[Federal Register Volume 63, Number 150 (Wednesday, August 5, 1998)]
[Notices]
[Pages 41835-41844]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-20769]


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ENVIRONMENTAL PROTECTION AGENCY

[PF-818; FRL-6017-1]


Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: This notice announces the initial filing of pesticide 
petitions proposing the establishment of regulations for residues of 
certain pesticide chemicals in or on various food commodities.
DATES: Comments, identified by the docket control number PF-818, must 
be received on or before September 4, 1998.
ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch, Information Resources and Services Division

[[Page 41836]]

(7502C), Office of Pesticides Programs, Environmental Protection 
Agency, 401 M St., SW., Washington, DC 20460. In person bring comments 
to: Rm. 119, CM #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Comments and data may also be submitted electronically to: <a href="/cdn-cgi/l/email-protection#2e415e5e03244a414d454b5a6e4b5e4f434f4742004b5e4f00494158">opp-
<span class="__cf_email__" data-cfemail="35515a565e50417550455458545c591b5045541b525a43">[email protected]</span></a>. Follow the instructions under ``SUPPLEMENTARY 
INFORMATION.'' No confidential business information should be submitted 
through e-mail.
    Information submitted as a comment concerning this document may be 
claimed confidential by marking any part or all of that information as 
``Confidential Business Information'' (CBI). CBI should not be 
submitted through e-mail. Information marked as CBI will not be 
disclosed except in accordance with procedures set forth in 40 CFR part 
2. A copy of the comment that does not contain CBI must be submitted 
for inclusion in the public record. Information not marked confidential 
may be disclosed publicly by EPA without prior notice. All written 
comments will be available for public inspection in Rm. 119 at the 
address given above, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: The product manager listed in the 
table below:

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                                   Office location/                     
        Product Manager            telephone number          Address    
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Sidney Jackson................  Rm. 268, CM #2, 703-    1921 Jefferson  
                                 305-7610, e-            Davis Hwy,     
                                 mail:<a href="/cdn-cgi/l/email-protection" class="__cf_email__" data-cfemail="f298939199819d9cdc819b969c978bb297">[email protected]</a>   Arlington, VA  
                                 pamail.epa.gov.                        
Beth Edwards..................  Rm. 206, CM #2, 703-    Do.             
                                 305-5400, e-mail:                      
                                 <a href="/cdn-cgi/l/email-protection#d4b1b0a3b5a6b0a7fab6b1a0bc94b1a4b5b9b5bdb8fadeb1a4b5fab3bba2"><span class="__cf_email__" data-cfemail="482d2c3f293a2c3b662a2d3c20082d38292529212466">[email protected]</span>
epa.gov</a>.                               
------------------------------------------------------------------------

SUPPLEMENTARY INFORMATION: EPA has received pesticide petitions as 
follows proposing the establishment and/or amendment of regulations for 
residues of certain pesticide chemicals in or on various food 
commodities under section 408 of the Federal Food, Drug, and Comestic 
Act (FFDCA), 21 U.S.C. 346a. EPA has determined that these petitions 
contain data or information regarding the elements set forth in section 
408(d)(2); however, EPA has not fully evaluated the sufficiency of the 
submitted data at this time or whether the data supports granting of 
the petition. Additional data may be needed before EPA rules on the 
petition.
    The official record for this notice of filing, as well as the 
public version, has been established for this notice of filing under 
docket control number [PF-818] (including comments and data submitted 
electronically as described below). A public version of this record, 
including printed, paper versions of electronic comments, which does 
not include any information claimed as CBI, is available for inspection 
from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal 
holidays. The official record is located at the address in 
``ADDRESSES'' at the beginning of this document.
    Electronic comments can be sent directly to EPA at:
    <a href="/cdn-cgi/l/email-protection#2b445b5b064f4448404e5f6b4e5b4a464a4247054e5b4a054c445d"><span class="__cf_email__" data-cfemail="e7889797ca8388848c8293a78297868a868e8bc9829786c9808891">[email protected]</span></a>


    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption. Comment and data 
will also be accepted on disks in Wordperfect 5.1 file format or ASCII 
file format. All comments and data in electronic form must be 
identified by the docket number (insert docket number) and appropriate 
petition number. Electronic comments on notice may be filed online at 
many Federal Depository Libraries.

List of Subjects

    Environmental protection, Agricultural commodities, Food additives, 
Feed additives, Pesticides and pests, Reporting and recordkeeping 
requirements.

    Dated: July 23, 1998.

James Jones,

Director, Registration Division, Office of Pesticide Programs.

Summaries of Petitions

    Petitioner summaries of the pesticide petitions are printed below 
as required by section 408(d)(3) of the FFDCA. The summaries of the 
petitions were prepared by the petitioners and represent the views of 
the petitioners. EPA is publishing the petition summaries verbatim 
without editing them in any way. The petition summary announces the 
availability of a description of the analytical methods available to 
EPA for the detection and measurement of the pesticide chemical 
residues or an explanation of why no such method is needed.

1. Interregional Research Project 4 (IR-4)

PP 6E4667

    EPA has received a pesticide petition (PP 6E4667) from the 
Interregional Research Project 4(IR4), proposing pursuant to section 
408(d) of the Federal Food, Drug, and Cosmetic Act, 21 U.S.C. 346a(d), 
to amend 40 CFR part 180 by establishing a tolerance for residues of 
pyridate, 0-(6-chloro-3-phenyl-4-pyridazinyl)-S-octyl carbonothioate 
and its metabolite 6-chloro-3-phenyl-pyridazine-4-ol (known as SAN 
1367), and conjugates of SAN 1367 in or on the raw agricultural 
commodity garbanzo beans (also known as chick peas) at 0.1 ppm.
    EPA has determined that the petition contains data or information 
regarding the elements set forth in section 408(d)(2) of the FFDCA; 
however, EPA has not fully evaluated the sufficiency of the submitted 
data at this time or whether the data support granting of the petition. 
Additional data may be needed before EPA rules on the petition. This 
notice contains a summary of the petitions prepared by Novartis Crop 
Protection, Inc. (formerly Sandoz Agro Inc.), the registrant.

2. Novartis Crop Protection, Inc.

PP 6F4754

    EPA has received a pesticide petition (PP 6F4754) from Novartis 
Crop Protection, Inc, proposing pursuant to section 408(d) of the 
Federal Food, Drug and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR 
Part 180 by establishing a tolerance for residues of pyridate, 0-(6-
chloro-3-phenyl-4-pyridazinyl)-S-octyl carbonothioate and its 
metabolite 6-chloro-3-phenyl-pyridazine-4-ol (known as SAN 1367), and 
conjugates of SAN 1367 in or on the raw agricultural commodities head 
and stem Brassica Subgroup 5A at 0.3 parts per million (ppm). (Sidney 
Jackson)

A. Residue Chemistry

    1. Plant metabolism. The metabolism of pyridate in plants is well 
understood based on studies with broccoli, corn, and peanut. Pyridate 
is rapidly broken down by hydrolysis to its major degradation product, 
SAN 1367. The SAN 1367 metabolite is further conjugated to glucoside 
and degraded.
    2. Analytical method. The proposed analytical method is ``Method of 
analysis of determination of residues of pyridate and its metabolites 
CL 9673

[[Page 41837]]

and conjugated CL 9673 in plant materials'', Report No. 758e, March 
1992, Agrolinz Agrarchemikalien Ges.m.b.H. (V/6).
    3. Magnitude of residues. Residue trials have been conducted with 
pyridate on the additional crops requested in the pending petitions. 
The proposed tolerances are recommended at the limit of determination 
for the method, which is the maximum expected residue from the 
geographically representative field trial data.
    Pyridate strongly adsorbs to soil and was shown to be immobile in 
soil column leaching studies. Pyridate has a short half-life, low water 
solubility, and low volatility. Due to its solubility and hydrolysis 
characteristics, pyridate will not persist in the environment.
    San 1367 is further degraded and mineralized to volatile CO2 and 
bound metabolites. It is susceptible to photolysis. Column leaching 
studies and field dissipation studies indicated that SAN 1367 tends to 
degrade faster than it is translocated below the 0-15 cm layer. 
Therefore under typical agricultural conditions and labeled uses, 
leaching of SAN 1367 is not an issue of concern.

B. Toxicological Profile

    Data are summarized below concerning the mammalian toxicity of 
pyridate. According to Novartis' interpretation of these data, pyridate 
is not a carcinogen or a mutagen, has low oral and dermal toxicity to 
mammals, and causes no reproductive or developmental effects.
    1. Acute toxicity. Results of a rat acute oral study showed a 
lethal dose LD<INF>50</INF> of 4,690 milligram/kilogram (mg/kg) body 
weight/day (bwt/day) (5,993 mg/kg in males and 3,544 mg/kg in females). 
In a rat acute dermal study, the LD<INF>50</INF> was shown to be >2,000 
mg/kg. A rat acute inhalation study yielded a LD<INF>50</INF> >4.37 mg/
milliliter (ml).
    Results of a primary eye irritation study in the rabbit indicated 
that pyridate is a mild irritant. A primary dermal irritation study 
showed pyridate to be a moderate skin irritant, whereas, a dermal 
sensitization study indicated it is a sensitizer.
    2. Genotoxicity. Pyridate was tested in the Ames test, mouse 
micronucleus assay, chromosome aberration assay with Chinese hamster 
ovary cells, the REC assay, and rat hepatocyte unscheduled DNA 
synthesis assay. Results were negative for mutagenicity and chromosome 
aberrations.
    3. Reproductive and developmental toxicity. A developmental 
toxicity study in the rat dosed at 0, 55, 165, 400, and 495 milligram/
kilograms/day (mg/kg/day) showed maternal toxicant no-observed effect 
level (NOEL) of 165 mg/kg/day, and developmental NOEL >495 mg/kg/day.
    A developmental toxicity study in the rabbit with doses of 0, 150, 
300, and 600 mg/kg/day showed a maternal toxicant NOEL of 300 mg/kg/day 
and developmental NOEL >600 mg/kg/day.
    Results of a multi-generational reproduction study with rats dosed 
at 0, 2.2, 10.8, and 67.5 mg/kg/day showed a NOEL of 10.8 mg/kg/day for 
maternal and developmental toxicity.
    4. Subchronic toxicity. Results of a 21-day dermal study showed a 
NOEL >1,000 mg/kg. A 90-day feeding study in rat dosed at 0, 62.5, 177, 
and 500 mg/kg/day showed a NOEL of 62.5 mg/kg/day. No neuropathological 
effects were found. A 90-day feeding study in dogs with doses of 0, 20, 
60 and 200 mg/kg/day showed a NOEL of 20 mg/kg/day. Slight degenerative 
myelopathy in the peripheral nerves was observed at the highest dose 
level (HDL), which is much higher than the NOEL and the expected 
exposure from field use.
    5. Chronic toxicity. A 1-year feeding study in dogs was conducted 
with doses of 0, 5, 20 and 60 mg/kg/day for 34-weeks. After week 34, 
the doses were increased to 30, 100, and 150 mg/kg/day because no toxic 
effects were evident at the lower doses. The final results showed a 
systemic NOEL of 20 mg/kg/day.
    A lifespan (121 week) chronic/carcinogenicity study in rats treated 
with analytical levels of 0, 2.2, 10.8, and 67.5 mg/kg/day (equivalent 
to 0, 48, 240, and 1,500 ppm) showed a systemic NOEL of 10.8 mg/kg/day 
(240 ppm) based on body weight depression. No carcinogenic potential 
was observed.
    In an 18- month carcinogenicity study, mice were fed doses of 0, 
400, 800, 1,600 and 7,000 ppm of pyridate. In males, dose levels were 
approximately 0, 47.7; 97.1; 169.5, and 882.6 mg/kg bwt/day; in 
females, dose levels were approximately 0, 54.5, 114.6, 204.3, and 
1,044.6 mg/kg bwt/day. NOEL was 800 ppm (97.1 mg/kg in males and 114.6 
mg/kg in females). Results showed no evidence of carcinogenicity.
    i. Chronic effects. The Reference Dose (RfD) has been established 
based on the chronic toxicity database. The RfD = 0.11 mg/kg bwt/day 
based on the NOEL of 10.8 mg/kg bwt/day from the lifespan rat 
oncogenicity study due to body weight depression in males, and assuming 
a safety factor of 100.
    ii. Acute effects. Acute dietary analysis compared the daily 
dietary exposure to the lowest NOEL for subchronic studies. EPA's 
current policy for Tier I analysis uses the conservation assumption 
that all residues are at a high end estimate or maximum, typically 
taken as the tolerance value. Acute dietary assessment for pyridate was 
generated by comparing the ratio of exposure and the NOEL from the 90-
day feeding study in dogs of 20 mg/kg bwt/day to determine a margin of 
exposure (MOE). The exposure estimate includes all current and pending 
tolerances from Novartis Agro, Inc. and IR-4. MOE of 100 or more are 
considered acceptable. For all subgroups evaluated, the MOE is greater 
than 140,000.
    iii. Carcinogenicity. Existing data demonstrate that there is no 
evidence of carcinogenicity in rats at 1,500 ppm (67.5 mg/kg/day) or 
mice at 7,000 ppm (883 mg/kg bwt/day in males, and 1,044.6 mg/kg bwt/
day in females). These data have been obtained at dosing in excess of 
any dietary exposure.
    6. Animal metabolism. Pyridate has been tested in rats, dogs, 
cattle,goats, and hens. In every study, pyridate was hydrolyzed to SAN 
1367 and rapidly excreted, primarily through the urine as SAN 1367 or 
its glucoside or glucuronide conjugates.
    Data from bovine metabolism and feeding studies established that 
the uses proposed do not yield secondary residues in meat and milk 
above the limit of detection. Novartis believes that data from 
metabolism and feeding studies in poultry established that at the 
maximum expected dietary burden from crops treated with pyridate will 
not result in quantifiable residues above the limits of the analytical 
method. Pyridate and its metabolites are not persistent and do not 
accumulate in animal systems.
    7. Metabolite toxicology. Pyridate has been tested in rats, dogs, 
cattle, goats, and hens. In every study, pyridate was hydrolyzed to SAN 
1367 and rapidly excreted, primarily through the urine as SAN 1367 or 
its glucoside or glucuronide conjugates. Pyridate and its metabolites 
are not persistent and do not accumulate in animal systems.

C. Aggregate Exposure

    Based on environmental fate data, pyridate is not expected to be 
found in drinking water. There are no non-crop uses for pyridate, and 
no non-occupational exposure for residential use. Exposure would be 
limited to dietary exposure described below. Novartis Agro has no 
information that would indicate that pyridate would have a mechanism of 
toxicity common to any other registered pesticide.

[[Page 41838]]

    1. Dietary exposure--food. Pyridate is registered for use in corn, 
peanut, and cabbage. The pending petitions add the use in grain 
sorghum, collards, and the stem and head Brassica subgroup. The 
potential dietary exposure of the population to residues of pyridate or 
its metabolites is calculated based on Theoretical Maximum Residue 
Contribution (TMRC) for all crops with pyridate use. The TMRC is a 
worst case estimate of dietary exposure since it assumes that 100% of 
all crops for which tolerances are established are treated with 
pyridate, and that pesticide residues are present at the tolerance 
levels. Novartis maintains that this method of calculation result in an 
overestimation of the exposure and is considered conservative. Dietary 
exposure is not expected in meat, milk, poultry, or eggs, based on cow 
and hen feeding studies, animal metabolism studies, and the fact the 
residue studies indicate that residues are not present in crops fed to 
animals above the limit of detection.
    2. Drinking water. Drinking water is not expected to be a means of 
exposure to pyridate. Environmental studies indicate that pyridate 
binds to the soil and is rapidly hydrolyzed into its metabolites. The 
metabolites are then photolyzed and further degraded and finally 
mineralized to CO<INF>2</INF>. Leaching studies and lysimeter studies 
indicate that under typical agricultural conditions, neither pyridate 
nor its metabolites were detected below 30 cm. Groundwater monitoring 
studies conducted in Europe have not confirmed any detection of 
pyridate or metabolites. Therefore significant movement of pyridate is 
not likely and is not a considerable factor in assessing human health 
risk.
    3. Non-dietary exposure. There are no registered uses for pyridate 
on residential or recreational turf. Therefore, non-dietary exposure of 
pyridate is not likely and not a factor in assessing human health risk.

D. Cumulative Effects

    Pyridate belongs to the pyridazine group of herbicidal compounds 
and has a unique mode of action in plants. Novartis does not have data 
to indicate a common mechanism of toxicity to other compounds in 
humans. Therefore, Novartis concludes that cumulative effects from 
common mechanisms of action are unlikely.

E. Safety Determination

    1. U.S. population. The RfD is calculated to be 0.11 mg/kg bwt/day. 
The estimates of exposure are based on conservative assumptions that 
all crops with a tolerance for pyridate are treated and that all 
residues found are at the maximum or tolerance level. The dietary 
exposure to the U.S. population for the current uses plus the garbanzo 
beans and Brassica uses is estimated at most to be 0.000019 mg/kg/day, 
which is 0.017% of the RfD. Therefore Novartis concludes that there is 
reasonable certainty of no harm from aggregate exposure of residues of 
pyridate or its metabolites including all dietary and other non-
occupational exposures.
    2. Infants and children. Pyridate is not a reproductive or 
developmental toxicant. Therefore no specific effects on infants and 
children are expected. Based on the weight of evidence of the toxicity 
studies, Novartis concludes that an additional safety factor is not 
warranted.
    Using the same assumptions as above, the exposure to infants and 
children is presented as a percent of RfD. The dietary exposure for the 
current uses plus the garbanzo beans and Brassica uses for non-nursing 
infants is estimated at 0.000045 mg/kg/day, which is 0.041% of the RfD. 
For children age 1-6, the estimated exposure is 0.000057 mg/kg/day, 
0.052% of the RfD, and exposure to children age 7-12 is estimated to be 
0.000044 mg/kg/day, which is 0.040% of the RfD. Therefore, Novartis 
concludes that there is reasonable certainty of no harm from aggregate 
exposure of residues of pyridate or its metabolites including all 
dietary and other non-occupational exposures.

F. International Tolerances

    No international tolerances have been established by CODEX 
Alimentarius Commission (Sidney Jackson).

3. Valent U.S.A. Company

PP 7F3485, 1F3949, 6F4648

    EPA has received a request from Valent U.S.A. Company, 1333 North 
California Boulevard, Suite 600, Walnut Creek, CA 94596-8025 proposing 
pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act, 
21 U.S.C. 346a(d), to amend 40 CFR 180.466 by establishing tolerances 
for residues of fenpropathrin, alpha-cyano-3-phenoxybenzyl 2,2,3,3-
tetramethylcyclopropanecarboxylate, in or on the raw agricultural 
commodities pome fruit (crop group 11) and grapes at 5.0 ppm, head and 
stem brassica (crop group 5A) at 3.0 ppm, citrus fruit (crop group 10) 
at 2.0 ppm, melons (crop group 9A) at 0.5 ppm, and in the processed 
products citrus oil at 50 ppm, raisins at 10 ppm, and dried citrus pulp 
at 4.0 ppm. The tolerances were first proposed in response to pesticide 
petitions PP 7F3485, 1F3949, and 6F4648. EPA has determined that the 
request contains data or information regarding the elements set forth 
in section 408(d)(2) of the FFDCA; however, EPA has not fully evaluated 
the sufficiency of the submitted data at this time or whether the data 
supports granting of the petition. Additional data may be needed before 
EPA rules on the petition.

 Background Information and Use Profile

    Fenpropathrin is the active ingredient in DANITOL 2.4 EC Spray (EPA 
Reg. No. 59639-35) and TAME 2.4 EC Spray (EPA Reg. No. 59639-77). To 
support DANITOL use, tolerances have been established on cottonseed; 
cottonseed oil; meat, meat byproducts, and fat of cattle, goats, hogs, 
horses, sheep and poultry; eggs; milkfat; peanuts; peanut hay; 
strawberries; and tomatoes. A time limited tolerance on red currants 
has been established to support a Section 18 in the state of Washington 
with an expiration date of December 31, 1998. The pending tolerances 
that are the subject of this notice of filing are on grapes and on the 
crop groups pome fruits (11), citrus (10), head and stem brassica (5A), 
and melons (9A), with associated processing products citrus oil, 
raisins, and dried citrus pulp.
    Fenpropathrin is a pyrethroid insecticide with broad spectrum 
activity on insects and mites. When formulated as the product DANITOL 
2.4 EC Spray the product is registered for agricultural use on outdoor 
terrestrial food crops. A separate fenpropathrin product, TAME 2.4 EC 
Spray, is registered for commercial, professional non-food use on 
indoor and outdoor ornamental and nursery stock. There are no uses 
registered for professional indoor pest control, termite prevention, 
homeowner use, or turf application.
    The products are applied as dilute emulsions in water directly to 
plants to control harmful insects and mites. In agriculture, depending 
on the crop and pest, the use rates vary from 0.15 to 0.4 pounds of 
active ingredient per acre (lb. ai./a), with a maximum total use on all 
crops of 0.8 lb. ai./a per season. Pre-harvest intervals (phi) range 
from 21-days on cotton to 1-day on citrus. Plant metabolism studies 
have shown that the plant and animal residues are best defined as 
parent fenpropathrin. Because of the mode of application and short phi, 
finite residues of fenpropathrin are often found on treated 
agricultural commodities requiring tolerances above the 0.01 ppm limit 
of quantitation of the residue analytical methodology. However, 
analyses of RAC samples from plants treated at the

[[Page 41839]]

maximum application rates, and minimum retreatment intervals and phi 
demonstrate that anticipated residues are much below tolerance levels. 
In addition, it has been demonstrated that fenpropathrin is not plant 
systemic and that residues occur only on plant parts that have been 
directly treated.

A. Residue Chemistry

     Summary. An extensive plant and animal metabolism data base 
demonstrates that the appropriate definition of aged fenpropathrin 
residue is parent. Ruminant and poultry metabolism followed by feeding 
studies have shown that the ratios of residues in feed to secondary 
residues in animal products are very low in most commodities, with 
higher (but still relatively low) ratios in body fat and milk fat. This 
section will describe metabolism and field residue data supporting the 
establishment of tolerances for residues of fenpropathrin in or on the 
raw agricultural commodities pome fruit (crop group 11) and grapes at 
5.0 ppm, head and stem brassica (crop group 5A) at 3.0 ppm, citrus 
fruit (crop group 10) at 2.0 ppm, melons (crop group 9A) at 0.5 ppm, 
and in the processed products citrus oil at 50 ppm, raisins at 10 ppm, 
and dried citrus pulp at 4.0 ppm The approved analytical method is 
capillary gas-liquid chromatography with flame ionization detection.
    1. Plant metabolism. The plant metabolism of fenpropathrin has been 
studied in five different crop plant species: cotton, apple, tomato, 
cabbage, and bean. Radiocarbon labeling has been in the cyclopropyl 
ring of the acid, in the aryl rings of the alcohol, and in the nitrile 
of fenpropathrin, a cyanohydrin ester. The permutations of radiocarbon 
label position and plant species yield a total of 17 separate, reviewed 
studies. Each of the studies involved foliar treatment of the plants 
under either greenhouse or field conditions and, while the actual 
treatment conditions and times to harvest and analyses varied from 
study to study, the results of the many studies are remarkably 
consistent. The total toxic residue is best defined as parent, 
fenpropathrin.
    Fenpropathrin remains associated with the site of application and 
only traces are found in seeds (e.g., bean or cotton) or in other parts 
of the plant not directly exposed to the application. Much of the 
parent residue can be removed from the plant material with a mild 
hexane/acetone or hexane rinse, demonstrating that the residue is 
located on or near the outside surface of the plant material. The 
primary metabolic pathway for fenpropathrin in plants is similar to 
that in mammals. There are no qualitatively unique plant metabolites; 
the primary aglycones are identical in both plants and animals.
    2. Analytical method. Adequate analytical methodology is available 
to detect and quantify fenpropathrin (and its metabolites) at residue 
levels in numerous matrices. The methods use solvent extraction and 
partition and/or column chromatography clean-up steps, followed by 
separation and quantitation using capillary column gas-liquid 
chromatography with flame ionization detection. The extraction 
efficiency has been validated using radiocarbon samples from the plant 
and animal metabolism studies. The enforcement methods have been 
validated at independent laboratories, and by EPA. The limit of 
quantitation for fenpropathrin in raw agricultural commodity samples is 
0.01 ppm.
    3. Magnitude of residues--i. Pome fruit (Crop Group 11). The 
proposed section 408 tolerance for fenpropathrin in/on Pome Fruit (Crop 
Group 11) is 5.0 ppm. The proposed tolerance will permit finite 
residues of fenpropathrin on pome fruit -- apple, pear, oriental pear, 
crabapple, and related fruits -- as a result of application of DANITOL 
2.4 EC Spray to orchards. The field residue data to support a 
fenpropathrin tolerance on the pome fruit crop grouping includes data 
on apples from 26 sites and pears from 18 sites providing data from 44 
sites across the U.S. The mean residue from all samples is 1.83 ppm. In 
the subset of samples that exactly fit the proposed use pattern the 
average residue is 0.83 ppm (n = 16, <greek-s>n -1 = 0.55 ppm) with a 
maximum value of 1.8 ppm.
    ii. Apples. The residue data base from apples that supports the 
proposed crop group tolerance includes all samples from field residue 
studies that were treated two or more times at 0.4 lb. ai./a with a 14-
day phi. These experiments were performed over 5- years at 26 sites in 
10 states. There were 38 separate treatments yielding 73 separate, 
treated samples for analysis. The average residue was 2.15 ppm (n = 
73,<greek-s>n -1 = 1.37 ppm). These data do not include supporting 
information at higher or lower rates, and harvested at different phi. 
In the 38-treatment data base there are only four treatments with only 
two applications that are completely consistent with the proposed use 
pattern that is limited to a maximum single application rate of 0.4 lb. 
ai./a, a seasonal maximum of 0.8 lb. ai./a, and a 14 phi. The highest 
average residue (HAR) found in these crop field trials for 
fenpropathrin on apples was 1.13 ppm. The average residue was 0.77 ppm 
(n = 8, <greek-s>n -1 = 0.40). Data obtained by separate analyses of 
peelings and pulp demonstrated that the bulk of fenpropathrin residues 
were located on the peeling of the apples.
    Five apple processing studies were performed. These studies 
demonstrated that fenpropathrin residues did not concentrate in apple 
juice (concentration factor all <<1, average = 0.06), but did 
concentrate in wet pomace (average concentration factor = 3.05). No 
additional tolerance for the processed product wet apple pomace is 
needed because the HAR times the average concentration factor for wet 
pomace is less than the proposed tolerance of 5 ppm (1.13 ppm x 3.05 = 
3.45 ppm).
    iii. Pears. The residue data base from pears that supports the 
proposed crop group tolerance includes all samples from field residue 
studies that were treated two or more times at 0.4 lb. ai./a with a 14-
day phi. These experiments were performed over 4-years at 18 sites in 5 
states. There were 30 separate treatments yielding 60 separate, treated 
samples for analysis. The average residue was 1.44 ppm (n = 60, 
<greek-s>n -1 = 1.01). This does not include supporting information at 
higher or lower rates, and harvested at different phi. In the 30-
treatment data base there are only four treatments with only 2 
applications that are completely consistent with the proposed use 
pattern, which is the same as in apples, and is limited to a maximum 
single application rate of 0.4 lb. ai./a, a seasonal maximum of 0.8 lb. 
ai./a, and a 14-day phi. The HAR found in these crop field trials for 
fenpropathrin on pears was 1.8 ppm. The average residue was 0.88 ppm (n 
= 8, <greek-s>n -1 = 0.69).
    iv. Grapes. The proposed section 408 tolerance for fenpropathrin on 
grapes is 5 ppm. The residue data base that supports the tolerance 
includes all samples from field residue studies that were treated 4- 
times at 0.2 lb. ai./a with a 21-day phi. Excluded from the calculation 
of the tolerance, and the chronic and acute exposure analyses is data 
from one site that were demonstrated to be outliers (The analytical 
determinations were very high, more than six sigma above the mean of 
the other determinations). These experiments were performed over 4-
years at 14 sites in 4 states. There were 14 separate treatments 
yielding 28 separate, treated samples for analysis. The average residue 
was 1.06 ppm (n = 28, <greek-s>n -1 = 0.71). This does not include 
supporting information at higher or lower rates, different numbers of 
applications, or different phi. The HAR

[[Page 41840]]

found in crop field trials for fenpropathrin on grapes was 3.1 ppm.
    Four processing studies yielding raisins and juice, and 5 
additional studies yielding grape juice only (total of 9), were 
performed. These studies demonstrated that fenpropathrin residues were 
greatly reduced in grape juice (concentration factor all <<1, average = 
0.06), but did concentrate in raisins (average concentration factor = 
1.76). An additional tolerance for the processed product raisins is 
needed because the HAR times the average concentration factor for 
raisins is greater than the proposed tolerance of 5 ppm (3.1 ppm x 1.76 
= 5.55 ppm). A Section 408 tolerance for fenpropathrin on raisins of 10 
ppm is proposed.
    v. Citrus. The proposed Section 408 tolerance for fenpropathrin on 
citrus fruit (Crop Group 10) is 2 ppm. The residue data base from 
citrus that supports the tolerance includes all samples from field 
residue studies that were completely consistent with the proposed use 
pattern of 2 applications at 0.4 lb. ai./a with a 1-day phi. In 
oranges, the experiments were performed over 5-years at 13 sites in 4 
states. There were 13 separate treatments yielding 24 separate, treated 
samples for analysis. The average residue in oranges was 0.39 ppm (n = 
24, <greek-s>n -1 = 0.35 ppm). In grapefruit, the experiments were 
performed in a single year at 7 sites in 3 states. There were 7 
separate treatments yielding 14 separate, treated samples for analysis. 
The average residue in grapefruit was 0.29 ppm (n = 14, <greek-s>n -1 = 
0.13 ppm). In lemons, the experiments were performed in a single year 
at 3 sites in 2 states. There were 3 separate treatments yielding 6 
separate, treated samples for analysis. The average residue in lemons 
was 0.52 ppm (n = 6, <greek-s>n -1 = 0.06 ppm).
    For the overall crop grouping citrus fruits the average residue was 
0.37 ppm (n = 44, <greek-s>n -1 = 0.28 ppm). The HAR found in all 
citrus crop field trials meeting the proposed use pattern for 
fenpropathrin on citrus was 1.2 ppm. These overall citrus data only 
include data from samples that are consistent with the proposed use 
pattern, and do not include supporting information at higher or lower 
rates, and harvested at different phi. Data obtained by separate 
analyses of peelings and pulp from oranges demonstrated that the bulk 
of fenpropathrin residues were located on the peeling, exterior, of the 
oranges.
    There are two processing studies performed in citrus (oranges) with 
processing to juice, dried citrus pulp, and citrus oil. The studies 
demonstrated that fenpropathrin did not concentrate in juice 
(concentration factor all <<1), but did concentrate in dried citrus 
pulp (average concentration factor = 2.6), and in citrus oil (average 
concentration factor = 40.5). Thus it can be calculated from the HAR 
that residues of 3.12 ppm (1.2 x 2.6) could occur in dried citrus pulp 
and 48.6 ppm (1.2 x 40.5) could occur in citrus oil. Since residues 
could be present in the not ``ready to eat'' commodities at levels 
(3.12, 48.6 ppm) appreciably higher than the proposed RAC tolerance of 
2 ppm, tolerances are being proposed. After rounding, the proposed 
tolerances are 4.0 ppm for dried citrus pulp, and 50.0 ppm for citrus 
oil.
    vi. Melons (Cantaloupe). The proposed Section 408 tolerance for 
fenpropathrin in/on melons (crop group 9A) is 0.5 ppm. The field 
residue data that support this proposal come from 10 locations in 7 
states. At these ten locations there was a total of 14 separate trials, 
yielding 36 separate, treated samples for analysis. Samples from 
treatments that were consistent with the proposed maximum use pattern -
- 0.2 lb. ai./a, 4 applications, 7-day spray interval, 7-day pre-
harvest interval -- gave 20 separate samples for analysis. The mean of 
the 20 determinations is 0.175 ppm (n = 20, <greek-s>n-1 = 0.077 ppm) 
and a maximum value of 0.31 ppm. Separate analyses of pulp and rind 
demonstrated that the bulk of the residues were present on the rind.
    vii. Head and Stem Brassica. A proposed Section 408 tolerance of 
3.0 ppm is proposed for fenpropathrin in/on Head and stem brassica 
(crop group 5A) -- cabbage, cauliflower, broccoli, brussels sprouts, 
and related non-leafy brassica. The field residue data to support a 
fenpropathrin tolerance on the crop grouping head and stem brassica 
includes data on broccoli from 7 sitesand cabbage from six sites 
providing data from 13 sites across the U.S. Samples from trials that 
were consistent with the proposed maximum use pattern for the crop 
group -- the first application at 0.2 lb. ai./a and 2 additional 
applications at 0.3 lb. ai./a (a total application of 0.8 lb. ai./a), 
7-day spray interval, 7-day pre-harvest interval -- gave a mean residue 
of 0.62 ppm(n = 26, <greek-s>n-1 = 0.69) with a maximum value of 2.8 
ppm.
    viii. Broccoli. Field residue data come from 7 locations in 4 
states. At these locations there were a total of 8 separate trials 
yielding 28 separate, treated samples for analysis. Samples from trials 
that were consistent with the proposed maximum use pattern gave 14 
separate samples for analysis. The mean of the 14 determinations is 
0.369 ppm (n = 14, <greek-s>n-1 = 0.157 ppm)and a maximum value of 0.58 
ppm.
    ix. Cabbage. Field residue data come from 6 locations in 6 states. 
At these six locations there was a total of 7 separate trials yielding 
26 separate, treated samples for analysis. Trials that were consistent 
with the proposed maximum use pattern gave 12 separate samples for 
analysis. The mean of the determinations is 0.92 ppm (n = 12, 
<greek-s>n-1 = 0.93 ppm) and a maximum value of 2.8 ppm. Analyses of 
cabbage heads with wrapper leaves removed demonstrated that the bulk of 
the residue was on the exterior of the cabbages with a mean residue of 
0.04 ppm (n = 12, <greek-s>n-1 = 0.05 ppm) and a maximum value of 0.19 
ppm.
    x. Secondary residues. Residues in animal feed may transfer to 
animal products, meat, milk, and eggs, used in human food. The existing 
tolerances on meat and meat by-products of cattle, goats, hogs, horses 
and sheep at 0.1 ppm, fat of cattle, goats, hogs, horses and sheep at 
1.0 ppm, milk fat (reflecting 0.08 ppm in whole milk) at 2.0 ppm, and 
poultry meat, fat, meat by-products and eggs at 0.05 ppm are, adequate 
to allow the addition of the proposed uses. Both chronic and acute 
dietary assessments show very low residue contribution from secondary 
residues in animal products to all population sub-groups.

B. Toxicological Profile

    Summary. The existing registrations and tolerances of fenpropathrin 
are supported at EPA by a complete toxicology data base. Toxicity 
endpoints of concern have been identified by the Agency's Health 
Effects Division, Hazard Identification Assessment Review Committee 
(Meeting July 17, 1997; Revised Memorandum November 14, 1997). The 
identified endpoints are an acute dietary of 6.0 mg/kg/day (systemic) 
and a chronic dietary of 2.5 mg/kg/day (RfD = 0.025 mg/kg/day, UF = 
100). No endpoints of concern were identified by the Committee for 
occupational or residential, dermal or inhalation exposures of any 
duration. Further, in the Revised Memorandum of November 14, 1997, the 
Committee concluded that an additional safety factor, beyond 100 was 
not needed to account for special sensitivity of infants and children 
to fenpropathrin. In a separate action, fenpropathrin has been 
evaluated for carcinogenicity by the HED RfD/Peer Review Committee. In 
a Memorandum from Dr. G. Z. Ghali to Mr. G. La Rocca dated March 18, 
1993, it was concluded that in valid studies with adequate doses that 
the compound ``did not alter the spontaneous tumor

[[Page 41841]]

profile in both rats and mice''. Fenpropathrin was classified as Group 
E.
    1. Acute toxicity. Oral LD<INF>50</INF> in the rat is 54.0 
milligram/kilogram (mg/kg) for males and 48.5 mg/kg for females - 
Toxicity Category I; dermal LD<INF>50</INF> is 1,600 mg/kg for males 
and 870 mg/kg for females - Category II; acute inhalation (impossible 
to generate sufficient test article vapor or aerosol to elicit 
toxicity) - Category IV; primary eye irritation (no corneal 
involvement, mild iris and conjunctival irritation) - Category III; and 
primary dermal irritation (no irritation) - Category IV. Fenpropathrin 
is not a sensitizer.
    2. Genotoxicity. Studies on gene mutation and other genotoxic 
effects: An Ames Assay was negative for Salmonella TA98, TA100, TA1535, 
TA1537, and TA1538; and E coli WP2uvrA (trp-) with or without metabolic 
activation. Sister Chromosome Exchange in CHO-K1 Cells - there were no 
increases in sister chromatid exchanges seen in the CHO-K1 cells 
treated with S-33206 or the DMSO vehicle. Cytogenetics in vitro (CHO/
CA) - negative for chromosome aberrations (CA) in Chinese hamster ovary 
(CHO) cells exposed in vitro to toxic doses ( > 30 nanogram) without 
activation; and to limit of solubility (1,000 nanogram) with 
activation. In Vitro Assay in Mammalian Cells - equivocal results - of 
no concern. DNA Damage/Repair in Bacillus subtilis - not mutagenic or 
showing evidence of DNA damage at > 5,000 nanogram/paper disk.
    3. Reproductive and developmental toxicity. In a developmental 
toxicity study in rats, pregnant female rats were dosed by gavage on 
gestation days 6-15 at 0 (corn oil control) 0.4, 1.5, 2.0, 3.0, 6.0, or 
10.0 mg/kg/day. The maternal no observed adverse effect level (NOAEL) 
is 6 mg/kg/day; maternal LEL is 10 mg/kg/day based on death, 
moribundity, ataxia, sensitivity to external stimuli, spastic jumping, 
tremors, prostration, convulsions, hunched posture, squinted eyes, 
chromodacryorrhea, and lacrimation; developmental NOAEL is > 10 mg/kg/
day.
    In a developmental toxicity study in rabbits, pregnant female New 
Zealand rabbits were dosed by gavage on gestation days 7 through 19 at 
0, 4, 12, or 36 mg/kg/day. Maternal NOEL is 4 mg/kg/day; maternal LEL 
is 12 mg/kg/day based on grooming, anorexia, flicking of the forepaws; 
developmental NOEL is > 36 mg/kg/day (HDT).
    A 3-generation reproduction study was performed in rats. Rats were 
dosed with fenpropathrin at concentrations of 0, 40, 120, or 360 ppm 
(0, 3.0, 8.9, or 26.9 mg/kg/day in males; 0, 3.4, 10.1, or 32.0 mg/kg/
day in females, respectively). Parents (male/female): Systemic NOEL = 
40 ppm (3.0/3.4 mg/kg/day). Systemic LEL = 120 ppm (8.9/10.1 mg/kg/day) 
based on body tremors with spasmodic muscle twitches, increased 
sensitivity and maternal lethality; reproductive NOEL = 120 ppm (8.9/
10.1 mg/kg/day). Reproductive LEL = 360 ppm (26.9/32.0 mg/kg/day) based 
on decrease mean F1B pup weight, increased F2B loss. Pups (male/
female): Developmental NOEL = 40 ppm (3.0/3.4 mg/kg/day). Developmental 
LEL = 120 ppm (8.9/10.1 mg/kg/day) based on body tremors, increased 
mortality.
    4. Subchronic toxicity. In a subchronic oral toxicity study, rats 
were dosed at concentrations of 0, 3, 30, 100, 300, or 600 ppm in the 
diet. The lowest effect level (LEL) is 600 ppm (30 mg/kg/day) based on 
body weight (bwt) reduction (female), body tremors, and increased brain 
(female) and kidney (male) weights. The NOEL is 300 ppm (15 mg/kg/day).
    In a subchronic oral toxicity study, dogs were dosed at 
concentrations of 0, 250, 500, or 1,000 ppm in the diet. A 1,000 ppm 
dog was sacrificed moribund during the third week after having tremors 
and showing other signs of poisoning caused by the test article. 
Because of this death, the dose for this group was reduced to 750 ppm 
for the remainder of the study. The LOEL is 250 ppm (7.25 mg/kg/day) 
based on signs of GI tract disturbance. There was no NOEL -- note dog 
chronic, below)
    In a 21-day dermal toxicity study, rabbits were dosed 5-days/week 
for 3 weeks on abraded or unabraded skin at doses of 0, 500, 1,200, or 
3,000 mg/kg/day. There were no dose-related effects on bwt, food 
consumption, clinical pathology, gross pathology, or organ weights. 
Trace or mild inflammatory cell infiltration was seen in the intact and 
abraded skin in all groups, including controls, and was attributed to 
the test article. The systemic NOEL is > 3,000 mg/kg/day. Local 
irritation only.
    Although a 21-day dermal toxicity study in rabbits is available the 
Agency has determined that rats are the most sensitive species to 
ascertain the dermal toxicity potential of pyrethroid insecticides. 
Although these data are lacking, EPA has sufficient toxicity data to 
support these tolerances and these additional studies are not expected 
to significantly change the risk assessment.
    5. Chronic toxicity. In a 1-year feeding study, dogs were dosed at 
0, 100, 250, or 750 ppm in the diet. The systemic LEL is 250 ppm (6.25 
mg/kg/day) based on tremors in all dogs. The neurologic NOEL is 100 ppm 
(2.5 mg/kg/day); the systemic NOEL is 100 ppm (2.5 mg/kg/day).
    In a chronic feeding/carcinogenicity study, rats were dosed at 0, 
50, 150, 450, or 600 ppm in the diet (0, 1.93, 5.71, 17.06, or 22.80 
mg/kg/day in males, and 0, 2.43, 7.23, 19.45, or 23.98 mg/kg/day in 
females). There was no evidence of carcinogenicity at any dose up to 
and including 600 ppm. The systemic NOEL (male) is 450 ppm (17.06 mg/
kg/day). The systemic NOEL (female) is 150 ppm (7.23 mg/kg/day). 
Systemic LEL (male) is 600 ppm highest dose tested (HDT) based on 
increased mortality, body tremors, increased pituitary, kidney, and 
adrenal weights. The systemic LEL (female) is 450 ppm (19.45 mg/kg/day) 
based on increased mortality and body tremors.
    In a chronic feeding/carcinogenicity study, mice were dosed at 0, 
40, 150, or 600 ppm in the feed (0, 3.9, 13.7, or 56.0 mg/kg/day in 
males, and 0, 4.2, 16.2, or 65.2 mg/kg/day in females). Mortality was 
highest during the final quarter of the study, but the incidence was 
similar in all dosed and control groups. No other indications of 
toxicity or carcinogenicity were seen. The systemic NOEL is <ls-thn-eq> 
600 ppm (HDT; male/female, 56.0/65.2 mg/kg/day). text.
    6. Animal metabolism. In a metabolism study in rats, animals were 
dosed with radiolabelled fenpropathrin radiolabelled in either the 
alcohol or acid portion of the molecule. Rats received 14 daily oral 
low-doses of 2.5 mg/kg/day of unlabelled fenpropathrin followed by a 
15th dose of either the alcohol or acid radiolabelled fenpropathrin. 
Groups of rats received a single dose of either of the 2 radiolabelled 
test articles at 2.5 mg/kg or 25 mg/kg. No clinical signs were seen in 
any rats.
    The major biotransformations included oxidation at the methyl group 
of the acid moiety, hydroxylation at the 4'-position of the alcohol 
moiety, cleavage of the ester linkage, and conjugation with sulfuric 
acid or glucuronic acid.
    Four metabolites were found in the urine of rats dosed with alcohol 
labeled fenpropathrin. The major metabolites were the sulfate conjugate 
of 3-(4'-hydroxyphenoxy)benzoic acid and 3-phenoxybenzoic acid (22-44% 
and 3-9% of the administered dose, respectively). The major urinary 
metabolites of the acid-labeled fenpropathrin were TMPA-glucuronic acid 
and TMPA-CH2OH (11-26% and 6-10% of the administered dose, 
respectively). None of the parent chemical was found in urine.
    The major elimination products in the feces included the parent 
chemical (13-34% of the administered dose) and four

[[Page 41842]]

metabolites. The fecal metabolites (and the percentage of administered 
dose) included CH2OH-fenpropathrin (9 20%), 4'-OH-fenpropathrin (4-
11%), COOH-fenpropathrin (2-7%), and 4'-OH-CH2OH-fenpropathrin (2-7%).
    There are no qualitatively unique plant metabolites . The primary 
aglycones are identical in both plants and animals; the only difference 
is in the nature of the conjugating moieties employed.
    The metabolism and potential toxicity of the small amounts of 
terminal plant metabolites have been tested on mammals. Glucoside 
conjugates of 3-phenoxy-benzyl alcohol and 3-phenoxybenzoic acid, 
administered orally to rats, were absorbed as the corresponding 
aglycones following cleavage of the glycoside linkage in the gut. The 
free or reconjugated aglycones were rapidly and completely eliminated 
by normal metabolic pathways. The glucose conjugates of 3-phenoxybenzyl 
alcohol and 3-phenoxy-benzoic acid are less toxic to mice than the 
corresponding aglycones.
    7. Endocrine disruption. No special studies to investigate the 
potential for estrogenic or other endocrine effects of fenpropathrin 
have been performed. However, as summarized above, a large and detailed 
toxicology data base exists for the compound including studies 
acceptable to the Agency in all required categories. These studies 
include evaluations of reproduction and reproductive toxicity and 
detailed pathology and histology of endocrine organs following repeated 
or long term exposure. These studies are considered capable of 
revealing endocrine effects and no such effects were observed.

C. Aggregate Exposure

    1. Dietary exposure. Toxicity endpoints of concern have been 
identified by the Agency's Health Effects Division, Hazard 
Identification Assessment Review Committee (July 17, 1997). The 
identified endpoints are a Chronic Dietary of 2.5 mg/kg/day (RfD = 
0.025 mg/kg/day, UF = 100) and an Acute Dietary of 6.0 mg/kg/day 
(systemic). Thus, both chronic and acute dietary exposure and risk 
analyses are necessary.
    2. Food. Chronic and acute dietary exposure analyses were performed 
for fenpropathrin using anticipated residues and accounting for 
proportion of the crop treated. The crops included in the analyses are 
the raw agricultural commodities cottonseed, currants, peanuts, 
strawberries, tomatoes, pome fruits, citrus, grapes, head and stem 
brassica, and melons; processed products from these crops; and the 
resulting secondary residues in meat, milk, and eggs. A report along 
with a supplemental report of these exposure/risk analyses has been 
submitted to the Agency including a detailed description of the 
methodology and assumptions used.
    Chronic dietary exposure was calculated for the U.S. population and 
26 population subgroups. The results from several representative 
subgroups are listed below. Chronic dietary exposure was at or below 
1.7 % of the reference dose with grapes and apples the commodities 
contributing the most to chronic exposure. Generally speaking, the 
Agency has no cause for concern if total residue contribution for 
published and proposed tolerances is less than 100% of the RfD.

  Summary of Chronic Dietary (Food) Exposures to Fenpropathrin Residues 
------------------------------------------------------------------------
                                               Exposure(mg/    Percent  
             Population Subgroup                kg bw/day)      ofRfD   
------------------------------------------------------------------------
Total U.S. Population (all seasons)                0.000165          0.7
Females (13+/Nursing)                              0.000285          1.1
Non-Hispanic other than B/W                        0.000246          1.0
Children (1-6 Years)                               0.000435          1.7
All Infants (<1 Year Old)                          0.000193          0.8
Non-Nursing Infants (<1 Year Old)                  0.000127          0.5
Nursing Infants (<1 Year Old)                      0.000351          1.4
------------------------------------------------------------------------

    Acute dietary exposure was calculated for the U.S. population, 
Females (13+/Pregnant/Not Nursing), and five children subgroups. The 
sub-population, Females (13+/Pregnant/Not Nursing), was included 
because the toxicity endpoint for acute dietary exposure identified by 
the Agency is based on clinical signs of toxicity in the dams from the 
rat developmental toxicity study. The calculated exposures and margins 
of exposure (MOE) for the higher exposed proportions of the subgroups 
are listed below. In all cases, margins of exposure exceed one-hundred.

             Calculated Acute Dietary Exposures to Fenpropathrin Residues in Food (per-capita days)             
----------------------------------------------------------------------------------------------------------------
                                                                 99th Percentile           99.9th Percentile    
                                                           -----------------------------------------------------
                    Population Subgroup                     Exposure(mg/               Exposure(mg/             
                                                             kg bw/day)       MOE       kg bw/day)       MOE    
----------------------------------------------------------------------------------------------------------------
U.S. Polulation...........................................      0.003296        1,821      0.010173          590
Females (13+/Pregnant/NotNursing).........................      0.002737         2192      0.005595         1072
Children 1-6..............................................      0.008461          709      0.020678          290
Children 7-12.............................................      0.005322        1,127      0.012195          492
All Infants...............................................      0.002963        2,025      0.029691          202
Nursing Infants (<1)......................................      0.007142          840      0.050337          119
Non-Nursing Infants (<1)..................................      0.001874        3,202      0.004863        1,234
----------------------------------------------------------------------------------------------------------------

    It should be noted that the numbers of individuals in the dietary 
survey of some population subgroups is small. These ``under 
represented'' subgroups are weighted to account for their proportions 
in the total U.S. Population and in various geographic and ethnic 
subpopulations. If in these under represented subgroups there are 
individuals with unusual dietary consumption patterns anomalous Monti 
Carlo selected diets will occur at the lower probability exposures 
(e.g. 99th and 99.9th percentiles) often times leading to 
unrealistically high calculated exposures. Such is the case for Nursing 
Infants (<1). Two of these babies were reported to be fed raw grapes. 
In one case, one nursing infant was reported to consume 310 grams of 
raw grapes in a single day. This is a very unusual diet for any infant. 
Because of this dietary anomaly, and the weighting factor for this 
population subgroup, the

[[Page 41843]]

MOE for nursing infants approaches 100.
    3. Drinking water. Since fenpropathrin is applied outdoors to 
growing agricultural crops, the potential exists for fenpropathrin or 
its metabolites to reach ground or surface water that may be used for 
drinking water. Because of the physical properties of fenpropathrin, 
the Agency has determined that it is unlikely that fenpropathrin or its 
metabolites can leach to potable groundwater.
    To further quantify potential exposure from drinking water, surface 
water concentrations for fenpropathrin were estimated using GENEEC 1.2. 
The average 56-day concentration predicted in the simulated pond water 
was 0.22 ppb. The residence time of fenpropathrin in surface water has 
been measured and is short. In pond studies, fenpropathrin half-lives 
in the water column were less than 1.5 days, thus this 56-day modeled 
half-life probably considerably overestimates any real surface water 
concentration. Using standard assumptions about bwt and water 
consumption, the chronic exposure from this drinking water would be 6.3 
x 10-6 and 2.2 x 10 -5 mg/kg bw/day for adults and children, 
respectively; less than 0.09 % of the RfD for children. Based on this 
worse case analysis, the contribution of water to the dietary risk is 
negligible.
    4. Non-dietary exposure. Fenpropathrin, as the product TAME 2.4 EC 
Spray, is registered for professional non-food use both indoors and 
outdoors on ornamentals and non-bearing nursery fruit trees. 
Fenpropathrin has no animal health, homeowner, turf, termite, indoor 
pest control, or industrial uses. Quantitative information concerning 
human exposure from this ornamental use is not available, but exposure 
to the general public from this use of fenpropathrin is expected to be 
minimal. It is important to note that no endpoints of concern were 
identified by the Health Effects Division, Hazard Identification 
Assessment Review Committee for occupational or residential, dermal or 
inhalation exposures of any duration. Thus, no risk assessment is 
needed.

D. Cumulative Effects

    Section 408(b)(2)(D)(v) requires that the Agency must consider 
``available information'' concerning the cumulative effects of a 
particular pesticide's residues and ``other substances that have a 
common mechanism of toxicity.'' Available information in this context 
include not only toxicity, chemistry, and exposure data, but also 
scientific policies and methodologies for understanding common 
mechanisms of toxicity and conducting cumulative risk assessments. For 
most pesticides, although the Agency has some information in its files 
that may turn out to be helpful in eventually determining whether a 
pesticide shares a common mechanism of toxicity with any other 
substances, EPA does not at this time have the methodologies to resolve 
the complex scientific issues concerning common mechanism of toxicity 
in a meaningful way.
    There are numerous other pesticidal compounds, pyrethroids and 
natural pyrethrins, that are structurally related to fenpropathrin and 
may have similar effects on animals. In consideration of potential 
cumulative effects of fenpropathrin and other substances that may have 
a common mechanism of toxicity, there are currently no available data 
or other reliable information indicating that any toxic effects 
produced by fenpropathrin would be cumulative with those of other 
chemical compounds. Thus, only the potential risks of fenpropathrin 
have been considered in this assessment of aggregate exposure and 
effects.
    Valent will submit information for EPA to consider concerning 
potential cumulative effects of fenpropathrin consistent with the 
schedule established by EPA at 62 FR 42020 (August 4, 1997) and other 
EPA publications pursuant to the Food Quality Protection Act.

E. Safety Determination

    The Food Quality Protection Act of 1996 introduces a new standard 
of safety, a reasonable certainty of no harm. To make this 
determination, at this time the Agency should consider only the 
incremental risk of fenpropathrin in its exposure assessment. Since the 
potential chronic and acute exposures to fenpropathrin are small (<< 
100 % of RfD, MOE <ls-thn-eq> 100) the provisions of the FQPA of 1996 
will not be violated.
    1. U.S. population--i Chronic exposure. Using the dietary exposure 
assessment procedures described above for fenpropathrin, calculated 
chronic dietary exposure resulting from residue exposure from existing 
and proposed uses of fenpropathrin is minimal. The estimated chronic 
dietary exposure from food for the overall U.S. population and many 
non-child/infant subgroups is 1.1 [Females (13+/Nursing), 0.000285 mg/
kg bw/day] to 0.4 % of the RfD. Addition of the small but worse case 
potential chronic exposure from drinking water (calculated above) 
increases exposure by only 6.3 x 10-6 mg/kg bw/day, and the maximum 
occupancy of the RfD from 1.14 % to 1.16 %. Generally, the Agency has 
no cause for concern if total residue contribution is less than 100 % 
of the RfD. It can be concluded that there is a reasonable certainty 
that no harm will result to the overall U.S. Population and many non-
child/infant subgroups from aggregate, chronic exposure to 
fenpropathrin residues.
    ii. Acute. The potential acute exposure from food to the U.S. 
population and various non-child/infant population subgroups (shown 
above) provide MOE values greatly exceeding 100. Addition of the worse 
case, but very small ``background'' dietary exposure from water is not 
sufficient to change the MOE values significantly (see table below). In 
a conservative policy, the Agency has no cause for concern if total 
acute exposure calculated for the 99.9th percentile yields a MOE of 100 
or larger. It can be concluded that there is a reasonable certainty 
that no harm will result to the overall U.S. Population and many non-
child/infant subgroups from aggregate, acute exposure to fenpropathrin 
residues.

             Aggregate U.S.Poulation Acute Dietary Exposure             
------------------------------------------------------------------------
                                                                99.9th  
                                               Exposure(mg/   Percentile
              Source of Exposure                 kgbw/day)      Margin  
                                                              ofExposure
------------------------------------------------------------------------
Chronic Water................................      0.000006            -
99.9th Percentile Acute Exposure -- Food.....      0.010173        589.8
99.9th Percentile Aggregate Acute Exposure                              
 Food + Water................................      0.010179        589.4
------------------------------------------------------------------------

    2. Infants and children. Safety Factor for Infants and Children: In 
assessing the potential for additional sensitivity of infants and 
children to residues of fenpropathrin, FFDCA section 408 provides that 
EPA shall apply an additional margin of safety, up to ten-fold, for 
added protection for infants and children in the case of threshold 
effects unless EPA determines that a different margin of safety will be 
safe for infants and children.
    The toxicological data base for evaluating pre- and post-natal 
toxicity for fenpropathrin is complete with respect to current data 
requirements. There are no special pre- or post-natal toxicity concerns 
for infants and children, based on the results of the rat and rabbit 
developmental toxicity studies or the 3-generation reproductive 
toxicity study in rats. EPA HED Hazard

[[Page 41844]]

ID Committee (Revised Memorandum, November 14,1997) has concluded that 
reliable data support use of the standard 100-fold uncertainty factor 
and that an additional uncertainty factor is not needed for 
fenpropathrin to be further protective of infants and children.
    3. Chronic risk. Using the conservative exposure assumptions 
described above, the percentage of the RfD that will be utilized by 
dietary (food only) exposure to residues of fenpropathrin ranges from 
0.5 % for Non-Nursing Infants (<1 year old), up to 1.7 % for Children 
(1 - 6 years). Addingthe worse case potential incremental exposure to 
infants and children from fenpropathrin in drinking water ( 2.2 x 10 -5 
mg/kg bw/day) to the chronic dietary exposure from food (0.000435 mg/kg 
bw/day) does not materially increase the aggregate, chronic dietary 
exposure and only increases the occupancy of the RfD by 0.09% to 1.8 % 
for Children (1 - 6 years). EPA generally has no concern for exposures 
below 100% of the RfD because the RfD represents the level at or below 
which daily aggregate dietary exposure over a lifetime will not pose 
appreciable risks to human health. It can be concluded that there is a 
reasonable certainty that no harm will result to infants and children 
from aggregate, chronic exposure to fenpropathrin residues.
    4. Acute. The potential acute exposure from food to the various 
child and infant population subgroups (shown above) provide MOE values 
exceeding 100. Addition of the worse case, but very small 
``background'' dietary exposure from water (2.2 x 10 -5 mg/kg bw/day) 
is not sufficient to change the MOE values significantly (see table 
below). In a conservative policy, the Agency has no cause for concern 
if total acute exposure calculated for the 99.9th percentile yields a 
MOE of 100 or larger. It can be concluded that there is a reasonable 
certainty that no harm will result to infants and children from 
aggregate, acute exposure to fenpropathrin residues.

       Aggregate Nursing Infants (> 1 Year) Acute Dietary Exposure      
------------------------------------------------------------------------
                                                                99.9th  
                                                  Exposure    Percentile
              Source of Exposure                 (mg/kg bw/   Margin of 
                                                    day)       Exposure 
------------------------------------------------------------------------
Chronic Water.................................     0.000022            -
99.9th Percentile Acute Exposure - Food.......     0.050337        119.2
99.9th Percentile Aggregate Acute Exposure                              
 Food + Water.................................     0.050359        119.1
------------------------------------------------------------------------

F. Safety Determination Summary

    Aggregate acute or chronic dietary exposure to various sub-
populations of children and adults demonstrate acceptable risk. 
Aggregate chronic dietary exposures to fenpropathrin occupy 
considerably less than 100% of the RfD, and all aggregate acute dietary 
MOE values exceed 100. Chronic and acute dietary risk to children from 
fenpropathrin should not be of concern. Further, fenpropathrin has no 
other uses, such as animal health, indoor pest control, homeowner use 
or turf applications, that could lead to unique, enhanced exposures to 
vulnerable sub-groups of the population. It can be concluded that there 
is a reasonable certainty that no harm will result to the U.S. 
Population or to any sub-group of the U.S. population, including 
infants and children, from aggregate chronic or aggregate acute 
exposures to fenpropathrin residues resulting from approved and pending 
uses.

G. International Tolerances

Codex Maximum Residue Limits
186 -- FENPROPATHRIN
Main uses -- 8 -- INSECTISCIDE/ACARACIDE
JMPR -- 83
ADI -- 0.03 mg/jg body weight (1993)
RESIDUE -- Fenpropathrin (fat soluble)

----------------------------------------------------------------------------------------------------------------
                                                    Commodity                                                   
-----------------------------------------------------------------------------------------------------------------
                Code                           Name           MRL (mg/kg)      Step         JMPR         CCPR   
----------------------------------------------------------------------------------------------------------------
MM 0812............................              Cattle meat    0.5 (fat)            6           93  ...........
ML 0812............................              Cattle milk        0.1 F            6           93  ...........
MO 0812............................     Cattle, Edible offal                                                    
                                                          of         0.05          CXL                    (1995)
SO 0691............................              Cotton seed            1          CXL                    (1995)
OC 0691............................   Cotton seed oil, Crude            3          CXL  ...........       (1995)
VO 0440............................                Egg plant          0.2            6           93  ...........
PE 0112............................                     Eggs     0.01 (*)          CXL  ...........       (1995)
VC 0425............................                  Gherkin          0.2          CXL     D (1995)             
FB 0269............................                   Grapes            5            6           93  ...........
VO 0445............................           Peppers, Sweet            1          CXL  ...........       (1995)
FP 0009............................              Pome fruits            5          CXL  ...........       (1995)
PM 0110............................             Poultry meat   0.02 (fat)          CXL  ...........       (1995)
PO 0111............................    Poultry, Edible offal                                                    
                                                          of     0.01 (*)          CXL  ...........       (1995)
V0 0448............................                   Tomato            1          CXL  ...........       (1995)
----------------------------------------------------------------------------------------------------------------

    There are small differences between the Section 408 tolerances and 
the Codex MRL values for secondary residues in animal products. These 
minor differences are mainly caused by differences in the methods used 
to calculate animal feed dietary exposure. The only substantial 
difference between the US tolerance and the Codex MRL value is for 
tomatoes. The JMPR reviewer required that the MRL exceed the highest 
field residue value rounded up to unit value. The EPA reviewer agreed 
with Valent that one set of field residue samples was possibly 
compromised by the presence of a high rate processing treatment nearby. 
High outliers were ignored, and the tolerance was set at 0.6 ppm. (Beth 
Edwards)
[FR Doc. 98-20769 Filed 8-4-98; 8:45 am]
BILLING CODE 6560-50-F


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