3250    90-Day Dermal

870.3465    90-Day Inhalation		yes

yes

yes

yes

yes	yes

yes

yes

yes

yes

870.3700a  Developmental Toxicity (rodent)

870.3700b  Developmental Toxicity (non-rodent)

870.3800    Reproduction		yes

yes

yes	yes

yes

yes

870.4100a  Chronic Toxicity (rodent)

870.4100b  Chronic Toxicity (non-rodent)

870.4200a  Carcinogenicity (rat)

870.4200b  Carcinogenicity (mouse)

870.4300    Chronic/carcinogenicity		no

yes

no

no

yes	-

yes

-

-

yes

870.5100    Mutagenicity—Gene Mutation - bacterial

870.5300    Mutagenicity—Gene Mutation - mammalian

870.5xxx    Mutagenicity—Structural Chromosomal Aberrations

870.5xxx    Mutagenicity—Other Genotoxic Effects		yes

yes

yes

yes	yes

yes

yes

yes

870.6100a  Acute Delayed Neurotoxicity (hen)

870.6100b  90-Day Neurotoxicity (hen)

870.6200a  Acute Neurotoxicity Screening Battery (rat)

870.6200b  90-Day Neurotoxicity Screening Battery (rat)

870.6300    Developmental Neurotoxicity		no

no

yes

no

yes	-

-

yes

-

no1

870.7485    General Metabolism

870.7600    Dermal Penetration		yes

no	yes

yes

Special Studies for Ocular Effects

Acute Oral (rat)

Subchronic Oral (rat)

Six-month Oral (dog)		no	-

1  Although classified unacceptable, a repeat DNT study is not required.
 See section 3.3.6 for more details.A.2	Toxicity Profiles TC \l2 "A.2
Toxicity Profiles

Table A.2.1a	Acute Toxicity Profile – Lambda-cyhalothrin.

Guideline Number	Study Type	MRI

Number(s)	Results	Toxicity Category

870.1100	Acute oral - rat	00151582	LD50 = 79 mg/kg (♂)

         = 56 mg/kg (♀)	II

870.1200	Acute dermal - rat	00151583	LD50 = 632 mg/kg (♂)

         = 696 mg/kg (♀)	II

870.1300	Acute inhalation - rat	40994701	LC50 = 0.065 mg/L (♂& ♀)	II

870.2400	Acute eye irritation 	00151586	Mild irritant.	II

870.2500	Acute dermal irritation - rabbit	00151584	Not an irritant.	IV

870.2600	Skin sensitization - guinea pig	00151585	Not a sensitizer in
the guinea pig.	N/A

Table A.2.1b	Acute Toxicity Profile –Cyhalothrin

Guideline Number	Study Type	MRID

243 mg/kg (♂)

         = 144 mg/kg (♀)	II

870.1200	Acute dermal - rat

Acute dermal - rabbit	00154865

00154865	LD50 > 1000 mg/kg
                                                    (♂& ♀)

LD50 > 2 g/kg  (♂& ♀)	II

III

870.1300	Acute inhalation - rat	00150847	LC50 = 0.173 mg/L (♂)

LC50 = 0.183 mg/L (♀)	II

870.2400	Acute eye irritation 	00154868	Moderate irritant without
irrigation; mild irritant with irrigation.	III

870.2500	Acute dermal irritation - rat

Acute dermal irritation - rabbit	00154867

00154867	Mild dermal irritant

Not an irritant.	IV

IV

870.2600	Skin sensitization - guinea pig	00154866	Not a sensitizer in
the guinea pig.	N/A

Table A.2.2	Subchronic, Chronic and Other Toxicity Profile.

Guideline Number	Study Type	MRID Number/Year/ Classification /Doses
Results

NA*	28-Day oral toxicity – rat

(cyhalothrin)	00153029

1984 Acceptable non-guideline

0, 2, 10, 25, 50, 75 mg/kg/day	NOAEL: 2 mg/kg/day

LOAEL: 10 mg/kg/day (clinical signs of neurotoxicity). At higher doses,
decreases in body weight gain and food consumption, and changes in organ
weights.

NA	28-Day oral toxicity – rat

(cyhalothrin)	00154806

1984 Acceptable non-guideline

0, 0.1, 0.5, 1.0, 2.0, or 25.0 mg/kg/day	NOAEL: 1.0 mg/kg/day

LOAEL: 2.0 mg/kg/day (decreases in mean body weight gain in females).

NA	28-Day oral toxicity – mouse

(cyhalothrin)	43241901

1981 Acceptable non-guideline

0, 0.65, 3.30, 13.5, 64.2, 309 mg/kg/day (males)

0, 0.80, 4.17, 15.2, 77.9, 294 mg/kg/day (females)	NOAEL: 64.2/77.9
mg/kg/day

LOAEL: 309/294 mg/kg/day (mortality, clinical signs of toxicity,
decreases in body weight gain and food consumption, changes in
hematology and organ weights, minimal centrilobular hepatocyte
enlargement).

870.3100	90-Day oral toxicity – rat

(cyhalothrin)	00154805

1981 Acceptable

0, 0.5, 2.5, 12.5 mg/kg/day	NOAEL: 2.5 mg/kg/day

LOAEL: 12.5 mg/kg/day (decreased body weight gain in males).

870.3100	90-Day oral toxicity – rat

(lambda-cyhalothrin)	00153028

1985 Acceptable

0, 0.5, 2.5, 12.5 mg/kg/day	NOAEL: 2.5 mg/kg/day

LOAEL: 12.5 mg/kg/day (reduced body weight gain and food consumption in
both sexes, and food efficiency in females).

870.3150	26-Week feeding study – dog

(cyhalothrin)	00154795

1981 Acceptable

0, 1.0, 2.5, 10.0 mg/kg/day	NOAEL: 1.0 mg/kg/day

LOAEL: 2.5 mg/kg/day (increase in liquid feces. At 10.0 mg/kg/day,
clinical signs of neurotoxicity)

870.3200	21-Day dermal toxicity – rat

(lambda-cyhalothrin)	44333802

1989 Acceptable

0, 1, 10 mg/kg/day for 6 hours/day for 21 consecutive days; 2-3
applications at 100 mg/kg/day, reduced to 50 mg/kg/day for 21
consecutive days.	NOAEL: 10 mg/kg/day

LOAEL: 50 mg/kg/day (clinical signs of toxicity, decreased body weight
and body weight gain).

870.3200	21-Day dermal toxicity – rabbit

(cyhalothrin)	00154869

1982 Acceptable

0, 10, 100, 1000 mg/kg/day for 6 hours/day, 5 days/week, for total of 15
applications.	NOAEL: 100 mg/kg/day

LOAEL: 1000 mg/kg/day (significant weight loss).

870.3465	21-Day inhalation toxicity – rat

(lambda-cyhalothrin)	41387702

1990 Acceptable non-guideline

0, 0.3, 3.3, 16.7 g/L (approximately 0, 0.08, 0.90, 4.5 mg/kg/day)
NOAEL: 0.08 mg/kg/day

LOAEL: 0.90 mg/kg/day (clinical signs of neurotoxicity, decreased body
weight gains, increased incidence of punctate foci in cornea, slight
reductions in cholesterol in females, slight changes in selected
urinalysis parameters).

870.3700a	Pre-natal developmental – rat

(cyhalothrin)	00154800

1981 Acceptable

0, 5, 10, 15 mg/kg/day

	Maternal NOAEL: 10 mg/kg/day

Maternal LOAEL: 15 mg/kg/day (uncoordinated limbs, reduced body weight
gain and food consumption).

Developmental NOAEL: 15 mg/kg/day (HDT)

Developmental LOAEL: > 15 mg/kg/day

870.3700b	Pre-natal developmental – rabbit

(cyhalothrin)	00154801

1981 Acceptable

0, 3, 10, 30 mg/kg/day

	Maternal NOAEL: 10 mg/kg/day

Maternal LOAEL: 30 mg/kg/day (reduced body weight gain and food
consumption).

Developmental NOAEL: 30 mg/kg/day (HDT)

Developmental LOAEL: > 30 mg/kg/day

870.3800	Reproduction and fertility effects – rat

(cyhalothrin)	00154802

1984 Acceptable

0, 0.5, 1.5, 5.0 mg/kg/day	Parental/Offspring NOAEL: 1.5 mg/kg/day

Parental/Offspring LOAEL: 5.0 mg/kg/day (decreased parental body weight
and body weight gain during premating and gestation periods and reduced
pup weight and weight gain during lactation).

Reproductive NOAEL: 5.0 mg/kg/day (HDT).

870.4100b	Chronic toxicity – dog

(lambda-cyhalothrin)	40027902

1986 Acceptable

0, 0.1, 0.5, 3.5 mg/kg/day	NOAEL: 0.1 mg/kg/day

LOAEL: 0.5 mg/kg/day (clinical signs of neurotoxicity).

870.4200	Carcinogenicity –

mouse

(cyhalothrin)	00150842

1984 Acceptable

0, 3, 15, 75 mg/kg/day	NOAEL: 15 mg/kg/day

LOAEL: 75 mg/kg/day (increased incidence of piloerection, hunched
posture; decreased body weight gain in males).  Not oncogenic under
conditions of study. HDT was inadequate; however, a new study not
required at this time.

870.4300	Carcinogenicity – rat

(cyhalothrin)	00154803

1984 Acceptable

0, 0.5, 2.5, 12.5 mg/kg/day	NOAEL: 2.5 mg/kg/day

LOAEL: 12.5 mg/kg/day (decreases in mean body weight).  Not oncogenic
under conditions of study.

870.6200a	Acute neurotoxicity screening battery – rat

(lambda-cyhalothrin)	44861510

1999 Acceptable

0, 2.5, 10, 35 mg/kg	NOAEL: 10 mg/kg

LOAEL: 35 mg/kg (clinical observations indicative of neurotoxicity, and
changes in FOB parameters).

870.6300	Developmental neurotoxicity

(lambda-cyhalothrin)	46449102

2004 Unacceptable

0, 25, 60, 150 ppm

0, 2, 4, 20 mg/kg/day	Maternal NOAEL: 4 mg/kg/day

Maternal LOAEL:  10 mg/kg/day (decreased body weight, body weight gain,
and food consumption).

Although Offspring neurotoxicity was seen with a LOAEL/NOAEL of 10/4, a
definitive LOAEL/NOAEL cannot be determined due to many data
insufficiencies.  (officially – for effects observed in the acceptable
parameters of the DNT study see Section 3.3.2).

870.7485	Metabolism and pharmacokinetics – rat	00151116, 00150852,
00150852,

00150852, 00153036, 00153037

1981, 1984, 1985 Acceptable when combined together.	In the rat,
approximately 55% of the oral dose is absorbed.  It is extensively
metabolized when absorbed. After subcutaneous administration, the
urinary/fecal excretion ratio is 2.5:1.0. Over 50% of the dose remained
in the carcass 7 days after a subcutaneous dose. Metabolism includes
cleavage of the ester to cyclopropylcarboxylic acid and a phenoxybenzyl
derivative. The distribution patterns and excretion rates in the
multiple oral dose studies are similar to the single oral dose studies.
There is accumulation of unchanged compound in the fat upon chronic
administration. Otherwise, cyhalothrin is rapidly metabolized and
excreted. Cyclopropyl carboxylic acid, 3 phenoxybenzoic acid,
glucuronide conjugated 3-4'- hydroxyphenoxy benzoic acid and a sulfate
conjugate were identified in the urine. Cyhalothrin is taken up slowly
by the fat and released slowly. It is rapidly released by blood,
kidneys, liver. The rate of metabolism of both enantiomer pairs are
likely identical (i.e. PP321 & PP563). The absorption, distribution,
metabolism and excretion patterns of PP321 and cyhalothrin following a
single dose of 1 mg/kg in the male rat appear to be identical.

870.7485	Metabolism and pharmacokinetics – dog	00150843, 00150852

1984 Acceptable when combined together.	In the dog, absorption of the
C14 benzyl label was 80% and absorption of the C14 cyclopropyl label was
48%. The metabolite patterns were different, indicating extensive
cleavage of the ester bond. Seven metabolites in urine were identified
for the benzyl label, and 12 metabolites for the isopropyl label. In the
feces, a large proportion of the radioactivity was due to unchanged
compound. Excretion in urine and feces was rapid (nearly all in 48
hours).

870.7600	Dermal penetration	44990402

1991 Acceptable

0.979, 0.099, 0.001 and 0.0008 mg/cm2 for 0.5, 1, 2, 4, 10, and 24
hours.	Absorption ranged from 3.46 to 15.89%.

870.7600	Dermal penetration	44333801

1984 Acceptable non-guideline

Dermal studies: 1.25 mg/50 cm2 dermal and 20 mg/800 cm2.  Dermal dose
washed quantitatively after 8 hours.

Oral study: 5 mg	Mild paresthesia of varying degrees was observed
following dermal dosing. The minimal oral absorption was estimated to be
from 50.35 to 56.71%. The minimal dermal absorption was estimated to be
from 0.115 to 0.122%. The estimated dermal absorption value of 1% was
determined by rounding these values up to the nearest whole number. No
metabolites were found near the limit of detection in plasma from the
oral dose study. Blood was not analyzed from the dermal study.

* NA = Not Applicable.

A.3	Executive Summaries TC \l2 "A.3  Executive Summaries

A.3.1	Subchronic Toxicity

	Non-Guideline	28-Day Oral Toxicity – Rat

	In a 28-day feeding study (MRID #00153029) in male and female SPF
AlpklAP Wistar-derived rats (16/sex/dose), cyhalothrin (PP563, 89.0%)
and PP654, an isomer mixture similar to cyhalothrin which contains both
cis and trans isomers (cyhalothrin contains only the cis isomer), were
fed in the diet at levels of 0, 20, 100, 250, 500, or 750 ppm (estimated
to be approximately 0, 2, 10, 25, 50, or 75mg/kg/day cyhalothrin, based
on use of very young animals; clinical signs upon which the NOAEL is
based started on day 3), and 500 or 750 ppm (approximately 50 or 75
mg/kg/day PP564). The animals were examined once daily for clinical
signs of toxicity.  Body weights, food consumption, hematological and
clinical chemistry parameters, ophthalmological examinations, urinalysis
parameters, organ weights, and macroscopic examinations were conducted
and/or measured.  For cyhalothrin, livers from up to 8/sex/group were
fixed in formol corrosive for microscopic examination.  The remaining
livers plus selected tissues (including sciatic nerves, brain, and
spinal cord) from 8/sex/group were fixed in formol saline for
microscopic examination.  The livers from the PP564 animals were
included in this group.  In addition, the left sciatic, and posterior
tibial nerves from 4 male and 4 female controls and high dose
cyhalothrin groups were fixed in formol glutaraldehyde for microscopic
examination.  With all remaining animals, only abnormal appearing
tissues were examined microscopically.  Livers from 6/sex/group were
taken for measurement of hepatic aminopyrine N-demethylase (APDM)
activity and electron microscopy.  Smooth endoplasmic reticulum (SER)
was quantified.

	At 20 ppm and above, a dose-related increase in APDM activity was
observed in males.  At 20 ppm, the increase was only slight (26.00
versus 22.30 tmoles HCHO/hr/g liver).  Slight hypersensitivity to touch
was observed in 4 females starting on day 2; however, this had a
variable dose-response.  At 100 ppm and above, a dose-related increase
in APDM activity was observed in females.  At 100 ppm, the increase was
only slight (14.21 versus 12.03 imoles HCHO/hr/g liver).  Clinical signs
included high stepping gait in 1 male on day 3, and slight
hypersensitivity to touch (2 males on days 2-4, 3 females on day 2) and
sound (2 males on day 23; again, variable dose-response).  At 250 ppm, 1
male and 2 females had high-stepping gait starting on day 2, 2 males had
ataxia starting on day 3, 3 males had hunched posture starting on day 4,
and 5 females had increased activity starting on day 4.  In addition,
significant decreases in mean body weight gain and food consumption
(both sexes), increases in mean relative liver weights, and decreases in
mean heart weights were observed at 250 ppm and above.  At 500 ppm and
above, high stepping gait, ataxia, hunched posture, tail erect,
increased activity, lack of grooming, and salivation were the major
dose-related clinical signs with cyhalothrin.  Reductions in serum
plasma triglyceride levels, and protein excretion levels in urine were
observed in males.  At higher dose levels, the reductions in serum
plasma triglyceride levels were observed in both sexes.  With PP564,
high stepping gait, ataxia, hunched posture, and increased activity in
females were observed, but to a lesser extent.  Reductions in serum
plasma triglyceride levels were also observed.  At 750 ppm an additional
clinical sign of loss of stability was observed in 1 male and 3 females.
 With PP564, similar clinical signs were observed as with cyhalothrin,
but to a lesser extent.  Loss of stability was not observed.

	The NOAEL for cyhalothrin is 20 ppm (2 mg/kg/day), and the LOAEL is 100
ppm (10 mg/kg/day), based on clinical signs of neurotoxicity.  At higher
dose levels, decreases in body weight gain and food consumption, and
changes in organ weights were also observed.  The NOAEL for PP564 is
less than 500 ppm (50 mg/kg/day).

	This study is classified as acceptable (non-guideline), and does not
satisfy any particular guideline requirement.

	Non-Guideline	28-Day Oral Toxicity – Rat

	In an oral toxicity study (MRID #00154806), SPF Wistar (Alderly Park
strain) rats (8/sex/dose) were dosed with cyhalothrin (89.2% ai) in the
diet at 0, 1, 5, 10, 20, or 250 ppm (approximately 0, 0.1, 0.5, 1.0,
2.0, or 25.0 mg/kg/day using a factor of 10 for young animals) for 28
days (MRID #00154806).  Animals were examined for clinical signs of
toxicity, and the following parameters were measured: body weights,
liver weights, and hepatic aminopyrene-N-demethylase (APDM) activity.
In addition, the livers were subjected to electron microscopic
examinations.

	No effects were observed at 1, 5, and 10 ppm.  At 20 ppm and above, a
reduction in mean body weight gain was observed in females (p < 0.05;
22% less than the control value for weeks 0-4); however, body weight was
not affected.  At 250 ppm, a reduction in mean body weight gain was
observed in males (13% less than the control value for weeks 0-4).  In
addition, increases and/or proliferation in APDM (14-40%), and smooth
endoplasmic reticulum (SER) was observed in both sexes.  Relative liver
weights were increased in males (7%); however, absolute liver weights
were not affected.

	The NOAEL is 10 ppm (1.0 mg/kg/day in females) and 20 ppm (2.0
mg/kg/day in males), and the LOAEL is 20 ppm (2.0 mg/kg/day in females),
and 250 ppm (25.0 mg/kg/day in males) based on decreases in mean body
weight gain in females at 20 ppm and above, and in males at 250 ppm, and
increases and/or proliferation in APDM and SER in both sexes at 250 ppm.

	This study is classified as acceptable (non-guideline), and does not
satisfy any particular guideline requirement.

	Non-Guideline	28-Day Oral Toxicity – Mouse

	Cyhalothrin (technical, no purity available) was tested in a 4-week
oral feeding study (MRID #43241901) in CD-l mice as a range-finding
study for the carcinogenicity study.  Twelve mice/sex/dose level were
tested at 0, 5, 25, 100, 500, or 2000 ppm in the diet (0, 0.65, 3.30,
13.5, 64.2, or 309 mg/kg/day for males, and 0, 0.80, 4.17, 15.2, 77.9,
or 294 mg/kg/day for females).

	At 2000 ppm, piloerection, abnormal gait (walking on toes), hunched
posture, increase in respiration rate, and emaciated appearance were
observed.  Six males and 3 females died during the study.  Both males
and females had a significant decrease in body weight gain over the
treatment period when compared to controls (-l g versus 5 g in controls
for males, p < 0.001, and 0 g versus 3 g in controls for females, p <
0.001) .  A decrease in food consumption was observed in both sexes
during the first week (60.8% of controls for males, and 62.5% of
controls for females), and in females for the remainder of the study
(82% of controls, p < 0.05).  Males had a slightly lower mean total
white blood cell count (6.8%).  The differential white cell count
revealed lower lymphocyte counts (58.7%), and higher neutrophil counts
(62.5% above controls), p < 0.01, for all hematological values in males
at this dose level.  Significantly higher APDM activity was observed in
both sexes (61.9% above controls for males, and 77.8% above controls for
females).  Slight increases in kidney weights (28.8% over controls for
males, p < 0.001), and liver weights (17% over controls for males, p <
0.05, and 3.1 % over controls for females) were observed.  In females,
the differences were not statistically significant.  Slightly lower
heart weights were also observed in females (87.7% of controls, p <
0.05).  Minimal centrilobular hepatocyte enlargement was observed in 2
of 12 females.

	At 500 ppm, piloerection was observed in several mice, several males
had low white blood cell counts (not statistically significant) as well
as marginally lower lymphocyte numbers (80%).  Significantly higher APDM
activity was observed in females (26.2% over controls).  Slightly higher
kidney weights were observed in males (13.5% over controls, p < 0.02),
and slightly lower heart weights were observed in females (93.0%, p <
0.05).

	At 100 ppm, piloerection was also observed in several mice.  One female
had an emaciated appearance.  Marginally lower lymphocyte numbers were
noted for males (79% of controls).  Significantly higher APOM activity
was observed in females (24.8% over controls).  Slightly higher kidney
weights were observed in males (13.0% over controls, p < 0.01), and
marginally lower heart weights were observed in females (87.7%, p <
0.01).

	The NOAEL is 500 ppm, and the LOAEL is 2000 ppm, based on mortality,
clinical signs of toxicity, decreases in body weight gain and food
consumption, changes in hematology and organ weights, and minimal
centrilobular hepatocyte enlargement.  The minimal effects observed at
500 and 100 ppm are not considered to be toxicologically significant.

	This study is not a guideline requirement, and thus does not satisfy
any guideline requirements.

	870.3100	90-Day Oral Toxicity – Rat

	In a 90-day feeding study (MRID #00154805) in male and female SPF
Alderley Park Wistar-derived rats, technical cyhalothrin (92.2% w/w
pyrethroids of which 96.8% was cyhalothrin) was fed in the diet at
levels of 0, 10, 50, or 250 ppm (estimated to be 0, 0.5, 2.5, or 12.5
mg/kg/day).  Twenty rats/sex/dose level were assigned.  The animals were
examined for clinical signs of toxicity.  Body weights, food
consumption, hematological and clinical chemistry parameters, urinalysis
parameters, organ weights, and macroscopic and microscopic observations
were recorded.  In addition, hepatic aminopyrine-N-demethylase activity
was measured.

	No significant treatment-related effects were observed at 0.5 or 2.5
mg/kg/day.  At 12.5 mg/kg/day, mean body weight (10-16% less than
controls) and body weight gain (13% less than controls) were
significantly reduced in males (p < 0.01).  Mean body weight was also
significantly reduced in females at this level, but only during the
first week (p < 0.05).  This decrease in body weight gain was
accompanied by a decrease in food consumption; however, there was no
effect on food utilization at any dose level.  Dietary palatability, and
food refusal with concurrent reduced body weight may be a factor.  A
dose-related reduction in mean red cell volume values was observed in
both sexes at all dose levels at week 13; however, a downward trend was
also observed in the controls.  Hemoglobin, hematocrit, and red blood
cell counts were elevated, indicating an opposite trend or an
accommodation.  Small isolated differences in selected clinical
chemistry parameters; however they were not dose related, or recurring
on the time basis, nor were they supported by microscopic findings.
Hence, neither the hematological nor the clinical chemistry changes are
considered compound-related.  Hepatic aminopyrine-N-demethylase activity
was increased in both sexes at 12.5 mg/kg/day, and in the males at 2.5
mg/kg/day.  This is a reversible, compensatory change usually considered
to be adaptive rather than an adverse toxicological response.

	The NOAEL is 2.5 mg/kg/day, and the LOAEL is 12.5 mg/kg/day, based on
decreased body weight gain in males.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a subchronic oral study (§82-1) in the rat.

	870.3100	90-Day Oral Toxicity – Rat

	In a 90-day feeding study (MRID #00153028) in male and female SPF
Alk/AP Wistar-derived rats (20/sex/dose), lambda-cyhalothrin (96.5%) was
fed in the diet at levels of 0, 10, 50, or 250 ppm (0, 0.5, 2.5, or 12.5
mg/kg/day).  The animals were examined once daily for clinical signs of
toxicity.  Body weights, food consumption, hematological and clinical
chemistry parameters, urinalysis parameters, organ weights, and
macroscopic and microscopic observations were recorded.

	No treatment-related effects were observed at 0.5 mg/kg/day.  At 2.5
mg/kg/day, increased mean liver weight, and increased activity of
hepatic aminopyrine-N-demethylase (APDM) were observed in males.  This
is considered to be an adaptive response.  At 12.5 mg/kg/day,
significantly reduced body weight gain and food consumption were
observed in both sexes, as well as increased mean liver weight, and
increased APDM activity in both sexes.  There was also a slight but
statistically significant reduction in food efficiency in females at
this dose level.

	The NOAEL is 2.5 mg/kg/day, and the LOAEL is 12.5 mg/kg/day, based on
reduction in body weight gain and food consumption in both sexes, and
food efficiency in females.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a subchronic feeding study (§82-1) in the
rat.

	870.3150	180-Day Oral Toxicity – Dog

	In a 26-week oral study in male and female beagle dogs (MRID
#00154795), six dogs/sex/dose level received technical cyhalothrin
(pyrethroid content = 92.2% w/w, of which 96.8% is cyhalothrin) via oral
administration in gelatin capsules.  The test chemical had been
dissolved in corn oil prior to placement in the capsules.  The following
dose levels were tested: 0, 1.0, 2.5, or 10.0 mg/kg/day.  The following
parameters were measured and/or recorded: daily clinical observations,
body weights, food consumption, ophthalmological examinations,
neurological examinations, clinical biochemistry, urinalysis, gross
necropsy, and microscopic examinations.

	At 1.0 mg/kg/day, a slight increase in the passage of liquid feces was
observed in both sexes combined (7% over the control group).  This was
the only effect observed at this dose level and it was not considered to
be of toxicological significance.

	At 2.5 mg/kg/day, liquid feces were observed at an increased rate (26%
over the control group, both sexes combined).  No other effects were
observed.  At this dose level, due to the greater number of animals
affected, and the greater increase in incidence, the liquid feces was
considered to be a toxicological effect.

	At 10.0 mg/kg/day, liquid feces were observed at an increased rate over
the control group (both sexes).  In addition, the following effects were
observed: increase in water consumption during first 4 weeks, vomiting,
usually within a few hours following dosing, and occasional unsteadiness
and/or muscular trembling.  During week 2, head shaking, and excessive
salivation were observed in several dogs.  These signs were observed
only occasionally during the subsequent test weeks.  One male had more
severe signs.  During the second week, excessive salivation, and head
shaking were noted.  On day 14, 3 hours post-dosing, the dog was in a
state of collapse, stiff-limbed, and frothing at the mouth with the
presence of vomitus.  It recovered in 6 hours.  In the following weeks
with this dog, there were periods of head shaking, salivation, loss of
appetite, episodes of collapse, muscular spasms, marked incoordination,
vocalization, and one episode of convulsive behavior (week 8).

	The NOAEL is 1.0 mg/kg/day, and the LOAEL is 2.5 mg/kg/day, based on an
increase in incidence of liquid feces.  At 10.0mg/kg/day, liquid feces,
and clinical signs of neurotoxicity (occasional unsteadiness and/or
muscular trembling, head shaking, excessive salivation, frothing at the
mouth, stiff-limbed, episodes of collapse, muscular spasms, marked
incoordination, vocalization, and one episode of convulsive behavior in
week 8) were observed.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a subchronic oral study (§82-1) in the dog.

	870.3200	21-Day Dermal Toxicity – Rat

	In a repeated-dose dermal toxicity study (MRID #44333802),
lambda-cyhalothrin (96.6% ai) was applied to the clipped skin of five
albino rats/sex/dose at dose levels of 1 or 10 mg/kg/day for 6 hours/day
for 21 consecutive days.  Five rats/sex were similarly treated with two
or three applications at 100 mg/kg/day, reduced to 50 mg/kg/day for 21
consecutive days.

	Two males which were found dead after three applications of 100
mg/kg/day had reduced, moderately atrophied seminal vesicles, and
slightly atrophied spleens.  Clinical signs indicative of neurotoxicity
were observed in the 100/50 mg/kg/day treatment groups.  Males exhibited
reduced splay reflex, downward curvature of the spine, splayed gait,
bizarre behavior, pinched-in sides, dehydration, reduced stability, and
thin appearance.  Females exhibited an increased incidence of tiptoe
gait, upward curvature of the spine, an increased incidence in signs of
urinary incontinence, urinary incontinence, chromodacryorrhea, and
reduced splay reflex.  The clinical signs commenced on day 2 of dosing.
Body weight gains for males were significantly reduced throughout the
study; the final gain was 58% lower than the control gain.  The final
mean body weight was 19% lower than the mean control value.  Body weight
gains for females were somewhat reduced only during the first half of
the study.  Food consumption was somewhat reduced for males throughout
the study.  No dermal irritation was observed at 100/50 mg/kg/day in
either sex.  No signs of clinical toxicity or dermal irritation in the
10 or 1 mg/kg/day treatment groups were considered to be
treatment-related.  No treatment-related differences in hematology or
clinical blood chemistry parameters, organ weights, or histopathology
were observed between the treatment and control groups.  No neoplastic
tissue was observed.

	The LOAEL is 50 mg/kg/day for both sexes, based on clinical signs of
toxicity and decreased body weight and body weight gain.  The NOAEL is
10 mg/kg/day for males and females.

	This dermal toxicity study is classified acceptable (§82-2), and
satisfies the guideline requirement for a repeated-dose dermal toxicity
study.

	870-3200	21-Day Dermal Toxicity – Rabbit

	In a repeated-dose dermal toxicity study (MRIDs #00154869, #41062701),
cyhalothrin (90.2% ai) was applied to the clipped skin of 10 New Zealand
White rabbits/sex/dose at dose levels of 10, 100, or 1000 mg/kg/day for
6 hours/day, 5 days/week, for a total of 15 applications.  One half the
animals had abraded skin, and the other half had non-abraded skin.  The
control group consisted of 14/sex treated with 2 ml/kg/day of
polyethylene glycol 300 (PEG 300).  The rabbits were observed daily for
clinical signs of toxicity, skin irritation, and individual body
weights.  Food consumption, hematology, and clinical chemistry
measurements were also taken.  Gross necropsy, and microscopic
examinations were conducted.

	There was no difference in clinical signs of toxicity between the
abraded and non-abraded animals.  No treatment-related clinical signs of
toxicity were observed at any dose level.  Some of the clinical signs
which are similar to those normally observed with pyrethroids were due
to physical injury.  In non-abraded animals, with the exception of low
dose males, all rabbits lost weight, including the controls.
Statistical significance in weight loss was achieved at 1000 mg/kg/day
in males.  This dose group lost 10% of their body weight.  The controls
lost <1% of their body weight.  In females, the controls lost 5% of
their body weight, and the 1000 mg/kg/day group lost 11% of their body
weight.  Food consumption in the high-dose group varied.  At times it
was less and at times it was more.  There was no consistent pattern.
Slight to severe irritation was observed in all test groups, including
controls.  In non-abraded animals, there appeared to be an increase in
the number of animals affected by irritation starting at 100 mg/kg/day.

	The NOAEL for dermal irritation is 10 mg/kg/day, and the LOAEL for
dermal irritation is 100 mg/kg/day.  The systemic NOAEL is 100 mg/kg/day
for both sexes.  The systemic LOAEL is 1000 mg/kg/day for both sexes,
based on significant weight loss when compared to the control groups.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a repeated dose dermal study (§82-2) in the
rabbit.

	870.3465	21-Day Inhalation – Rat

	In a 21-day inhalation study (MRID #41387702), 10/sex/dose SPF
Alpk:APfSD Wistar-derived albino rats were exposed nose-only 6
hours/day, 5 days/week, for 21 days to lambda-cyhalothrin (81.5% pure)
at 0, 0.3, 3.3, or 16.7 µg/L (estimated to be approximately 0, 0.08,
0.90, or 4.5 mg/kg/day).  The MMAD ranged from 1.47 to 1.91 µm, and the
GSD ranged from 1.02 to 2.24 µm.

	No treatment-related effects were observed at 0.3 µg/L.  At 3.3 µg/L,
the following was observed: salivation, lachrymation, paw flicking
(males only), tail erections, and splayed gait (males only); decreased
body weight (94-95%, p < 0.05) and body weight gain (53-65%, p < 0.01)
of control values; an increased incidence of punctate foci on the comea;
slight reductions in cholesterol levels in females (p < 0.05); decreased
urine volume in males, slightly raised specific gravity of the urine in
both sexes, and reductions in urinary protein levels in males.  At 16.7
µg/L, the following was observed: salivation, lachrymation, auditory
hypoaesthesia, paw flicking, tail erection, splayed gait, decreased
activity, reduced foot withdrawal (males only), head flicking, reduced
righting reflex, shaking (males only), sides pinched in, reduced splay
reflex, decreased visual placing response, absent puma reflex (females
only), ungroomed appearance (females only), tiptoe gait (males only),
respiratory noise; decreased body weight (85-88%, p < 0.01) and body
weight gain (<3-14%, p < 0.01 of control values); decreased food
consumption (46-91% ♂, 56-87% ♀ of controls); changes in selected
clinical chemistry values, particularly in females; decreased urine
volume, increased urine specific gravity, and decreased urinary protein.
 There was also a slight increase in the incidence of alveolitis in high
dose females.

	The NOAEL is 0.3 µg/L (0.08 mg/kg/day), and the LOAEL is 3.3 µg/L
(0.90 mg/kg/day), based on clinical signs of neurotoxicity, decreased
body weight gains, increased incidence of punctate foci in the cornea,
slight reductions in cholesterol in females, and slight changes in
selected urinalysis parameters.

	This inhalation toxicity study is classified as acceptable
(non-guideline), and does not satisfy any particular guideline
requirement.  The study is too short for a guideline study, and
individual animal data were not provided.

A.3.2	Pre-Natal Developmental Toxicity

	870.3700a	Pre-Natal Developmental Toxicity Study - Rat

	In a developmental toxicity study (MRID #00154800), technical
cyhalothrin (89.25%) was administered by gavage to 24 SPF CD rats/dose
at the following dose levels: 0, 5, 10, or 15 mg/kg/day during the
gestation period (days 6 through 15).  Maize oil was used as the
vehicle.

	No treatment-related effects were observed in the dams at dose levels
of either 5 or 10 mg/kg/day.  At 15 mg/kg/day, uncoordinated movements
in the limbs were observed in two dams, one from gestation days 8-10,
and the other from gestation days 12-18.  In addition, a statistically
significant reduction in mean body weight gain was observed, both during
dosing (70% of control value), and throughout the entire gestation
period (88% of control value).  The adjusted mean gestational body
weight gain was 67% of the control value.  Mean body weight gain was
comparable to the control group during the post-dosing period.  Food
consumption was also significantly reduced during gestation days 6-12
(77-91%).  No treatment-related developmental effects were observed at
any dose level.

	The maternal NOAEL is 10 mg/kg/day, and the maternal LOAEL is 15
mg/kg/day, based on uncoordinated movements in the limbs starting on
gestation day 8, and reduced body weight gain and food consumption
during the dosing period.

	The developmental NOAEL is greater than 15 mg/kg/day (HDT).  No
developmental effects were observed.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a study (§83-3) in the rat.

	870.3700b	Pre-Natal Developmental Toxicity Study - Rabbit

	In a developmental toxicity study (MRID #00154801), technical
cyhalothrin (89.25%) was administered by gavage to 18-22 New Zealand
White rabbits/dose at the following dose levels: 0, 3, 10, or 30
mg/kg/day, during the gestation period (days 6 through 18).  Corn oil
was used as the vehicle.

	No treatment-related effects were observed in the does at dose levels
of either 3 or 10 mg/kg/day.  At 30 mg/kg/day, a statistically
significant reduction in mean body weight gain was observed from
gestation days 6-9, when compared to the control group.  Mean body
weight gain was 48% of the control value during the dosing period.  It
was 122% of the control value during the post-dosing period, and 88% of
the control value for the entire gestation period (days 0-28).  The %
adjusted mean gestational body weight gain was 59% of the control value.
 Food consumption was also significantly reduced during gestation days
6-15 (71-77%).  No treatment-related developmental effects were observed
at any dose level.

	The maternal NOAEL is 10 mg/kg/day, and the maternal LOAEL is 30
mg/kg/day, based on decreased body weight gain during the dosing period.

	The developmental NOAEL is 30 mg/kg/day (HDT).  No effects were
observed.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a study (§83-3) in the rabbit.

A.3.3	Reproductive Toxicity

	870.3800	Reproduction and Fertility Effects - Rat

	In the three-generation reproduction study (MRID #00154802), groups of
5 male and 30 female SPF Wistar-derived rats/dose were fed technical
cyhalothrin (89.2%) in the diet at 0, 10, 30, or 100 ppm (approximately
0, 0.5, 1.5, or 5.0 mg/kg/day).  The pre-mating periods were 12 weeks
for the F0 animals, and 11 weeks for the F1 and F2 animals.

	Parental toxicity was observed as decreased mean body weight and body
weight gain during the pre-mating and gestation periods at 5.0
mg/kg/day.  There were no other treatment-related effects.  Offspring
toxicity was observed as reduced mean pup weight and pup weight gains
during lactation, again at 5.0 mg/kg/day.  No other treatment-related
effects were observed.

	The parental/offspring systemic NOAELs are 1.5 mg/kg/day, and the
parental/offspring systemic LOAELs are 5.0 mg/kg/day, based on decreased
mean body weight and body weight gain during the pre-mating and
gestation periods, and reduced mean pup weight and pup weight gain
during lactation.  The reproductive NOAEL is 5.0 mg/kg/day (highest dose
tested).

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a multi-generation reproduction study
(§83-4) in the rat.

A.3.4	Chronic Toxicity

	870.4100a	Chronic Toxicity – Rat

	See Section A.3.5, 870.4300 (Chronic/Carcinogenicity – Rat).

	870.4100b	Chronic Toxicity - Dog

	In a chronic toxicity study (MRID #40027902), beagle dogs (6/sex/dose)
were given oral administration of gelatin capsules containing
lambda-cyhalothrin (96.5%) at 0, 0.1, 0.5, or 3.5 mg/kg/day, 7
days/week, for 12 months.  The test chemical had been dissolved in corn
oil prior to placement in the capsules.  The following parameters were
measured and/or recorded: daily clinical observations, body weights,
food consumption, ophthalmological examinations, clinical biochemistry,
urinalysis, gross necropsy, and microscopic examinations.

	No treatment-related toxicity was observed at 0.1 mg/kg/day.  At 0.5
mg/kg/day, 1 male and 1 female dog exhibited gait abnormalities, with
the effects seen in the male 7-hours post dosing during week 2, and
again 2 days later immediately after dosing, and in the female 4 times
during week 9.  Convulsions were seen in two other dogs (both males);
the convulsions appeared to be precipitated by the stress of handling or
noise.  At 3.5 mg/kg/day, the principal neurological clinical signs
following dosing were ataxia (all dogs, apparent from day 2 in 2 dogs,
observed 3-7 hours post-dosing), muscle tremors and convulsions,
occasional subdued behavior, worn or bleeding claws, regurgitation of
food during first 2 weeks, and fluid feces in all dogs.  Treatment had
no effect on body weights, hematology, clinical chemistry, urinalysis,
gross or histopathology.

	The NOAEL is 0.1 mg/kg/day, and the LOAEL is 0.5 mg/kg/day, based on
clinical signs of neurotoxicity.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a study (§83-1) in the dog.

	A.3.5	Carcinogenicity

	870.4200	Carcinogenicity (Feeding) - Mouse

	Groups of 52/sex CD-1 mice (MRID #00150842) were fed technical
cyhalothrin (89.25%) in the diet at 0, 20, 100, or 500 ppm
(approximately 0, 3, 15, or 75mg/kg/day) for 104 weeks.  In addition, 4
satellite groups of 12 mice/sex were fed the same dietary
concentrations, and terminated at week 52.

	No treatment-related effects were observed at 3 mg/kg/day.  At 15
mg/kg/day, an increased incidence of piloerection was observed in males
between weeks 13 and 52.  This was the only observed effect at 15
mg/kg/day.  After week 52, the incidences of piloerection were
comparable to the control group.  At 75 mg/kg/day, an increased
incidence of piloerection was observed in both sexes, and hunched
posture was observed up to 78 weeks, particularly in males.  After 78
weeks, the incidences of hunched posture were similar between treated
and control groups.  Decreased body weight gain was also observed in
males during the first 13 weeks (54% of the control group).  Mean body
weight was 10 percent lower than the controls at week 13.  For the
entire two years, body weight gain in males was 77% of the control
value.

	On 2/12/1993 and 6/16/1994, the HED RfD/Peer Review Committee concluded
that cyhalothrin was not tested at a sufficiently high dose level for an
adequate carcinogenicity study in mice.  Following the decision by the
Committee, Toxicology Branch 1 (TB-1) determined that there was not
enough toxicological concern to warrant a requirement for a new
carcinogenicity study in the mouse at that time.  However, there was
sufficient concern about the adequacy of dosing in this study that
additional testing may be required in the future.  This decision was
based on data from the mouse chronic feeding/oncogenicity study, the
28-day range finding study in the mouse, and the results from mouse and
rat carcinogenicity studies conducted with similar pyrethroids.

	The 2/12/1993 RfD/Peer Review Committee also had concern over the
increased incidences of mammary tumors in females (1/52, 0/52, 7/52,
6/52).  On 6/16/1994, the HED RfD/Peer Review Committee evaluated the
study in more detail, and noted that the concurrent control value was
low when compared to historical control values.  Because of the
equivocal nature of the findings, and in view of the inadequacy of the
dose levels tested, the Committee concluded that the chemical should be
classified as a Group B chemical.

	The LOAEL for systemic chronic toxicity is 75 mg/kg/day, based on an
increased incidence of piloerection and hunched posture, and decreased
mean body weight gain in males, and the NOAEL is 15 mg/kg/day.

	Under the conditions of the study, cyhalothrin is not considered to be
oncogenic in mice. However, there is concern over the adequacy of the
dosing in the study, and additional testing may be required in the
future, particularly if new uses result in significantly higher residues
in human foods, and/or there is significantly higher occupational (or
future residential) exposure due to changes in parameters such as the
method of application.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a chronic feeding/oncogenicity study (§83-5)
in the mouse.

	870.4300	Carcinogenicity Study - Rat

	In a chronic feeding/carcinogenicity study in rats (MRID #00154803),
groups of 52 male and 52 female AlpklAP strain rats were fed 0, 10, 50,
or 250 ppm (0, 0.5, 2.5, or 12.5 mg/kg/day) cyhalothrin (89.2%) in the
diet for 2 years.  Additional groups of 20 males and females were added
to each dose level as extras, and for the purpose of interim sacrifice.

	No treatment-related effects were observed at either 0.5 or 2.5
mg/kg/day.  At 12.5 mg/kg/day, decreased mean body weight (11% for
males, and 8.5% for females) and food consumption in both sexes were
observed.  There were no neurological effects noted.

	The LOAEL for chronic toxicity in rats is 12.5 mg/kg/day, and the NOAEL
is 2.5 mg/kg/day, based on decreases in mean body weight.

	Under the conditions of the study, there was no indication of oncogenic
activity for this chemical.

	This study is classified as acceptable (guideline), and satisfies the
guideline requirements for a chronic feeding/oncogenicity study (§83-5)
in the rat.

A.3.6	Neurotoxicity

	870.6200	Acute Neurotoxicity Screening Battery

	In this acute oral neurotoxicity study (MRID #44861510),
lambda-cyhalothrin in corn oil was administered in a single dose by
gavage to 10 Alpk:APSD rats/sex/dose at doses of 2.5, 10, or 35 mg/kg.
Functional observation battery (FOB) and motor activity measurements
were performed during week 1 (acclimation), day 1 (at 7 hours
post-dosing), day 8, and day 15.  Five animals/sex/group were sacrificed
by perfusion fixation, and subjected to neuropathological examination.

	No animals died during the study.  No treatment-related changes in body
weight, body weight gain; food consumption, motor activity, or gross
pathology were observed.  No differences relative to concurrent controls
were observed in brain widths or dimensions.  No treatment- related
findings were observed in the 2.5 mg/kg group.

	At 10 mg/kg, the following clinical signs were observed (# incidences):

(1) increased breathing rate (males 5, females 5),

(2) slight piloerection (males 1, females 3),

(3) signs of urinary incontinence (1, females only),

(4) upward spine curvature (2, females only), and

(5) urinary incontinence (3, males only).

None of the clinical signs were observed in the concurrent controls.
The following observations were noted during the day 1 FOB: slight signs
of salivation (1, males only); slight signs of urinary incontinence (1,
females only); and slight urinary incontinence (2, males only).  None of
the clinical observations were observed in the concurrent controls.
These findings are not considered to be adverse, and very few animals
were observed to have effects.

	At 35 mg/kg, clinical signs were similar in nature to those observed in
the FOB, and consisted of the following (# incidences):

(1) slightly decreased activity (males 7, females 3),

(2) ataxia (males 5, females 5),

(3) increased breathing rate (males l6, females 13),

(4) piloerection (males 27, females 20),

(5) reduced stability (males 2, females 4),

(6) sides pinched in (males 3, females 4),

(7) signs of salivation (males 6, females 11),

(8) signs of urinary incontinence (males 2, females5),

(9) stains around mouth (males 4, females 3),

(10) tiptoe gait (males 5, females 3),

(11) un-groomed appearance (males 3, females 2),

(12) upward curvature of the spine (males 25, females 20), and

(13) urinary incontinence (males 5, females 7).

	The following findings were noted during the FOB on day 1:

(1) slightly decreased activity (2, males only),

(2) slight ataxia (males-3, females 2),

(3) extreme ataxia (2, females only),

(4) lacrimation (males- 1, females-2),

(5) slight piloerection (males-6, females-7),

(6) moderately reduced stability (1, females only),

(7) extremely reduced stability.  (1, females only),

(8) moderate salivation (1, males only),

(9) extreme salivation (males-i, females-i),

(10) slight signs of salivation (males-6, females-4),

(11) moderate signs of salivation (1, females, only),

(12) sides pinched in (1, females only),

(13) slight tip toe gait (males-4, females-I),

(14) upward curvature of the spine (males-8, females-8),

(15) tremors (1, females only),

(16) slight signs of urinary incontinence (males-l, females- 1), and

(17) slight urinary incontinence (thales-3,females-6).

Landing foot-splay values were decreased on day 1 (121%, p < 0.05), and
decreased (p < 0.05 or 0.01) hindlimb grip strength was observed on days
1, 8, and 15 (119%, 131%, 132%) in males.  Females displayed increased
time to tail-flick on day 1 (171%, p < 0.05).  In addition, one female
was found to have minimal pigmentation of the olfactory bulb, but no
other associated pathology.  Minimal fiber degeneration of the sciatic
nerve was observed in another female.

	The LOAEL for this study is 35 mg/kg, based on clinical observations
indicative of neurotoxicity, and changes in FOB parameters.  The NOAEL
for this study is 10 mg/kg.

	This acute oral neurotoxicity study is classified as acceptable
(§81-81aI), and satisfies the guideline requirements for an acute
neurotoxicity screening battery in rats.

870.6300	Developmental Neurotoxicity Test

		In a developmental neurotoxicity study (MRID 46449102),
Lambda-cyhalothrin (87.7% a.i., batch #P31 (BX E624)) was administered
in the diet to 30 mated female Alpk:APfSD (Wistar-derived) rats/group at
nominal concentrations of 0, 25, 60 or 150 ppm from gestation day (GD) 7
through day 23 post partum.  Average doses to the animals, adjusted for
purity, were 1.8, 4.3, and 10.0 mg/kg/day, respectively, during
gestation and 4.0, 9.4, and 23.1 mg/kg/day, respectively, during
lactation.  Dietary concentrations were based on the results of a
preliminary developmental neurotoxicity study (MRID 46449101).  A
Functional Observational Battery (FOB) was performed on all dams on GDs
10 and 17 and on lactation days (LDs) 2 and 9.  On postnatal day (PND)
5, litters were culled to yield four males and four females (as closely
as possible).  Offspring, representing at least 20 litters/dose, were
allocated for detailed clinical observations and assessment of motor
activity, auditory startle response, and learning and memory.  Neural
tissues were collected from selected offspring (10/sex/dose,
representing 20 litters) on PND 12 and at study termination (PND 63).
Pup body weights were recorded, and the age of sexual maturation was
assessed (vaginal opening in females and preputial separation in males).

		In the dams, no treatment-related effects were observed on mortality,
reproductive performance, or gross pathology.  Treatment-related
maternal toxicity included decreased (p (0.05 or 0.01) body weights,
body weight gains, and food consumption during gestation and lactation
at the high dose (150 ppm).  At this dose, absolute maternal body
weights were consistently decreased by 8-9%, compared to controls,
throughout the treatment period and persisting through LD 15.

		The maternal LOAEL is 150 ppm (10.0 mg/kg/day during gestation), based
on decreased body weight, body weight gain, and food consumption.  The
maternal NOAEL is 60 ppm (4.3 mg/kg/day during gestation).

		In offspring, no treatment-related effects were observed on clinical
signs, developmental landmarks, the functional observational battery,
brain weights, macroscopic neuropathology, or microscopic
neuropathology.

		A significant decrease (6%; p (0.01) in the number of pups surviving
from PNDs 1-5 (pre-cull), compared to controls, was observed at 150 ppm.
 Survival was unaffected by treatment with 25 or 60 ppm.

	Pup body weights and body weight gains were consistently lower (p
(0.01) in both sexes at 150 ppm from PNDs 5-29, with a maximum decrease
in body weight of 12%, compared to controls.

The motor activity data were considered inadequate for assessment.  Of
the control animals, habituation was only observed in PND 22 females.
Although habituation might not be expected in PND 14 animals (e.g., the
pups’ eyes may still be closed, and their brains may not yet be
developed enough so that habituation is possible), failure for all but
one of the other control groups to properly habituate indicates a lack
of an adequate assessment of this parameter in this study.

No treatment-related effects were seen in auditory startle response in
PND 23 males or females or in PND 61 males.  In PND 61 females,
decreases in maximum auditory startle response were seen in all treated
groups for repetitions 11-50, compared to controls.  The magnitude of
the decreases were similar across all doses (i.e., the dose-response was
flat), and the decreases reached statistical significance at the low and
high doses (p ( 0.01).  However, while the behavior of the treated PND
61 females is different from the controls, it is not possible to
determine whether this difference is due to treatment or if it is
because the PND 61 control females failed to exhibit the expected
habituation.  Failure for these animals to properly habituate indicates
an inadequate assessment of auditory startle in the PND 61 females
tested in this study. Habituation was evident in PND 61 males.

		High-dose females showed differences in water maze performance on PNDs
21 and 24.  Learning was affected on PND 21, in that mean time to
completion was longer, and the proportion of successful trials was lower
than controls for cut-off times ranging from 3-10 seconds.  When the
cut-off was expressed in relation to the time taken to complete the
straight channel, the group mean success rate at 1.5 the straight
channel swim time on PND 21 was decreased, although this change was not
statistically significant.  When memory was tested on PND 24, high-dose
females showed only a slight increase in the mean time per trial,
compared to controls, but the proportion of successful trials for
cut-off times from 3-9 seconds were still decreased.  Treatment-related
effects on learning and memory were not seen in PND 59/62 females or in
males at either time point.

At the high dose, statistically significant decreases were seen in the
molecular layer of the preculminate fissure of the cerebellum (13%), the
overall width of the hippocampus (7%), and the level 3 dorsal cortex 1
(7%) of PND 12 males.  In PND 12 females, statistically significant
decreases were observed at 150 ppm in the level 5 dorsal cortex (6%),
the level 4 dorsal cortex (7%), the thalamus width (4%), and the
thalamus/cortex width (4%).  At PND 63, a statistically significant
decrease (7%) was observed in the level 3 piriform cortex of high-dose
males.  Data for these measurements at the mid and low doses should be
provided to confirm whether or not the effects are limited to the high
dose.

	The offspring NOAEL/LOAEL cannot be determined due to the lack of brain
morphometrics at the low and mid doses, as well as inadequate
assessments of auditory startle response in PND 61 females and of motor
activity.

This study is classified Unacceptable/Guideline and does not satisfy the
guideline requirement for a developmental neurotoxicity study in rats
(OPPTS 870.6300, §83-6).  The motor activity data were considered
inadequate for assessment.  It was not possible to determine whether the
difference in auditory startle response between treated and control PND
61 females was due to treatment because the PND 61 control females
failed to exhibit the expected habituation.  Finally, morphometric data
at the mid and low doses were not available for the measurements in
which effects were observed at the high dose.

A.4	References (in MRID order)

00153029	Tinston, D.; Banham, P.; Chart, I.; et al. (1984) PP563: 28-day
Feeding Study in Rats: Summary Report: CTL Study No. PR0337: Report No.
CTL/P/1056. Unpublished study prepared by Imperial Chemical Industries,
PLC. 79 p.

00153035	Colley, J.; Dawe, S.; Heywood, R.; et al. (1984) Cyhalothrin:
Potential

		Tumorigenic and Toxic Effects in Prolonged Dietary Administration to
Mice: Addendum to Final Report: No. CTL/C/1260: No. ICI/395/83668.
Unpublished study prepared by Imperial Chemical Industries, PLC. 70 p.

00150842	Colley, J.; Dawe, S.; Heywood, R.; et al. (1984) Cyhalothrin:
Potential

		Tumorigenic and Toxic Effects in Prolonged Dietary Administration to
Mice: Final Report Vol. 3.: Rept No. ICI/395. Unpublished study prepared
by Huntingdon Research Centre, 553 p.

00153028	Hart, D.; Banham, P.; Chart, I.; et al. (1985) PP321: 90 Day
Feeding Study in Rats: CTL Study No. PR0584: Report No. CTL/P/I 045.
Unpublished study prepared by Imperial Chemical Industries, PLC. 76 p.

00154795	Chesterman, H.; Heywood, R.; Allen, T.; et al. (1981)
Cyhalothrin: Oral Toxicity Study in Beagle Dogs (Final Report: Repeated
Daily Dosing for 26 Weeks): Report No. ICI/326/8 162. Unpublished study
prepared by Huntingdon Research Centre. 210 p.

00154800	Killick, M. (1981) Cyhalothrin: Oral (Gavage) Teratology Study
in the Rat: CTL Study Number RR 0170: Report No. 2661-72/208.
Unpublished study prepared by Hazleton Laboratories Europe Ltd. 171 p.

00154801	Killick, M. (1981) Cyhalothrin: Oral (Gavage) Teratology Study
in the New Zealand White Rabbit: CTL Study Number RB 0169: Report No.
2700-72/211.  Unpublished study prepared by Hazleton Laboratories Europe
Ltd. 173 p.

00154802	Milburn, G.; Banham, P.; Godley, M, et al. (1984) Cyhalothrin:
Three-Generation Reproduction Study in the Rat: Report No: CTL/P/906.
Unpublished study prepared by Imperial Chemical Industries PLC. 1916 p.

00154803	Pigott, G.; Chart, I.; Godley, M., et al. (1984) Cyhalothrin:
Two Year Feeding Study in Rats: Report No: CTLJP/980: hand Individual
Animal Data Supplement: Report No: CTL/P/980So. Unpublished study
prepared by Imperial Chemical Industries. 2687 p.

00154804	Colley, I.; Dawe, S.; Heywood, R.; et al. (1984) Cyhalothrin:
Potential

		Tumorigenic and Toxic Effects in Prolonged Dietary Administration to
Mice: (Final Report): Report No. ICI 395/83668. Unpublished study
prepared by Huntingdon Research Centre. 849 p.

00154805	Lindsay, S.; Chart, I.; Godley, M.; et al. (1981) Cyhalothrin:
90-Day Feeding Study in Rats: Report No: CTL/P/629. Unpublished study
prepared by Imperial Chemical Industries PLC. 539 p.

00154806	Moyes, A.; Godley, M.; Hall, M., et al. (1984) Cyhalothrin:
28-Day Feeding Study in the Rat (Second Study): Summary Report: Report
No: CTL/P/1013. Unpublished study prepared by Imperial Chemical
Industries PLC. 33 p.

00154869	Henderson, C.; Jackson, S. (1982) Cyhalothrin: Subacute Dermal
Toxicity Study in Rabbits: Report No. CTL/P/680. Unpublished study
prepared by Imperial Chemical Industries PLC. 64 p.

B

D

¤

h<

$

d

k

¢

Ï

9

[

‹

¿

À

Á

Â

Ô

ö

Ÿ

¡

¸

½

Á

Â

Ó

Ô

Õ

Ý

Þ

á

â

ó

õ

ö

ù

ú

#ö

jø

h„

h„

h„

摧優5

h

h

h

h

萑ː葠ː摧珼±

h0

&

h÷u

h7

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

ਁ䠃愀϶H

ਁ䠃愀϶H

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

ਁ䠃愀϶H

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

㐀ۖĀ̊H䠃昀Ĵ

ਁ䠃愀϶H

h÷u

$

愀Ĥ摧痷

愀Ĥ摧痷

摧痷

@

䀆

䀆

䀆

䀆

䀆

䀆

䀆

䀆

h

h

h

h

†

›

Î

@

@

@

@

@

@

kd

愀Ĥ

愀Ĥ

ø

愀Ĥ

ø

愀Ĥ

ø

愀Ĥ

ø

&

&

&

@

@

@

耀䀆

耀䀆

耀䀆

耀䀆

耀䀆

耀䀆

耀䀆

h-

# h-

# h-

	ô

	ô

	ô

@

# h-

@

 h-

 h-

# h-

	”

&

H

I

J

L

M

b

c

d

…

’

Ÿ

¢

´

µ

·

¸

¹

¼

&

M

¹

,

ƒ

è

'

(

)

+

,

/

9

?

H

I

L

N

h

i

l

n

~

€

‚

ƒ

†

•

š

£

¤

¥

§

©

É

Ê

Í

Ï

ã

ä

æ

ç

è

ë

ú

&

&

&

&

&

„@

„Àô^„@

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

&

$ h-

 h-

 h-

# h-

 h-

 h-

#̀Ĥ옍)

!̀Ĥ옍)

#̀Ĥ옍)

@

ô

ô

ô

ô

ô

ô

ô

@

@

@

@

@

@

@

ð

T

½

¾

×

ã

í

 h-

 h-

萏֠萑褐葞֠葠褐ᜀ40387701, Cyhalothrin: Subacute Dermal Toxicity
in Rabbits: Proj. ID CTL/P/680. Unpublished study prepared by ICI
Central Toxicology Laboratory. 5 p.

41387702	Hext, P. (1990) Lambda-Cyhalothrin Production Material: 21-day
Sub-acute Inhalation Toxicity Study in the Rat: Lab Project Number:
CTL/P/2772: MROI 35. Unpublished study prepared by ICI Central
Toxicology Laboratory. 102 p.

43227901	Athis, J. (1994) Comments on February 1993 EPA RID/Peer Review
of Lambda-Cyhalothrin 1-Year Dog Study. Unpublished study prepared by
ICI Central Toxicology Laboratory. 14 p.

43232101	Stonard, M. (1991) First Amendment to PP321: 1-Year Oral Dosing
Study in Dogs: Lab Project Number: CTL/P/l 316. Unpublished study
prepared by ICI Central Toxicology Laboratory. 96 p.

43241901	Colley, J.C.; Dawe, S; et al. (1981) Cyhalothrin: 4-Week Dose
Range Finding Study in Mice.  CTL/C/1039 Unpublished study prepared by
Huntingdon Research Center, Huntingdon, Cambridgeshire, England

43241902	Athis, J. (1994) Comments on February 1993 EPA Rfd/Peer Review
of

		Cyhalothrin Oncogenicity/Chronic Feeding Study in Mice (Accession
Number<PHONE_NUMBER>16). Unpublished study prepared by Zeneca
Agrochemicals. 12 p.

43241903	Athis, J.; Pigott. G. (1994) Additional Comments on February
1993 EPA

		RfD/Peer Review of Lambda-Cyhalothrin 1-Year Dog Study (MRID
#40027902). Unpublished study prepared by Zeneca Agrochemicals. 7 p.

43245301	Athis, J. (1994) Additional Comments on February 1993 EPA
Rfd/Peer Review of Lambda-Cyhalothrin 1-Year Dog Study (MRID #40027902).
Unpublished study prepared by Zeneca Agrochemicals, Central Toxicology
Lab Cheshire, UK. 4 p.

44333802	Leah, A. (1989) Lambda-cyhalothrin: 21-Day dermal toxicity to
the rat. ICI Central Toxicology Laboratory, Alderley Park, Macclesfield,
Cheshire, UK. Laboratory Report Number CTL/P/2532. Laboratory Study
Number LR0526. June 20, 1989. Unpublished.

44861510	Brammer, A. (1999) Lambda-cyhalothrin: Acute neurotoxicity
study in rats. Central Toxicology Laboratory, Cheshire, UK. Laboratory
Project Identification Number: CTL/P/615l, Study Number: AR6699. April
13, 1999. Unpublished.

46449102	Milburn, G. M. (2004) Lambda-Cyhalothrin: Developmental
neurotoxicity study in rats.  Syngenta Limited, Alderley Park,
Macclesfield, Cheshire, UK SK 10 4TJ.  Laboratory study number RR0969;
November 3, 2004.  Unpublished.

AppendiX B:  Metabolism Assessment

B.1.	Metabolism Guidance and Considerations

Table B.1	Summary of Degradate Formation from Degradation of
Lambda-cyhalothrin.

Study Type	Source	Degradate and Maximum Concentration

Compound Ia (% Applied) 1	Compound Ib (% Applied) 2	Degradate XV (%
Applied) 3

Aqueous Photolysis	MRID #44861501	13.7 at 282 hours (cyclopropane ring).
 	7.1% at 282 hours (cyclopropane ring).  	Others: 3-phenoxybenzoic acid
was 25.0% at 247 hours; phenoxybenzaldehyde was a minor degradate (5.5%
at 247 hours).

Aerobic Aquatic Metabolism	MRID #44861506	11.4% at 30 days in a 98 day
study, and 11.4% at 14 days in the sediment of the SL sediment system.

	NA 4	11.4% at 30 days, and 10.6% at 30 days in the sediment of the SL
sediment system.

Aerobic Aquatic Metabolism	MRID #44367402	14.4% at 14 days, and 0.7 to
3.3% from 4 to 30 days in the sediment of the sand sediment system.  	NA
0.4-1.3% at 0.125-7 days, and 8.7at 7 days in the sediment of the sand
sediment system.

Terrestrial Field Dissipation	MRID #40052407	Transformation products
monitored at the two sites were reported to be at low levels.

Data for hydrolysis, soil photolysis, aerobic soil metabolism, and
anaerobic aquatic metabolism were not available.

1. Compound Ia =
(1RS)-cis-3(ZE)-2-chloro-3,3,3-trifluro-1-propenyl)-2,2-dimethylcyloprop
ane-carboxylate.

2. Compound Ib =
(1RS)-trans-3-(ZE-2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclo
propane-carboxylic acid.

 α-(S) cis α-(R) α-cyano-3-(4-hydroxy-phenoxy) benzyl
3-(Z-2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclo-propanecarbo
-	xylate.

4. NA = Not Applicable.

AppendiX C:  Human Research REFERENCES

+	õ

	”

+	õ

+	õ

	”

+	õ

	”

 h-

"halothrin in Man.; Zeneca Report #CTL/P/4208, Study #XH2429; MRID
#44333801; J.R. March, B.H. Woolen, and M.F. Wilks; 1/28/1994.

	The Pesticide Handlers Exposure Database, Version 1.1 (Electronic
Database); The PHED Task Force, 1995; (Task Force members: Health
Canada, US Environmental Protection Agency, and the National
Agricultural Chemicals Association); released February, 1995.

	Page   PAGE  1  of   NUMPAGES  71