[Federal Register Volume 63, Number 111 (Wednesday, June 10, 1998)]
[Notices]
[Pages 31768-31771]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-15177]


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ENVIRONMENTAL PROTECTION AGENCY

[PF-810; FRL-5793-1]


FMC Corporation; Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: This notice announces the initial filing of a pesticide 
petition proposing the establishment of regulations for residues of a 
certain pesticide chemical in or on various food commodities.
DATES: Comments, identified by the docket control number PF-810, must 
be received on or before July 10, 1998.
ADDRESSES: By mail submit written comments to: Information and Records 
Integrity Branch, Public Information and Services Divison (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 by following 
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

[[Page 31769]]

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. 1132 at the address given above, from 8:30 
a.m. to 4 p.m., Monday through Friday, excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: Joanne Miller, Registration Support 
Branch, Registration Division (7505C), Office of Pesticide Programs, 
Environmental Protection Agency, 401 M St., SW, Washington, DC 20460. 
Office location, telephone number, and e-mail address: Rm. 237, Crystal 
Mall CM #2, 1900 Jefferson Davis Highway, Arlington, VA 22202, (703) 
305-6224; e-mail: <a href="/cdn-cgi/l/email-protection#68050104040d1a4602070906060d280d180905090104460d1809460f071e"><span class="__cf_email__" data-cfemail="8ce1e5e0e0e9fea2e6e3ede2e2e9cce9fcede1ede5e0a2e9fceda2ebe3fa">[email protected]</span></a>.
SUPPLEMENTARY INFORMATION: EPA has received a pesticide petition as 
follows proposing the establishment and/or amendment of regulations for 
residues of certain pesticide chemical 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 this petition 
contains 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-810] (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#274857570a4348444c4253674257464a464e4b0942574609404851"><span class="__cf_email__" data-cfemail="472837376a2328242c2233072237262a262e2b6922372669202831">[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 FRL-5793-1 and appropriate petition 
number. Electronic comments on this proposed rule 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: May 26, 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. FMC Corporation

PP 6G4615

    EPA has received a pesticide petition (PP 6G4615) from FMC 
Corporation, 1735 Market Street, Philadelphia, PA 19103, 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 extending a temporary 
tolerance for the combined residue of the herbicide carfentrazone-ethyl 
(ethyl-alpha-2-dichloro-5-[4-(difluoromethyl)-4,5-dihydro-3-methyl-5-
oxo-1H-1,2,4-triazol-1-yl]-4-fluorobenzene-propanoate) and its major 
wheat metabolites: carfentrazone-ethyl chloropropionic acid (alpha, 2-
dichloro-5-[4-difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4-
triazol-1-yl]-4-fluorobenzenepropanoic acid), 3-hydroxymethyl-F8426-
chloropropionic acid (alpha,2-dichloro-5-[4-difluoromethyl)-4,5-
dihydro-3-hydroxymethyl-5-oxo-1H-1,2,4-triazol-l-yl]-4-
fluorobenzenepropanoic acid), and 3-desmethyl-F8426 chloropropionic 
acid (alpha, 2-dichloro-5-[4-difluoromethyl)-4,5-dihydro-5-oxo-1H-
1,2,4-triazol-l-yl]-4-fluorobenzenepropanoic acid) in or on wheat raw 
agricultural commodities: 0.2 ppm in or on wheat hay, 0.2 ppm in or on 
wheat straw, 0.2 ppm in or on wheat grain; and extending tolerance for 
combined residue of the herbicide carfentrazone-ethyl (ethyl-alpha-2-
dichloro-5-[4-(difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4-
triazol-1-yl]-4-fluorobenzene-propanoate) and its major corn 
metabolites: carfentrazone-ethyl chloropropionic acid (alpha, 2-
dichloro-5-[4-difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4-
triazol-l-yl]-4-fluorobenzenepropanoic acid),and 3-desmethyl-F8426 
chloropropionic acid (alpha, 2-dichloro-5-[4-difluoromethyl)-4,5-
dihydro-5-oxo-1H-1,2,4-triazol-1-yl]-4-fluorobenzenepropanoic acid) in 
or on corn raw agricultural commodities: 0.15 ppm in or on corn forage, 
0.15 ppm in or on corn fodder, 0.15 ppm in or on corn grain.
    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 supports granting of the 
petition. Additional data may be needed before EPA rules on the 
petition.

A. Residue Chemistry

    1. Plant metabolism. The metabolism of carfentrazone-ethyl in 
plants is adequately understood. Corn and wheat metabolism studies with 
carfentrazone-ethyl have shown uptake of material into plant tissue 
with no significant movement into grain or seeds. All three plants 
extensively metabolized carfentrazone-ethyl and exhibited a similar 
metabolic pathway. The residues of concern are the combined residues of 
carfentrazone-ethyl and carfentrazone-ethyl- chloropropionic acid.
    2. Analytical method There is a practical analytical method for 
detecting and measuring levels of carfentrazone and its metabolites in 
or on food with a limit of quantitation that allows monitoring of food 
with residues at or above the levels set in the tolerances. The 
analytical method for carfentrazone-ethyl involves separate analyses 
for parent and its metabolites. The parent is analyzed by GC/ECD. The 
metabolites are derivatized with boron trifluoride and acetic anhydride 
for analysis by GC/MSD using selective ion monitoring.
    3. Magnitude of residues. Carfentrazone-ethyl 50DF was applied 
postemergent to 28 wheat trials, and 24 corn trials in the appropriate 
EPA regions. The RAC's were harvested at

[[Page 31770]]

the appropriate growth stages and subsequent analyses determined that 
the residues of carfentrazone-ethyl and its metabolites will not exceed 
the proposed tolerances of 1.0, 0.3, 0.2 and 0.1 ppm for wheat forage, 
hay, straw and grain, respectively; 0.1 ppm each for corn forage, 
fodder, and grain. Residue data from a cow feeding study demonstrated 
that no accumulation of carfentrazone-ethyl or its metabolites occurred 
in milk or tissues.

B. Toxicological Profile

    1. Acute toxicity. Carfentrazone-ethyl demonstrates low oral, 
dermal and inhalation toxicity. The acute oral LD<INF>50</INF> value in 
the rat was greater than 5,000 milligram/Kilograms (mg/kg), the acute 
dermal LD<INF>50</INF> value in the rat was greater than 4,000 mg/kg 
and the acute inhalation LC<INF>50</INF> value in the rat was greater 
than 5.09 mg/L/4h. Carfentrazone-ethyl is non-irritating to rabbit skin 
and minimally irritating to rabbit eyes. It did not cause skin 
sensitization in guinea pigs. An acute neurotoxicity study in the rat 
had a systemic no-observed-adverse-effect level (NOAEL) of 500 mg/kg 
based on clinical signs and decreased motor activity levels; the NOAEL 
for neurotoxicity was greater than 2,000 mg/kg highest dose tested 
(HDT) based on the lack of neurotoxic clinical signs or effects on 
neuropathology.
    2. Genotoxicty. Carfentrazone-ethyl did not cause mutations in the 
Ames assay with or without metabolic activation. There was a positive 
response in the Chromosome Aberration assay without activation but a 
negative response with activation. The Mouse Micronucleus assay (an in 
vivo test which also measures chromosome damage), the CHO/HGPRT forward 
mutation assay and the Unscheduled DNA Synthesis assay were negative. 
The overwhelming weight of the evidence supports the conclusion that 
Carfentrazone-ethyl is not genotoxic.
    3. Reproductive and developmental toxicity. Carfentrazone-ethyl is 
not considered to be a reproductive or a developmental toxin. In the 2-
generation reproduction study, the NOEL for reproductive toxicity was 
greater than 4,000 ppm (greater than 323 to greater than 409 mg/kg/
day). In the developmental toxicity studies, the rat and rabbit 
maternal NOELs were 100 mg/kg/day and 150 mg/kg/day, respectively. The 
developmental NOEL for the rabbit was greater than 300 mg/kg/day which 
was the HDT and for the rat the NOEL was 600 mg/kg/day based on 
increased litter incidences of thickened and wavy ribs at 1,250 mg/kg/
day. These two findings (thickened and wavy ribs) are not considered 
adverse effects of treatment but related delays in rib development 
which are generally believed to be reversible.
    4. Subchronic toxicity 90-day feeding studies were conducted in 
mice, rats and dogs with carfentrazone-ethyl. The NOEL for the mouse 
study was 4,000 ppm (571 mg/kg/day), for the rat study was 1,000 ppm 
(57.9 mg/kg/day for males; 72.4 mg/kg/day for females) and for dogs was 
150 mg/kg/day. A 90-day subchronic neurotoxicity study in the rat had a 
systemic NOEL of 1,000 ppm (59.0 mg/kg/day for males; 70.7 mg/kg/day 
for females) based on decreases in body weights, body weight gains and 
food consumption at 10,000 ppm; the neurotoxicity NOEL was greater than 
20,000 ppm (1178.3 mg/kg/day for males; 1433.5 mg/kg/day for females) 
which was the HDT.
    5. Chronic toxicity. Carfentrazone-ethyl is not carcinogenic to 
rats or mice. A 2-year combined chronic toxicity/oncogenicity study in 
the rat was negative for carcinogenicity and had a chronic toxicity 
NOEL of 200 ppm (9 mg/kg/day) for males and 50 ppm (3 mg/kg/day) for 
females based on red fluorescent granules consistent with porphyrin 
deposits in the liver at the 500 and 200 ppm levels, respectively. An 
18-month oncogenicity study in the mouse had a carcinogenic NOEL that 
was greater than 7,000 ppm (>1090 mg/kg/day for males; >1296 mg/kg/day 
for females) based on no evidence of carcinogenicity at the HDT. A 1-
year oral toxicity study in the dog had a NOEL of 50 mg/kg/day based on 
isolated increases in urine porphyrins in the 150 mg/kg/day group (this 
finding was not considered adverse).
    Using the Guidelines for Carcinogen Risk Assessment, carfentrazone-
ethyl should be classified as Group ``E'' for carcinogenicity -- no 
evidence of carcinogenicity -- based on the results of carcinogenicity 
studies in two species. There was no evidence of carcinogenicity in an 
18-month feeding study in mice and a 2-year feeding study in rats at 
the dosage levels tested (DLT). The doses tested are adequate for 
identifying a cancer risk. Thus, a cancer risk assessment is not 
necessary.
    6. Animal metabolism. The metabolism of carfentrazone-ethyl in 
animals is adequately understood. Carfentrazone-ethyl was extensively 
metabolized and readily eliminated following oral administration to 
rats, goats, and poultry via excreta. All three animals exhibited a 
similar metabolic pathway. As in plants, the parent chemical was 
metabolized by hydrolytic mechanisms to predominantly form 
carfentrazone-ethyl-chloropropionic acid which was readily excreted.
    7. Endocrine disruption. An evaluation of the potential effects on 
the endocrine systems of mammals has not been determined; however, no 
evidence of such effects were reported in the chronic or reproductive 
toxicology studies described above. There was no observed pathology of 
the endocrine organs in these studies. There is no evidence at this 
time that carfentrazone-ethyl causes endocrine effects.

C. Aggregate Exposure

    Dietary exposure--i. Acute dietary. The Agency has determine that 
there is no concern for an acute dietary risk assessment since the 
available data do not indicate any evidence of significant toxicity 
from a 1-day or single event exposure by the oral route Federal 
Register of September 30, 1997 (62, FR 189). Thus an acute dietary risk 
assessment is not necessary.
    ii. Food. Dietary exposure from the proposed uses would account for 
1.3% or less of the RfD in subpopulations (including infants and 
children).
    iii. Drinking water. Studies have indicated that carfentrazone-
ethyl will not move into groundwater, therefore water has not been 
included in the dietary risk assessment.
    iv. Non-dietary exposure. No specific worker exposure tests have 
been conducted with carfentrazone-ethyl. The potential for non-
occupational exposure to the general population has not been fully 
assessed. No specific worker exposure tests have been conducted with 
carfentrazone-ethyl.

D. Cumulative Effects

    EPA is also required to consider the potential for cumulative 
effects of carfentrazone-ethyl and other substances that have a common 
mechanism of toxicity. EPA consideration of a common mechanism of 
toxicity is not appropriate at this time since EPA does not have 
information to indicate that toxic effects produced by carfentrazone-
ethyl would be cumulative with those of any other chemical compounds; 
thus only the potential risks of carfentrazone-ethyl are considered in 
this exposure assessment.

E. Safety Determination

    1. U.S. population. Using the conservative exposure assumptions 
described and based on the completeness and reliability of the toxicity 
data, the aggregate exposure to carfentrazone-ethyl will utilize 0.61% 
of the RfD for the US population. EPA generally has no concern for 
exposures below 100% of the RfD. Therefore,

[[Page 31771]]

based on the completeness and reliability of the toxicity data and the 
conservative exposure assessment, there is a reasonable certainty that 
no harm will result from aggregate exposure to residues of 
carfentrazone-ethyl, including all anticipated dietary exposure and all 
other non-occupational exposures.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of carfentrazone-ethyl, 
EPA considers data from developmental toxicity studies in the rat and 
rabbit and the 2-generation reproduction study in the rat. The 
developmental toxicity studies are designed to evaluate adverse effects 
on the developing organism resulting from pesticide exposure during 
prenatal development. Reproduction studies provide information relating 
to effects on the reproductive capacity of males and females exposed to 
the pesticide. Developmental toxicity was not observed in developmental 
toxicity studies using rats and rabbits. In these studies, the rat and 
rabbit maternal NOELs were 100 mg/kg/day and 150 mg/kg/day, 
respectively. The developmental NOEL for the rabbit was greater than 
300 mg/kg/day which was the HDT and for the rat was 600 mg/kg/day based 
on increased litter incidences of thickened and wavy ribs. These two 
findings are not considered adverse effects of treatment but related 
delays in rib development which are generally believed to be 
reversible.
    In a 2-generation reproduction study in rats, no reproductive 
toxicity was observed under the conditions of the study at 4,000 ppm 
which was the HDT.
    Section 408 of the FFDCA provides that EPA may apply an additional 
safety factor for infants and children in the case of threshold effects 
to account for pre- and post-natal toxicity and the completeness of the 
database. Based on the current toxicological data requirements, the 
database relative to pre- and post-natal effects for children is 
complete and an additional uncertainty factor is not warranted. 
Therefore at this time, the provisional RfD of 0.06 mg/kg/day is 
appropriate for assessing aggregate risk to infants and children.

F. Reference Dose

    Using the conservative exposure assumptions described above, the 
percent of the RfD that will be utilized by aggregate exposure to 
residues of carfentrazone-ethyl for non-nursing infants (<1-year old) 
would be 0.28% and for children 1-6 years of age would be 1.37% (the 
most highly exposed group). Based on the completeness and reliability 
of the toxicity data and the conservative exposure assessment, there is 
a reasonable certainty that no harm will result to infants and children 
from aggregate exposure to the residues of carfentrazone-ethyl 
including all anticipated dietary exposure.

G. International Tolerances

    There are no Codex Alimentarius Commission (Codex) Maximum Residue 
Levels (MRLs) for carfentrazone-ethyl on any crops at this time. 
However, MRLs for small grains in Europe have been proposed which 
consist of carfentrazone-ethyl and carfentrazone-ethyl-chloropropionic 
acid.
[FR Doc. 98-15177 Filed 6-9-98; 8:45 am]
BILLING CODE 6560-50-F


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