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canola oil Pesticide Petition Filing 12/97



[Federal Register: December 17, 1997 (Volume 62, Number 242)]
[Notices]               
[Page 66083-66091]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr17de97-73]

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ENVIRONMENTAL PROTECTION AGENCY

[PF-782; FRL-5759-1]

 
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-782, must 
be received on or before January 16, 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. 1132, CM #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Comments and data may also be submitted electronically to: opp-
docket@epamail.epa.gov. 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. 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: The product manager listed in the 
table below:

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                                   Office location/                     
        Product Manager            telephone number          Address    
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Joanne Miller (PM 23).........  Rm. 237, CM #2, 703-    1921 Jefferson  
                                 305-6224, e-mail:       Davis Hwy,     
                                 miller.joanne@epamail   Arlington, VA  
                                 .epa.gov.                              
James Tompkins (PM 25)........  Rm. 239, CM #2, 703-    Do.             
                                 305-5697, e-mail:                      
                                 tompkins.james@epamai                  
                                 l.epa.gov.                             
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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-782] (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:
    opp-docket@epamail.epa.gov


    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-782] 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: December 3, 1997.

Peter Caulkins,

Acting 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.


[[Page 66084]]


2. E.I. du Pont de Nemours and Company

PP 1F4032

    EPA has received a pesticide petition (PP 1F4032) from E.I. du Pont 
de Nemours and Company, Barley Mill Plaza, Walker's Mill Bldg. 37, 
Wilmington, DE 19880-0038, proposing

[[Page 66086]]

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 ethametsulfuron in or on the raw agricultural commodity 
canola 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 supports granting of 
the petition. Additional data may be needed before EPA rules on the 
petition.

A. Residue Chemistry

    1. Plant metabolism. The qualitative nature of the residues of 
ethametsulfuron methyl is adequately understood. The unmetabolized 
parent compound was the major residue found in a canola metabolism 
study up to 30 days after application. The principal route of metabolic 
breakdown of ethametsulfuron methyl in canola is dealkylation from the 
triazine ring. The initial step in the metabolic breakdown is 
deethylation to form O-deethyl ethametsulfuron methyl. Further 
metabolism forms N-demethyl-O-deethyl ethametsulfuron methyl and more 
minor polar metabolites. For purposes of establishing the proposed 
tolerance, the parent compound ethametsulfuron methyl is the only 
residue of concern.
    The available metabolism studies indicate that total radioactive 
residues found in mature seeds, when rapeseed was treated at a rate 
equivalent to the proposed application rate, ranged from 0.008 to 0.012 
ppm. These terminal residues may consist of the parent compound, O-
deethyl ethametsulfuron methyl, O-deethyl-N-demethyl ethametsulfuron 
methyl and other minor metabolites.
    2. Analytical method. Analytical methods are available to measure 
the parent compound in oil seeds, and in oil seed processing fractions. 
The quantification of ethametsulfuron methyl is by normal phase high 
performance liquid chromatography (HPLC) using a photoconductivity 
detector. The Limit of Quantitation (LOQ) for the analytical method is 
0.02 ppm.
    3. Magnitude of residues--i. Magnitude of the residue in plants.  
The results of the seed analyses from canola/seed show that no 
detectable residues of ethametsulfuron methyl were found in canola/seed 
harvested 60 to 137 days after treatment at exaggerated rates of 3X of 
the normal application rate.
    ii. Magnitude of the residue in processed commodities. Analyses of 
canola processed fractions (whole seed, pressed cake, desolventized 
meal, crude oil, pressed oil, solvent extracted oil, degummed oil, 
refined washed oil, refined bleached oil, and deodorized oil) show that 
levels of ethametsulfuron methyl were found to be less than 0.02 ppm, 
the limit of quantitation of the method in all of the fractions 
evaluated. All of the processed fractions were obtained from seed 
harvested 92 days after application at proposed use rates and 
exaggerated rates.

B. Toxicological Profile

    1. Acute toxicity. Based on EPA criteria, ethametsulfuron methyl is 
relatively non-toxic, and be categorized as Toxicity Category IV (oral 
and inhalation routes) and Category III (dermal exposure). 
LD50s are >5,000 mg/kg for acute oral toxicity in rats, 
>2,000 mg/kg for acute dermal toxicity in rabbits, and >5.7 mg/L for 
acute inhalation toxicity in rats. For technical grade active 
ingredient, primary eye irritation in rabbits is classified as Tox Cat 
II. For formulated product, primary eye irritation in rabbits is 
classified as Tox Cat IV. Primary dermal irritation in rabbits is 
classified as Tox Cat IV. Dermal sensitization in guinea pigs is 
classified as ``Not a skin sensitizer.''
    2. Genotoxicity. This compound was negative in the following tests 
that have been conducted to determine the genotoxic and mutagenic 
potential of ethametsulfuron methyl: Mutagenicity assays conducted in 
bacteria (Ames test) and in cultured Chinese Hamster Ovary cells; a 
test that measures the induction of chromosomal aberrations in bone 
marrow cells isolated from rats treated with ethametsulfuron methyl; 
micronuclei induction in bone marrow cells from mice; and negative in a 
text that measures DNA damage in cultured rat liver cells. Based on the 
weight of these data, E.I du Pont concludes that ethametsulfuron methyl 
is neither genotoxic or mutagenic.
    3. Reproductive and developmental toxicity. A 2-generation, four 
litter reproduction study with CD rats treated with dietary levels of 
0, 250, 5,000, 20,000 ppm of ethametsulfuron methyl failed to reveal 
any evidence suggestive of an adverse effect on reproductive potential. 
A NOEL was indicated at the mid dose level of 5,000 ppm (equivalent to 
approx. 433 mg/kg b.w./day, actual intake) based on significantly 
(p<0.5) decreased body weights in the high dose treated F0 and F1 
generation males.
    A developmental toxicity study of ethametsulfuron methyl in rabbits 
indicated that dams administered 4,000 mg/kg (highest dose tested) had 
a higher mortality rate, lower food consumption and body weight gains, 
increased incidences of gross clinical signs of toxicity and of 
abortions, and increased absolute and relative liver weights. Absolute 
and relative liver weights were also slightly greater for dams 
administered 1,000 mg/kg. There were no compound-related effects 
observed for dams administered 250 mg/kg.
    Dams administered 4,000 mg/kg also had a decrease in the number of 
live fetuses. This was related to an increase in the number of early 
resorptions. There were no other compound-related effects on the dams, 
nor were there any effects on fetal weights, malformations or 
variations incidences. The NOELs for this study were 250 mg/kg for the 
dams and 1,000 mg/kg for the fetus. Ethametsulfuron methyl was neither 
teratogenic in rabbits nor uniquely toxic to the conceptus.
    A developmental toxicity study was also conducted in rats treated 
at doses of 0, 60, 250, 1,000, or 4,000 mg/kg. Among the dams of the 
groups given ethametsulfuron methyl, no compound-related mortality or 
clinical abnormalities were observed. For the treatment period, the 
high dose group had a lower weight gain and significantly decreased 
food consumption compared to the control group. No other significant 
differences in body weight changes or food consumption were observed. A 
significant trend was indicated for mean fetal weight and the mean 
fetal weight of the high dose group was lower than that of the control 
group. No significant differences were observed in the rates of 
malformations or developmental variations. Under the conditions of the 
study, the apparent no effect level for the dam and fetus was 1,000 mg/
kg/day. Thus ethametsulfuron methyl was not uniquely toxic to the 
conceptus nor was it teratogenic in rats.
    4. Subchronic toxicity--i. Rat. A 90-day feeding study followed by 
a 1-generation reproduction phase in rats at dietary levels of 0, 100, 
1,000, and 5,000 ppm of ethametsulfuron methyl failed to elicit any 
signs of overt toxicity or any adverse effect on reproductive 
performance at levels as high as 5,000 ppm (equivalent to 0.5% of the 
diet or approximately 409 mg/kg b.w./day, actual intake). The No 
Observed Adverse Effect Level (NOAEL) for this study was, therefore, 
the high dose level of 5,000 ppm.
    ii. Mouse. A 90-day dietary feeding study in CD-1 mice at levels of 
0, 50, 500, 2,500 and 5,000 ppm indicated a No Observed Effect Level 
(NOEL) for females and a NOAEL for males set at

[[Page 66087]]

the high dose level of 5,000 ppm (equivalent to approximate 687 mg/kg 
b.w./day, actual intake for males).
    iii. Dog. Dietary administration of technical ethametsulfuron 
methyl to dogs for 90 days at levels of 0, 100, 3,500 or 10,000 ppm 
failed to reveal any evidence of treatment-related toxicity at levels 
as high as 10,000 ppm (equivalent to 1% of the diet or approximately 
386 mg/kg b.w./day, based on actual intake).
    5. Chronic toxicity--i. Rat. Administration of ethametsulfuron 
methyl to Sprague-Dawley rats for up to 24 months at dietary levels of 
0, 50, 500 and 5,000 ppm revealed a NOAEL for in-life parameters of 
5,000 ppm (equivalent to 238.5 mg/kg b.w./day, actual intake), based on 
questionable toxicological significance of decreased (p<0.05) serum 
sodium levels in both the 5,000 ppm treated males and females during 
the first 12 months of treatment. The effects on serum sodium levels in 
the high dose groups were described as mild (representing a decrease in 
2-6% of the control values) and occurring in the absence of any 
associated pathological changes in the kidney. Treatment with the test 
material at dietary levels as high as 5,000 ppm (equivalent to 0.5% of 
the diet) failed to elicit any evidence of treatment-related neoplastic 
potential.
    ii. Dogs. Chronic dietary administration of the test material to 
dogs at levels of 0, 250, 3,000 and 15,000 ppm for 1-year indicated a 
NOEL of 3,000 ppm, equivalent to approximately 87 mg/kg b.w./day actual 
intake, based on compound-related effects expressed in the 15,000 ppm 
treated group as decreased body weight gain and food efficiency values 
in the males. Significantly decreased serum sodium levels in both sexes 
at the high dose treated level were not associated with any evidence of 
renal pathology. In the absence of any collaborative clinical or 
pathological findings differences in organ weights relative to body or 
brain weight were considered to be of doubtful biological significance.
    iii. Mouse. Administration of the test material to CD-1 mice at 
dietary levels of 0, 25, 500, and 5,000 ppm for the period of up to 78 
weeks failed to reveal any overt signs of treatment-related toxicity of 
dietary levels of up to 5,000 ppm (equivalent to 818 mg/kg bwt/day, 
actual intake). Although a direct effect of treatment on body weights 
or weight gains could not be established, overall body weight gain in 
the 5,000 ppm treated male mice was depressed (non-significant, p>0.05) 
by 10% when compared to the controls. There was no evidence of any 
treatment-related oncogenic potential.
    6. Animal metabolism. When administered via oral gavage to rats, 
ethametsulfuron methyl was rapidly metabolized and excreted in the 
urine and feces. Within 3 days, greater than 90% of the administered 
dose was excreted by male rats and greater than 80% was excreted by 
females. Approximately 50% of the administered dose was excreted as 
unchanged ethametsulfuron methyl. The remainder was converted 
predominately to N-demethyl ethametsulfuron methyl and O-deethyl 
ethametsulfuron methyl, which are considered by by-products of 
cytochrome P450-mediated reactions. Less than 0.02% of the administered 
dose remained in the carcass or tissues. There was no significant or 
preferential accumulation of ethametsulfuron methyl or its metabolites 
in any tissue. Because of the short excretion half-life, repeated daily 
exposures are not expected to result in significant body burdens of 
ethametsulfuron methyl.
    7. Metabolite toxicology. There is no evidence that the metabolites 
of ethametsulfuron methyl as identified as either the plant or animal 
metabolism studies are of any toxicological significance.
    8. Endocrine effects. No special studies investigating potential 
estrogenic or endocrine effects of ethametsulfuron methyl have been 
conducted. However, the standard battery of required toxicology studies 
have been completed. These 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. Based on these studies there is no evidence to suggest that 
ethametsulfuron methyl has an effect on the endocrine system.

C. Aggregate Exposure

    1. Dietary exposure--i. Food. Based on the residue data and the 
proposed single-crop use, potential for dietary exposure of 
ethametsulfuron methyl from food sources is extremely low. Residue 
studies have shown no residues above the LOQ (residues <0.02 ppm) in 
any canola seed samples evaluated, including the canola oil processed 
fractions. No dietary exposure is anticipated from secondary residues 
in meat or milk. Although canola meal is considered a minor feedstuff 
for cattle and poultry (representing a maximum of 15% of an animal's 
diet), field residue studies showed ethametsulfuron methyl residues 
were all below the LOQ (<0.02 ppm) in all of the canola RACs and 
processed fractions, including meal, even when the crop was treated at 
2-3X the proposed maximum use rate.
    Direct human consumption of canola as a food commodity in the 
United States is extremely low. Canola is a minor crop in the U.S., and 
the only canola fraction used as a food product is the refined canola 
oil. A dietary risk evaluation (DRES) was conducted to determine the 
theoretical maximum residue contribution of ethametsulfuron methyl in 
the diet as a result of agricultural use on canola. Unfortunately, 
consumption data for canola oil does not exist in the 1977-1979 food 
consumption database used in EPA's DRES system, since at that time, 
canola oil was not a significant part of the U.S. diet. Since 1977 more 
canola oil is used in U.S. homes, although total production and usage 
are still minor when compared to other edible oils such as soybean oil.
    Conservative assumptions were used to estimate canola consumption 
in the United States. The USDA's Oilseed Analysis Division has 
indicated that an average of 1.1 billion pounds of canola oil was used 
in the United States annually over the past 5 years. The dietary 
exposures that might occur by way of canola oil consumption can be 
estimated by taking the average annual use of canola oil in the United 
States (includes both domestically produced and imported canola oils) 
and dividing it by the approximate US population of 266.3 million 
people. This provides a per-capita consumption estimate for the general 
population. Using this approach, total canola oil consumption on a 
grams per kg body weight per day was calculated by dividing by the 
average days in a year and average body weight of a person (60 kg). The 
60 kg value is used by the US EPA as part of their ``Food Factor'' 
system, and is also supported by taking the average weight of children 
between the ages of 6 months to 19 years (36 kg) and the average weight 
of adults of 70 kg and assuming a 69 year life span (as proposed in the 
review draft of the US EPA's Exposure Factors Handbook). Using these 
assumptions, canola oil consumption was calculated to be 0.088 g/kg bw/
day.
    While this method provides a useful approximation of canola 
consumption, this is clearly a conservative estimate for risk 
assessment purposes, since this estimate assumes that all of the canola 
oil used in the US is indeed ingested. In reality, not all the oil that 
is used in cooking or deep-fat frying is consumed but instead, is 
discarded or recycled. Another indication that the consumption value of 
0.088 g/kg bw/day is an over-estimate is from the USDA's 1989-1992 food 
survey (not yet included in the EPA's DRES system),

[[Page 66088]]

 which indicates canola oil consumption is 0.00023 g/kg/day for the 
general U.S. population.
    Using the consumption estimate of 0.088 g canola oil/ kg bw/day for 
the general US population, and assuming that 100% of the canola crop is 
treated with ethametsulfuron methyl and all canola consumed contains 
residues at the proposed tolerance level of 0.1 ppm, the theoretical 
maximum residue contribution of ethametsulfuron methyl in the diet is 
calculated to be 0.00001 mg/kg/day or <0.01% of the RfD of 0.87 mg/kg/
day.
    ii. Drinking water. Another potential source of dietary exposure to 
pesticides are residues in drinking water. There is no established 
Maximum Concentration Level (MCL) for ethametsulfuron methyl in water. 
Based on the low use rate of ethametsulfuron methyl, and a use pattern 
that is not widespread (since the only proposed use is on a minor 
crop), DuPont does not anticipate residues of ethametsulfuron in 
drinking water and exposure from this route is unlikely.
    2. Non-dietary exposure. Ethametsulfuron methyl is not registered 
for any use which could result in non-occupational, non-dietary 
exposure to the general population. Ethametsulfuron methyl is a 
herbicide with proposed use only on canola. There are no other food 
uses, nor are there any residential or non-crop uses of this active 
ingredient. Therefore, the only potential for non-occupational 
aggregate exposure would come from dietary intake.

D. Cumulative Effects

    Ethametsulfuron methyl belongs to the sulfonylurea class of 
compounds. Other compounds in this class are registered herbicides. 
However, the herbicidal activity of the sulfonylureas is due to the 
inhibition of acetolactase synthase (ALS), an enzyme only found in 
plants. ALS is part of the biosynthetic pathway leading to the 
formation of branched chain amino acids. Animals lack ALS and this 
biosynthetic pathway. This lack of ALS contributes to the low toxicity 
of the sulfonylurea compounds in animals. There is no evidence to 
indicate or suggest that ethametsulfuron methyl has any toxic effects 
on mammals that would be cumulative with those of any other chemicals.

E. Safety Determination

    1. U.S. population. Using the conservative exposure assumptions 
described above and based on the most sensitive species chronic NOEL of 
87 mg/kg and a Reference Dose (RfD) of 0.87 mg/kg/day, the proposed use 
of ethametsulfuron methyl on canola is expected to utilize 0.001% of 
the RfD for the general U.S. population. Generally, exposures below 100 
percent of the RfD are of no concern because the RfD represents the 
level at or below which daily aggregate dietary exposure over a 
lifetime will not pose risk to human health. Thus, DuPont concludes 
that there is a reasonable certainty that no harm will result from 
aggregate exposure to ethametsulfuron methyl resulting from proposed 
agricultural use on canola.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of ethametsulfuron 
methyl, data were considered from developmental toxicity studies in the 
rat and rabbit, and a multi-generation reproduction study in rats. The 
developmental toxicity studies demonstrated that even at the high oral 
doses used in these studies (up to 4,000 mg/kg in rabbits and rats), no 
teratogenic effects were found in either species nor was the compound 
found to be uniquely toxic to the conceptus.
    The 2-generation reproduction study in rats treated at dietary 
levels as high as 20,000 ppm on a daily basis throughout 2 generations 
(equivalent to 1,582 mg/kg/day for males and 1817 mg/kg/day for 
females), showed no evidence of effects on reproductive performance in 
the adults, or evidence of gross or histopathological effects in the 
adult or weanling rats in any test group. This study indicates that 
ethametsulfuron methyl is not a reproductive toxicant.
    As mentioned previously, canola oil is a very minor component of 
the diet, and thus had not been included as part of the 1977-79 food 
survey used in EPA's DRES system. DuPont is not aware of specific food 
survey data concerning consumption of canola oil by infants and 
children. However, the 1977-79 food survey database does provide 
consumption data for other edible oils for each of the population 
subgroups, including infants and children. This data indicate that non-
nursing infants consume more soybean and coconut oil than any of the 
other 22 population subgroups, specifically consuming 4.2 times more 
soybean oil and 49.1 times more coconut oil than the consumption by the 
general US population. The data also show that children 1-6 consume 
more corn, cottonseed, peanut and sunflower oil than any other subgroup 
listed, to a maximum of 2 times more than the general U.S. population. 
Using these data and making the most conservative assumption to 
extrapolate to canola oil, we can estimate that infants and children 
consume 49 times more canola oil than does the U.S. population, and 
calculate an approximate daily consumption of 4.3 g canola oil/kg body 
weight. If we use the additional conservative assumptions that all the 
canola oil consumed contains ethametsulfuron methyl residues at 
tolerance levels of 0.1 ppm, we calculate that the maximum theoretical 
residue concentration of ethametsulfuron methyl in the infants' and 
children's diets would be 0.00049 mg/kg/day or <0.05% of the RfD.
    As indicated above, DuPont concludes that infants and children have 
a low potential for ethametsulfuron methyl exposure because of both the 
low level of canola oil in the diet, and the absence of detectable 
residues in field-treated canola. The toxicology profile of 
ethametsulfuron methyl demonstrates low mammalian toxicity, and results 
from the developmental and reproduction studies indicate that there is 
no additional sensitivity for infants and children. Therefore, DuPont 
concludes that an additional safety (uncertainty) factor is not 
warranted and the RfD of 0.87 mg/kg body weight/day, which utilizes a 
100-fold safety factor, is appropriate to assure a reasonable certainty 
of no harm to infants and children from aggregate exposure to 
ethametsulfuron methyl.

F. International Tolerances

    Ethametsulfuron methyl and its end-use product Muster are 
registered only in Canada on canola/rape and mustard with a MRL value 
of 0.1 ppm. A CODEX tolerance for ethametsulfuron methyl has not been 
established. (Jim Tompkins)


[FR Doc. 97-32936 Filed 12-16-97; 8:45 am]
BILLING CODE 6560-50-F