[Federal Register Volume 63, Number 37 (Wednesday, February 25, 1998)]
[Notices]
[Pages 9528-9532]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-4812]


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

ENVIRONMENTAL PROTECTION AGENCY

[PF-795; FRL-5775-3]


Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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

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-795, must 
be received on or before March 27, 1998.
ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch (7502C), Information Resources and Services 
Division, 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: opp-
[email protected]. 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 
Virginia address given above, from 8:30 a.m. to 4 p.m., Monday through 
Friday, excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: By mail: Paul Schroeder, Registration 
Division, (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, 401 M. St., SW., Washington, DC 20460. Office 
location and telephone number: Rm. 255, CM #2, 1921 Jefferson Davis 
Highway, Arlington, VA, 703-305-6602, e-mail: 
[email protected].

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-795] (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:
    [email protected]


    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 5.1/6.1 or ASCII file 
format. All comments and data in electronic form must be identified by 
the docket control number [PF-795] and appropriate petition number. 
Electronic comments on this 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: February 18, 1998.

James Jones,

Director, Registration Division, Office of Pesticide Programs.

Summaries of Petitions

    Petitioner summaries of the pesticide petitions are printed below 
as required

[[Page 9529]]

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.

Uniroyal Chemical Company

PP 6G4771

    EPA has received a pesticide petition (PP 6G4771) from Uniroyal 
Chemical Co., Inc., Bethany, Connecticut 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 
the combined residues of the insect growth regulator, diflubenzuron and 
metabolites convertible to p-chloroaniline, expressed as diflubenzuron 
in or on rice at 0.02 parts per million (ppm) and rice straw at 0.8 
ppm. The proposed analytical method for detecting and measuring 
residues of diflubenzuron and 4-chloroaniline is gas chromatography 
with electron capture detection. p-Chloroaniline is determined using an 
internal standard method and detected by mass spectrometry.
    Pursuant to the section 408(d)(2)(A)(I) of the FFDCA, as amended, 
Uniroyal Chemical Company has submitted the following summary of 
information, data and arguments in support of their pesticide petition. 
This summary was prepared by Uniroyal Chemical and EPA has not fully 
evaluated the merits of the petition. EPA edited the summary to clarify 
that the conclusions and arguments were the petitioners and not 
necessarily EPA's and to remove certain extraneous material.

A. Toxicology Profile

    1. Data summary. Diflubenzuron is not acutely toxic and is not an 
irritant. In a 3-week dermal toxicity study in rats the no observed 
effect level (NOEL) for systemic toxicity was 20 milligrams/kilograms 
(mg/kg/day). In developmental toxicity studies in rats and rabbits, 
diflubenzuron was without maternal or developmental effects at doses up 
to 1,000 mg/kg/day. Systemic effects were seen on parental animals in a 
rat reproduction study at doses of 1,000 and 100,000 ppm; however, 
there were no reproductive effects and the NOEL for reproductive 
toxicity was greater than 5,000 mg/kg/day. In a chronic dog feeding 
study, target organ effects were seen in the blood and liver. 
Methemoglobinemia was evident at dose levels of 10 mg/kg/day and 
greater. The NOEL for chronic toxicity in dogs was 2 mg/kg/day. In a 
chronic rat feeding study, target organ effects were seen in the blood, 
liver, spleen and bone marrow. Methemoglobinemia was evident at doses 
of 160 ppm and greater. The NOEL for chronic toxicity in rats was 2 mg/
kg/day. Diflubenzuron was negative in a complete battery of 
mutagenicity assays. In a mouse oncogenicity study, diflubenzuron was 
negative at doses up to 1,429 mg/kg/day. Additionally, diflubenzuron 
was negative for carcinogenicity in a rat chronic feeding study at 
doses up to 500 mg/kg/day. None of the studies conducted on 
diflubenzuron have provided evidence of endocrine organ involvement.
    2. Acute toxicity. Studies for diflubenzuron technical indicate the 
acute oral toxicity in rats and mice is >4,640 mg/kg, and the acute 
dermal toxicity in rats is >10,000 mg/kg. The acute inhalation 
LC50 in rats is >35 mg/l (6 hours). Diflubenzuron technical 
is not an eye or skin irritant to rabbits, and is not a dermal 
sensitizer in guinea pigs.
    To assess subacute dermal toxicity, diflubenzuron was applied to 
the backs of male and female CD rats for 3 weeks at dose levels of 20, 
500 and 1,000 mg/kg/day. Hematology evaluation showed reductions in red 
blood cell (RBC), hemoglobin (Hgb) and hematocrit values at 500 and 
1,000 mg/kg/day. An increased incidence of polychromasia, hypochromasia 
and anisocytosis was seen at 500 and 1,000 mg/kg/day. An increase in 
methemoglobin and sulfhemoglobin values was seen at 1,000 mg/kg/day. 
The NOEL for systemic toxicity was 20 mg/kg/day.
    3. Developmental/reproductive effects. In a rat developmental 
toxicity study, diflubenzuron was administered by oral gavage to 
pregnant female rats at dosage levels of 0, 1, 2 and 4 mg/kg/day. No 
treatment related effects were seen. A subsequent study was conducted 
in pregnant Sprague Dawley rats at a dose of 0 and 1,000 mg/kg/day. No 
maternal toxicity was observed. The incidence of fetuses with skeletal 
abnormalities was slightly increased in the treated group, but was 
within historical background range. The NOEL for maternal and 
developmental toxicity in rats was greater than 1,000 mg/kg/day.
    Diflubenzuron was also administered by oral gavage to pregnant New 
Zealand White rabbits at dosage levels of 0, 1, 2 and 4 mg/kg/day. No 
treatment related effects were seen. A subsequent study was conducted 
in pregnant rabbits at a dose of 0 and 1,000 mg/kg/day. No maternal or 
developmental toxicity was seen. The NOEL for maternal and 
developmental toxicity in rabbits was greater than 1,000 mg/kg/day.
    In a rat reproduction study, diflubenzuron was fed to two 
generations of male and female rats at dietary concentrations of 0, 10, 
20, 40, and 160 ppm. No effects were seen on parental body weight gain 
and there were no reproductive effects. A subsequent study was 
conducted on 1-generation (one litter) of rats at dietary 
concentrations of 0, 1,000 and 100,000 ppm. Systemic effects were seen 
in adults at these doses but there was no effect on reproductive 
parameters. The NOEL for reproductive toxicity was greater than 100,000 
ppm (5 g/kg/day).
    4. Chronic effects. Diflubenzuron was given by capsule to male and 
female Beagle dogs for one year at dose levels of 0, 2, 10, 50 and 250 
mg/kg/day. Body weight gain was slightly reduced in females at 250 mg/
kg/day. Absolute liver and spleen weights were increased in males given 
50 and 250 mg/kg/day. A reduction in hemoglobin and mean corpuscular 
hemoglobin concentration, with an elevation in reticulocyte count, was 
seen at 50 and 250 mg/kg/day. Methemoglobin and sulfhemoglobin values 
were increased at doses of 10 mg/kg/day and greater. Histopathological 
findings were limited to pigmented macrophages and Kupffer cells in the 
liver at doses of 50 and 250 mg/kg/day. The NOEL for chronic toxicity 
in dogs was 2 mg/kg/day.
    Diflubenzuron was fed to male and female Sprague Dawley rats for 2 
years at dose levels of 0, 156, 625, 2,500 and 10,000 ppm. 
Methemoglobin values were elevated in female rats at all dose levels 
and in male rats at the two highest dose levels. Sulfhemoglobin was 
elevated in females, only, at dose levels of 2,500 and 10,000 ppm. Mean 
corpuscular volume (MCV) and reticulocyte counts were increased in high 
dose females. Spleen and liver weights were elevated at the two highest 
doses. Histopathological examination demonstrated an increase in 
hemosiderosis of the liver and spleen, bone marrow and erythroid 
hyperplasia and areas of cellular alteration in the liver. In another 
study diflubenzuron was administered to male and female CD rats for 2 
years at dose levels of 0, 10, 20, 40 and 160 ppm. Elevated 
methemoglobin levels were seen in high dose males and females. No 
additional effects, including carcinogenic findings, were observed. The 
NOEL for chronic toxicity in rats was 40 ppm (2 mg/kg/day).

[[Page 9530]]

    5. Carcinogenicity. A 91-week oncogenicity study in CFLP mice was 
conducted at doses of 0, 16, 80, 400, 2,000 and 10,000 ppm. There was 
no increase in tumor incidence as a result of diflubenzuron 
administration. Target organ effects included: increased methemoglobin 
and sulfhemoglobin values, Heinz bodies, increased liver and spleen 
weight, hepatocyte enlargement and vacuolation, extramedullary 
hemopoiesis in the liver and spleen, siderocytosis in the spleen and 
pigmented Kupffer cells. A NOEL for these effects was 16 ppm (2 mg/kg/
day).
    Diflubenzuron was fed to male and female Sprague Dawley rats for 2 
years at dose levels of 0, 156, 625, 2,500 and 10,000 ppm. 
Methemoglobin values were elevated in female rats at all dose levels 
and in male rats at the two highest dose levels. Blood sulfhemoglobin 
was elevated in females, only, at dose levels of 2,500 and 10,000 ppm. 
MCV and reticulocyte counts were increased in high dose females. Spleen 
and liver weights were elevated at the two highest doses. 
Histopathological examination demonstrated an increase in hemosiderosis 
of the liver and spleen, bone marrow and erythroid hyperplasia and 
areas of cellular alteration in the liver. There was no increase in 
tumor formation. In another study diflubenzuron was administered to 
male and female CD rats for 2 years at dose levels of 0, 10, 20, 40 and 
160 ppm. Elevated methemoglobin levels were seen in high dose males and 
females. No additional effects, including carcinogenic findings, were 
observed.
    NCI/NTP conducted chronic feeding and gavage studies with p-
chloroaniline (PCA), a minor metabolite of diflubenzuron, in Fischer 
344 rats and B6C3F1 mice.
    PCA was administered in the diet to Fischer 344 rats at dietary 
concentrations of 250 and 500 ppm for 78 weeks, followed by a 24-week 
observation period. A slight body weight depression was seen in high 
dose females rats, compared to controls. Survival was reduced in high 
dose males compared to controls. In male rats there was a slight 
increase in uncommon fibromas or fibrosarcomas of the spleen, which was 
not statistically significant. Non-neoplastic proliferative and chronic 
inflammatory lesions were found in spleens of treated rats. It was 
concluded that, under the conditions of the assay, sufficient evidence 
was not found to establish the carcinogenicity of PCA for Fischer 344 
rats.
    PCA was administered 5 days/week by oral gavage, as a hydrochloride 
salt in water, to male and female F344/N rats at doses of 0, 2, 6 or 18 
mg/kg/day. Mean body weights of dosed rats were generally within 5% of 
those of controls throughout the study. High dose animals generally 
showed mild hemolytic anemia and dose-related methemolglobinemia. Non-
neoplastic lesions seen were bone marrow hyperplasia, hepatic 
hemosiderosis and splenic fibrosis, suggesting treatment related 
effects on the hematopoietic system. Adrenal medullary hyperplasia was 
observed in high dose female rats. The incidence of uncommon sarcomas 
of the spleen was significantly increased in high dose male rats. A 
marginal increase in pheochromocytomas of the adrenal gland was seen in 
high dose male and female rats. It was concluded that, under the 
conditions of this 2 year gavage study, there was clear evidence of 
carcinogenic activity of PCA hydrochloride for male F344/N rats and 
equivocal evidence of carcinogenic activity of PCA hydrochloride for 
female F344/N rats.
    PCA was administered in the diet to B6C3F6 mice at dietary 
concentrations of 2,500 and 5,000 ppm for 78 weeks followed by a 13-
week observation period. A body weight depression was seen in treated 
mice of both sexes, compared to controls. An increased incidence of 
hemangiomas and hemangiosarcomas in spleen, kidney, liver and other 
sites was seen in treated mice of both sexes, however this increase was 
not statistically significant compared to controls. Non-neoplastic 
proliferative and chronic inflammatory lesions were found in spleens of 
treated mice. The evidence was considered insufficient to conclusively 
relate the hemangiomatous tumors in mice to compound administration. It 
was concluded that, under the conditions of the assay, sufficient 
evidence was not found to establish the carcinogenicity of PCA for 
B6C3F1 mice.
    PCA hydrochloride was administered 5 days/week by oral gavage to 
male and female B6C3F1 mice at doses of 0, 3, 10, or 30 mg/kg/day. Mean 
body weights of high dose male and female mice were generally within 5% 
of those of controls throughout the study. The incidence of 
hepatocellular adenomas or carcinomas (combined) was increased in a 
non-dose-dependent manner in treated male mice. Metastasis of carcinoma 
to the lung was seen in the high dose group. An increased incidence of 
hemangiosarcomas of the liver or spleen was seen in high dose male 
mice. It was concluded that, under the conditions of this 2 year gavage 
study, there was some evidence of carcinogenic activity of PCA 
hydrochloride for male B6C3F1 mice and no evidence of carcinogenic 
activity of PCA hydrochloride for female B6C3F1 mice.
    6. Mutagenicity. Diflubenzuron did not show any mutagenic activity 
in point mutation assays employing S. typhimurium, S. cerevisiae, or 
L5178Y Mouse Lymphoma cells. Diflubenzuron did not induce chromosomal 
aberrations in Chinese Hamster Ovary cells and it did not induce 
unscheduled DNA synthesis in human WI-38 cells. Diflubenzuron was also 
negative in Mouse Micronucleus and Mouse Dominant Lethal assays and it 
did not induce cell transformation in Balb/3T3 cells.
    7. Endocrine effects. The standard battery of required studies has 
been completed and evaluated to determine potential estrogenic or 
endocrine effects of diflubenzuron. These studies include an evaluation 
of the potential effects on reproduction and development, and an 
evaluation of the pathology of the endocrine organs following repeated 
or long-term exposure. These studies are generally considered to be 
sufficient to detect any endocrine effects. No such effects were noted 
in any of the studies with diflubenzuron.
    8. Rat metabolism. Diflubenzuron (DFB) in rats at a single dose of 
100 mg/kg and 5 mg/kg single and multiple oral doses depicted limited 
absorption from the gastrointestinal tract. No major difference was 
observed between the single and multiple doses. In single dose 
treatments, after 7 days, 20 and 3% of the applied dose 5 and 100 mg/
kg, respectively, were excreted in urine while 79 and 98% of the 
applied dose 5 and 100 mg/kg, respectively, were eliminated in the 
feces. Very little bioaccumulation in the tissues was observed. Several 
metabolites were observed in the urine which are, among others, 2,6-
diflurobenzoic acid (DFBA), 2,6-difluorophippuric acid, 2,6-
difluorobenzamide (DFBAM), and 2-hydroxydiflubenzuron (2-HDFB). An 
unresolved peak that was p-chloroaniline (PCA) and/or p-
chlorophenylurea (CPU) was found. This latter peak accounted for about 
2% of the administered dose (5 mg/kg). In the feces, only unchanged 
parent compound was detected.

B. Aggregate Exposure

    1. Dietary exposure--i. Diflubenzuron. The dietary exposure from 
diflubenzuron (DFB) was estimated based on the average residue values 
from the various currently labeled raw agricultural commodities (RACs) 
and the proposed rice use. Percent of crop treated was also factored 
into the estimate. Current animal commodity tolerances, which

[[Page 9531]]

adequately cover the rice use, were used for meat, milk, and egg 
products. The dietary exposure analysis was estimated based on 1977 
USDA food consumption data.
    For the general U.S. population (48 states, all seasons), the 
dietary exposure of diflubenzuron was estimated as 0.000706 mg/kg/day. 
For nursing and non-nursing infants, the exposure was estimated as and 
0.000799 and 0.003461 mg/kg/day, respectively. For children, the 
exposure was 0.001888 and 0.001178 mg/kg/day for 1-6 year olds and 7-12 
year olds, respectively.
    ii. p-Chloroaniline and related product. The dietary exposure 
estimate for PCA and related products is a conservative estimate, in 
that it includes rice straw as an animal feed. Rice straw, however, 
will be restricted as a animal feed, in the proposed Experimental Use 
Program. The dietary exposure from p-chloroaniline (PCA) and a related 
product, 4-chlorophenylurea (CPU), which have been detected in some 
food products was also determined. EPA has used a 2% in vivo conversion 
factor of DFB to PCA for foods derived from plant products. For 
mushrooms, PCA and CPU average residue data was combined with a 2% in 
vivo conversion of DFB to PCA. Calculations for levels of PCA/CPU in 
animal products were based on metabolism studies, extrapolation to 
anticipated animal dietary burdens and the 2% conversion of DFB to PCA. 
The percent treated of each crop was also factored into the exposure 
estimate.
    For the general U.S. population, the dietary exposure of PCA/CPU 
was estimated as 0.000001 mg/kg/day. For nursing and non-nursing 
infants, the exposure was estimated as 0.000002 and 0.000006 mg/kg/day, 
respectively. For children, the exposure was 0.000004 and 0.000002 mg/
kg/day for 1-6 year olds and 7-12 year olds, respectively.
    2. Drinking water exposure. Diflubenzuron degrades in soil 
relatively quickly with an aerobic half-life ranging from 3-7 days. 
Major degradates include difluorobenzoic acid (DFBA) and CPU. DFBA is 
further metabolized through decarboxylation and ring cleavage by soil 
microbes whereas CPU is slowly degraded to soil-bound entities. Under 
anaerobic aquatic conditions, diflubenzuron has a half-life of 34 days 
with the main degradates being DFBA and CPU. In surface water, 
diflubenzuron is degraded by microbes with a half-life of 5-10 days. 
The soil mobility of diflubenzuron is considered quite limited based on 
a number of experimental studies as well as by computer modeling. CPU 
has also been shown to be relatively immobile in soil. Although DFBA 
shows mobility in soil, it is rapidly degraded. Therefore, based on 
results of laboratory and field studies, it is not likely that 
diflubenzuron or its degradates will impact ground water quality to any 
significant extent. Thus the aggregate risk to diflubenzuron does not 
include drinking water.
    3. Non-occupational exposure. Diflubenzuron is a restricted use 
pesticide based on its toxicity to aquatic invertebrates. This 
restricted use classification makes it unavailable for use by 
homeowners. Occupational uses of diflubenzuron may expose people in 
residential locations, parks, or forests treated with diflubenzuron. 
Based on very low residues detected in forestry dissipation studies, 
low dermal absorption rate (0.05%), and extremely low dermal and 
inhalation toxicity, these uses are expected to result in insignificant 
risk, and will, therefore, not be included in the aggregate risk 
assessment. Reference: ``Reregistration Eligibility Document: 
Diflubenzuron,'' EPA, August 1997.

C. Cumulative Risk

    Uniroyal Chemical Co. has considered the potential for cumulative 
effects of diflubenzuron and other substances with a common mechanism 
of toxicity. The mammalian toxicity of diflubenzuron is well defined. 
We are not aware of any other pesticide product registered in the 
United States that could be metabolized to p-chloroaniline. For this 
reason, consideration of potential cumulative effects of residues from 
pesticidal substances with a common mechanism of action as 
diflubenzuron is not appropriate. Thus only the potential exposures to 
diflubenzuron were considered in the total exposure assessment.

D. Safety Determination

    1. U.S. population. Based on the available toxicology and exposure 
data base for diflubenzuron, Uniroyal has determined that the total 
possible non-occupational aggregate exposure from diflubenzuron would 
occur from the dietary exposure route. Dietary exposure to the general 
U.S. population from diflubenzuron was estimated at 0.000706 mg/kg/day. 
Based on the 0.02 mg/kg/day RfD (reference dose) derived from the dog 
chronic NOEL of 2 mg/kg/day and a 100-fold safety factor, this dietary 
exposure is 3.5% of the RfD.
    For PCA and CPU, Uniroyal has also determined that the total 
possible non-occupational aggregate exposure would occur from the 
dietary exposure route. Dietary exposure to the general U.S. population 
from PCA/CPU was estimated as 0.000001 mg/kg/day. The risk from 
diflubenzuron-derived PCA/CPU can be estimated using a linear 
extrapolation of the dose-response from the rat chronic study conducted 
by the National Toxicology Program in which rats were dosed via gavage 
with p-chloroaniline hydrochloride 5 days/week for 103 weeks (NTP TR 
351). EPA has determined the q1* as 0.059 by combining the incidences 
of splenic sarcomas from both male and female rats.
    Although EPA has assumed that CPU is also carcinogenic purportedly 
based on its structural similarity to PCA, Uniroyal has indicated to 
the Agency in previous correspondence that this assumption is not 
warranted. It may be more appropriate to compare the carcinogenicity 
potential of CPU to acetanilide, which is also a structural analog of 
CPU, and for which no evidence of carcinogenicity has been demonstrated 
possibly because the N-hydroxy metabolite is not formed in significant 
amounts. Formation of the N-hydroxy metabolite of CPU is also remote. 
Uniroyal has also argued that it is unlikely that significant 
degradation of CPU to form PCA would occur, since based on the known 
animal metabolism of phenylureas, only a small amount of aniline 
derivatives are produced. The major metabolic pathway for the 
phenylureas is ring hydroxylation and n-dealkylation, a process that 
would maintain the integrity of the parent urea molecule. Therefore, it 
would not be appropriate to combine CPU residues with PCA. However, for 
this safety assessment we have conservatively estimated the risk from 
dietary exposure to both PCA and CPU combined.
    Using the q1* of 0.059 from the combined male and female incidence 
of splenic tumors in rats, the risk to the general U.S. population from 
dietary exposure to diflubenzuron-derived PCA/CPU is 8.7x10-
8.
    2. Infants and children. The same assumptions as for the general 
U.S. population were used for the dietary exposure risk determination 
in infants and children. The dietary exposure of diflubenzuron was 
calculated as 0.000799 mg/kg/day and 0.003461 mg/kg/day respectively 
for nursing and non-nursing infants. These values are 4% and 17.3% 
respectively of the RfD for diflubenzuron. The dietary exposure from 
diflubenzuron in children 1-6 and 7-12 years old was determined as 
0.001888 mg/kg/day and 0.001178 mg/kg/day, respectively. These values 
are 9.4% and 5.9% of the RfD, respectively.
    As previously discussed, the NOELs for maternal and developmental 
toxicity in rats and rabbits were greater than

[[Page 9532]]

1,000 mg/kg/day, and the NOEL for reproductive toxicity was greater 
than 5,000 mg/kg/day. Therefore, based on the completeness and 
reliability of the toxicity data and the conservative exposure 
assessment, Uniroyal concludes that there is reasonable certainty that 
no harm will result in infants and children from aggregate exposure to 
residues of diflubenzuron and its conversion products containing the p-
chloroaniline moiety.

E. Residues in the Raw Agricultural Commodity and Processed Food/Feed

    1. Nature of residues in plants and livestock. The nature of the 
residue in plants and livestock is adequately understood. In plants, 
the metabolism of diflubenzuron was investigated in soybeans, oranges 
and rice. The main component of residues in rice was CPU; levels of PCA 
were negligible to non-detectible. The main component of the residues 
in soybeans and oranges was the parent diflubenzuron (DFB). A 
considerable portion of the residues were bound. DFB showed very 
limited absorption and translocation in plants with most of the 
residues remaining on the surface.
    In livestock, goats treated for three days at about 1X (10 ppm 
feeding level) the dietary burden of C14 DFB gave DFB 
equivalent of C14 = 7-9 ppb in milk, 217-262 ppb in liver, 
16-19 ppb in kidney, about 1 ppb in muscle, and about 4 ppb in fat. 
Milk residues were mainly CPU and DFBAM. PCA was not detectable. Liver 
residues were DFB, 2-hydroxy DFB, CPU, and DFBAM. Again, PCA was not 
detected at this dose however, it was detected in studies conducted at 
about 22X dose. Chickens were dosed with C14 DFB at 5 ppm 
level for 1-28 days. Residues in tissues as DFB equivalent were highest 
in liver and kidney. The main residues in tissues and eggs were DFB and 
DFBA. Trace amount of PCA and its acetanilide were detected, but not 
confirmed, in liver kidney and egg white.
    2. Magnitude of residues and proposed tolerances. An adequate 
number of separate residue trials have been conducted with 
diflubenzuron on rice. Analyses of these trials show that the maximum 
total residue for diflubenzuron and its conversion products PCA and CPU 
will be at or below 0.01 ppm.
    A tolerance has been requested for the combined residues of 
diflubenzuron and metabolites convertible to p-chloroaniline expressed 
as diflubenzuron on rice at 0.01 ppm. The proposed tolerance is 
adequate to cover residues likely to be present from the use of 
diflubenzuron on rice. Therefore, no special processing to reduce the 
residues will be necessary.
    The meat by-products tolerances are adequate to cover residues 
resulting from the rice use. Uniroyal Chemical has submitted 
calculations from a goat metabolism study which supports the 0.05 ppm 
tolerance in meat by-products. Therefore, no increase in the meat by-
products tolerances should be necessary.

F. Practical Analytical Method

    Practical analytical methods for detecting levels of DFB, CPU and 
PCA, in or on food with a limit of detection that allows monitoring of 
the residue at or above the level set in the tolerance was used to 
determine residues in rice and its respective processed fractions.
    Residues of the individual analytes are detectable and quantifiable 
using three separate analytical methods. Residues of DFB are extracted 
from rice with dichloromethane. Extracts are purified with deactivated 
florisil. An aliquot of the extract is hydrolyzed with phosphoric acid 
and the DFB is partitioned into hexane. The resulting extract is 
derivatized in heptafluorobutyric anhydride (HFBA). Quantification of 
DFB is accompanied by gas chromatography using an electron capture 
detector.
    The analytical method for quantitation of the 4-chlorophenylurea 
requires ethyl acetate extraction of the residue from the matrix. 
Column chromatography is utilized for clean-up of the extract 
immediately prior to derivitization with HFBA. Derivatized extracts are 
analyzed by gas chromatography equipped with an electron capture 
detector.
    The analysis for the determination of PCA residues in rice matrices 
utilizes an internal standard method. Samples of matrix to be analyzed 
are fortified with the internal standard. Residues of 12C-PCA and the 
internal standard are subjected to acid and base hydrolysis. The final 
extract is passed through florisil column for clean-up and derivatized 
with HFBA in hexane. An aliquot of the derivatized extract is analyzed 
by gas chromatography using a mass spectrometry detector in the 
selective ion monitoring mode. Recovery of PCA is determined by the 
combined peak areas for the two mass spectral ions obtained from the 
derivatized 12C-PCA relative to the response factor derived from the 
combined areas of the corresponding two mass spectral ions from the 
internal standard.

G. List of All Pending Tolerances and Exemptions

    A tolerance for diflubenzuron on range grass at 4.0 ppm is pending. 
There are no exemptions from tolerance for diflubenzuron.

H. List International Tolerances (Code MRLs)

    There are no Codex Alimentarius Commission maximum residue levels 
for residues of diflubenzuron on rice. The Codex MRL on citrus is 1.0 
mg/kg vs. 0.05 ppm for U.S. tolerance. The Codex MRL for mushrooms is 
0.1 mg/kg vs. 0.2 ppm for U.S. tolerance. The Codex MRL for soybeans is 
0.1 mg/kg/ vs. 0.05 ppm for the U.S. The Codex MRL is 1 mg/kg for 
apples, Brussels sprouts, cabbage, pears, plums and tomatoes for which 
there are no U.S. tolerances. The Codex MRL for meat, milk and eggs is 
0.05 mg/kg/ which is the same as the established U.S. tolerances.

[FR Doc. 98-4812 Filed 2-24-98; 8:45 am]
BILLING CODE 6560-50-F