PMEP Home Page --> Pesticide Active Ingredient Information --> Herbicides, Growth Regulators and Desiccant --> 1-naphthaleneacetic acid to rimsulfuron --> quizalofop-p-ethyl (Assure, Super) --> quizalofop-p-ethyl (Assure, Super) Pesticide Petition Filing 12/97

quizalofop-p-ethyl (Assure, Super) Pesticide Petition Filing 12/97



[Notices]               
[Page 66077-66083]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr17de97-72]

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

ENVIRONMENTAL PROTECTION AGENCY

[PF-781; FRL-5758-3]

 
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-781, must 
be received on or before January 16, 1998.
ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch, Information Resources and Services Division 
(7502C), 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:

------------------------------------------------------------------------
                                   Office location/                     
        Product Manager            telephone number          Address    
------------------------------------------------------------------------
James Tompkins (PM 25)........  Rm. 265, CM #2, 703-    1921 Jefferson  
                                 305-7801, e-            Davis Hwy,     
                                 mail:tompkins.james@e   Arlington, VA  
                                 pamail.epa.gov.                        
Elizabeth Haeberer............  Rm. 207, CM #2, 703-    Do.             
                                 308-2891, e-mail:                      
                                 haeberer.elizabeth@ep                  
                                 amail.epa.gov.                         
------------------------------------------------------------------------

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-781]

[[Page 66078]]

(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 file format or ASCII 
file format. All comments and data in electronic form must be 
identified by the docket number PF-781 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: December 4, 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.


2. E. I. Du Pont de Nemours & Company

PP 5F4545

    EPA has received a pesticide petition (PP 5F4545) from E. I. Du 
Pont de Nemours & Company (DuPont), P.O. Box 80038, Wilmington, DE 
19880-0038. 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 to 
establish an exemption from the requirement of a tolerance for 
quizalofop (2-[4-(6-chloroquinoxalin-2-yl)oxy) phenoxy]) - propanoic 
acid], and quizalofop ethyl [ethyl-2- [4-(6-chloroquinoaxalin-2-yl)oxy) 
phenoxy) propanoat in or on the raw agricultural commodities canola 
seed and canola meal . The proposed analytical method involves 
homogenization, filtration, partition and cleanup with analysis by high 
performance liquid chromatography using UV detection. 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. Quizalofop-p ethyl ester is metabolized by 
cleavage at three sites as follows:
    (i) Primary pathway is hydrolysis of the ethyl ester to form the 
quizalofop-p acid, then (ii) Cleavage of the enol ether linkage in the 
acid, between the phenyl and quinoxalinyl rings, to form phenols, and 
(iii) Cleavage of the ether linkage between the isopropanic group and 
the phenyl ring to form a phenol.
    The plant metabolism data show that quizalofop-p ethyl ester does 
not translocate, but is rapidly hydrolyzed to the corresponding acid; 
then the phenols conjugate with the plant sugars. Metabolism studies in 
soybeans using the racemic mixture quizalofop ethyl ester and the 
resolved D+ isomer show nearly identical pathways.
    The nature of the quizalofop-p ethyl ester residue in plants is 
adequately understood. The residues of concern are quizalofop-p ethyl 
ester and its acid metabolite, quizalofop-p, and the S enantiomers of 
both the ester and the acid, all expressed as quizalofop-p ethyl ester.
    2. Analytical method. An adequate analytical methodology (high-
pressure liquid chromatography using either ultraviolet or fluorescence 
detection) is available for enforcement purposes in Vol. II of the Food 
and Drug Administration Pesticide Analytical Method (PAM II, Method I).
    Adequately validated residue analytical methods, LAN-1 and LAN-3, 
were used to gather the magnitude of the quizalofop-p, its acid 
metabolite, phenols 1, 2, and 4, residue data on canola and canola 
processed commodities.
    3. Magnitude of residues. Dupont proposes establishing tolerances 
for the combined residues of quizalofop (2-[4-(6-chloroquinoaxalin-2-
yl)oxy) phenoxy])-propionic acid], and quizalofop ethyl [ethyl-2- [4-
(6-chloroquinoxalin-2-yl)oxy) phenoxy) propanoat for the raw 
agricultural commodities canola seed at 1.0 parts per million (ppm) and 
canola meal at 1.5 ppm.

B. Toxicological Profile

    1. Acute toxicity. Several acute toxicology studies were conducted 
and the overall results placed technical grade quizalofop ethyl in 
toxicity Category III. These include the following studies in Category 
III: acute oral toxicity (LD50s 1,480 and 1,670 for female 
and male rats, respectively) and eye irritation (mild effects; 
reversible within 4-days). Dermal toxicity (LD50 > 5,000 mg/
kg; rabbit), inhalation toxicity (LC50 > 5.8 mg/L; rat) and 
dermal irritation were classified within Category IV. Technical 
quizalofop ethyl was not a dermal sensitizer.
    2. Genotoxicty. Technical quizalofop ethyl was negative in the 
following genotoxicity tests: bacterial gene mutation assays with E. 
coli and S. typhimurium; gene mutation assays in Chinese hamster 
ovary(CHO) cells ; in vitro DNA damage assays with B. subtillis and in 
rat hepatocytes; and an in vitro chromosomal aberration test in CHO 
cells.
    3. Reproductive and developmental toxicity. Studies supporting the 
registration include: A developmental toxicity study in rats 
administered dosage levels of 0, 30, 100, and 300 milligrams/kilogram/
day (mg/kg/day) highest dose tested (HDT). The maternal toxicity no-
observed effect level (NOEL) was 30 mg/kg/day and a developmental 
toxicity NOEL was greater than 300 mg/kg/day (HDT). The maternal NOEL 
was based on reduced food consumption and increased liver weights. A 
developmental toxicity study in rabbits administered dosage levels of 
0, 7, 20, and 60 mg/kg/day with no developmental effects noted at 60 
mg/kg/day (HDT). The maternal toxicity NOEL was 20 mg/kg/day based on 
decreases in food consumption and body weight gain at 60/mg/kg/day 
(HDT). A 2-generation reproduction study in rats fed diets containing 
0, 25, 100 or 400 ppm (or approximately 1, 1.25, 5, and 20 mg/kg/day, 
respectively) with a developmental (systemic effects) NOEL of 1.25 mg/
kg/day for F2B weanlings based on increased liver weights 
and increased incidence of eosinophilic changes in the livers at 5.0 
mg/kg/day. These liver changes were considered to be physiological or 
adaptive changes to compound exposure among weanlings. When access to 
the mother's feed is available, it is a common observation that young 
rats will begin consuming chow prior to complete weaning at 21-days of 
age. Consumption could not be quantified; therefore, the maternal 
consumption was assumed as the NOEL (if normalized on a body weight 
basis, exposures to the weanling rats were likely higher). The parental 
NOEL of 5.0 mg/kg/day was based on decreased body weight and premating 
weight gain in males at 20 mg/kg/day (HDT).
    4. Subchronic toxicity. A 90-day study was conducted in rats fed 
diets containing 0, 40, 128, 1,280 ppm (or approximately 0, 2, 6.4 and 
64 mg/kg/day, respectively). The NOEL was 2 mg/kg/day. This was based 
on increased liver weights at 6.4 mg/kg. A 90-day feeding study in mice 
was conducted with diets that contained 0, 100, 316 or 1,000 ppm (or 
approximately 0, 15, 47.4, and 150 mg/kg/day, respectively). The NOEL 
was > 15 mg/kg/day lowest dose tested (LDT) based on increased liver 
weights and reversible histopathological effects in the liver at the 
LDT. A 6-month feeding study in dogs was conducted with diets that 
contained 0, 25, 100 or 400 ppm (or approximately 0, 0.625, 2.5, and 10 
mg/kg/day, respectively). The NOEL was 2.5 mg/kg/day based on increased 
blood urea nitrogen at 10 mg/kg/day. A 21-day dermal study was 
conducted in rabbits at doses of 0, 125, 500 or 2,000 mg/kg/day. The 
NOEL was 2,000 mg/kg/day (HDT).
    5. Chronic toxicity. An 18-month carcinogenicity study was 
conducted in CD-1 mice fed diets containing 0, 2, 10, 80 or 320 ppm (or 
approximately 0, 0.3, 1.5, 12, and 48 mg/kg/day, respectively). There 
were no carcinogenic effects observed under the conditions of the study 
at levels up to and including 12 mg/kg/day. A marginal increase in the 
incidence of hepatocellular tumors was observed at 48 mg/kg/day, the 
(HDT) which exceeded the maximum tolerated

[[Page 66081]]

dose (MTD). (Please see the discussion by the EPA HED Carcinogenicity 
Peer Review Committee.)
    A 2-year chronic toxicity/carcinogenicity study was conducted in 
rats fed diets containing 0, 25, 100 or 400 ppm (or 0, 0.9, 3.7, and 
15.5 mg/kg/day for males and 0, 1.1, 4.6, and 18.6 mg/kg/day for 
females, respectively). There were no carcinogenic effects observed 
under the conditions of the study at levels up to and including 18.6 g/
kg/day (HDT). The systemic NOEL was 0.9 mg/kg/day based on altered red 
cell parameters and slight/minimal centrilobuler enlargement of the 
liver at 3.7 mg/kg/day.
    A 1-year feeding study was conducted in dogs fed diets containing 
0, 25, 100 or 400 ppm (or approximately 0, 0.625, 2.5, and 10 mg/kg/
day, respectively). The NOEL was 10 mg/kg/day (HDT).
    The Carcinogenicity Peer Review Committee (CPRC) of HED has 
evaluated the rat and mouse cancer studies on quizalofop along with 
other relevant short-term toxicity studies, mutagenicity studies, and 
structure activity relationships. The CPRC concluded, after three 
meetings and an evaluation by the OPP Science Advisory panel, that the 
classification should be a Category D (not classifiable as to human 
cancer potential). No new cancer studies were required.
    The first CPRC review tentatively concluded that quizalofop should 
be classified as a Category B2 (probable human carcinogen). That 
classification was based on liver tumors in female rats, ovarian tumors 
in female mice, and liver tumors in male mice. This classification was 
downgraded to a Category C (possible human carcinogen) at a second CPRC 
review. The change in classification was due to a reexamination of the 
liver tumors in female rats and ovarian tumors in female mice. The 
first peer review had found a statistically significant positive trend 
for liver carcinomas in female rats. Subsequent to this conclusion the 
tumor data was reevaluated, and the revaluation showed a reduced number 
of carcinomas. Although there remained a statistically significant 
positive trend for carcinomas in the study, the CPRC concluded that the 
carcinomas were not biologically significant given the few carcinomas 
identified (one at the mid-dose and two at the high dose). Noting that 
this level of carcinomas was within historical levels, the CPRC 
concluded that administration of quizalofop did not appear to be 
associated with the liver carcinomas.
    As to the ovarian tumors in female mice, the CPRC had first 
attached importance to the fact that these tumors were statistically 
significant at the high dose as compared to historical control values 
although statistically significant when compared to concurrent 
controls. However, review of further historical control data showed 
that the level of ovarian tumors in the quizalofop study was similar to 
the background rate in several other studies. Given this information 
and that the quizalofop study showed no hyperplasia of the ovary, no 
signs of endocrine activity related to ovarian function, and no dose 
response relationship, the CPRC concluded that the ovarian tumors were 
probably not compound-related.
    The findings of the second CPRC review were presented to EPA's 
Scientific Advisory Panel (SAP). The SAP concurred with the CPRC 
conclusion that the liver tumors in female rats and the ovary tumors in 
female mice showed no evidence of carcinogenicity. However, the SAP 
disagreed with CPRC's classification of quizalofop as a Category C 
based on the liver tumors in male mice. The SAP concluded that the 
mouse liver tumors did not support such a classification because the 
tumors occurred at a dose above the MTD and because they were not 
statistically significant if a ``p'' value of less than 0.05. The SAP 
believed that such greater statistical rigor was appropriate for 
variable tumor endpoints such as male mouse liver tumors.
    Following the SAP review, the CPRC changed the classification for 
quizalofop to Category D. The Category D classification is based on an 
approximate doubling in the incidence of male mice liver tumors between 
controls an the high dose. This finding was not considered strong 
enough to warrant the finding of a Category C (possible human 
carcinogen) since the increase was of marginal statistical 
significance, occurred at a high dose which exceeded the predicted MTD, 
and occurred in a study in which the concurrent control for liver 
tumors was somewhat low as compared to the historical controls, while 
the high dose control group was at the upper end of previous historical 
control-groups.
    EPA has found the evidence on the carcinogenicity of quizalofop-p 
ethyl ester in animals to be equivocal and therefore concludes that 
quizalofop-p ethyl ester does not induce cancer in animals within the 
meaning of the Delaney clause. Important to this conclusion was the 
following evidence: (1) The only statistically significant tumor 
response that appears compound-related was seen at a single dose in a 
single sex in a single species; (2) the response was only marginally 
statistically significant; (3) the response was only significant when 
benign and malignant tumors were combined; (4) the tumors were in the 
male mouse liver; (5) the tumors were within historical controls; and 
(6) the mutagenicity studies were negative. Although in some 
circumstances a finding of animal carcinogenicity would be made despite 
any one, or even several, of the six factors noted, the combination of 
all of these factors here cast sufficient doubt on the reproducibility 
of the response in the high dose male mouse that EPA concludes the 
evidence on carcinogenicity is equivocal.
    6. Animal metabolism. The metabolism of quizalofop ethyl in animals 
(rat, goat and poultry) is well understood. 14C-phenyl and 
14C-quinoxaline quizalofop ethyl ester metabolism studies 
have been conducted in each species. There are similarities among these 
species with respect to metabolism. Quizalofop ethyl is rapidly and 
extensively metabolized and rapidly excreted by rats. The principal 
metabolites were the quizalofop-p acid and two dechlorinated 
hydroxylated forms of the acid. Tissue residues were minimal and there 
was no evidence of accumulation of quizalofop ethyl or its metabolites 
in the rat.
    The primary pathway in ruminants is hydrolysis of the ethyl ester 
to form the quizalofop-p methyl ester. In poultry, the primary 
metabolic pathway is also the hydrolysis of the ethyl ester to form the 
quizalofop-p acid, then the methyl esterification to form the 
quizalofop methyl ester becomes a minor pathway.
    The nature of the quizalofop ethyl ester residue in livestock is 
adequately understood. The residues of concern are quizalofop ethyl, 
quizalofop methyl, and quizalofop, all expressed as quizalofop ethyl.
    7. Metabolite toxicology. There is no evidence that the metabolites 
of quizalofop ethyl as identified as either the plant or animal 
metabolism studies are of any toxicological significance.

C. Aggregate Exposure

    1. Dietary exposure. Quizalofop ethyl is a herbicide with proposed 
use on canola. The only potential for non-occupational aggregate 
exposure would come from dietary intake.
    An analysis of chronic dietary risk was conducted to determine the 
impact of the possible addition of canola to the Assure label. A 
Reference Dose (RfD) of 0.009 mg/kg/day was used in the analyses. 
Consumption data for canola

[[Page 66082]]

had to be estimated using various production and usage statistics.
    2. Food. The first step in the analysis was to run the TAS 
(Tolerance Assessment System) program using current tolerances with an 
RfD of 0.009 mg/kg/day. The Theoretical Maximum Residue Concentration 
(TMRC), based on the current tolerances, was 0.000288 mg/kg/day for the 
U.S. population (48 states) and 0.000759 mg/kg/day for the population 
subgroup with the highest estimated exposure (non-nursing infants > 1-
yr. old). For the U.S. population subgroup this represents 
approximately 3.2% of the RfD while for the most exposed population 
this represents approximately 8.4% of the RfD. Based on the risk 
estimates arrived at in this analysis, chronic dietary risk from the 
current uses of Assure is minimal.
    Unfortunately the 1977-1979 food consumption database does not 
contain any consumption data for canola oil. At the time the survey was 
conducted, 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 as compared to soybean oil. 
Conservative assumptions were used to estimate canola consumption in 
the U.S. The USDA's Oilseed Analysis Division indicated that an average 
of 1.1 billion pounds of canola oil was used in the U.S. annually over 
the past 5-years. The dietary exposures that might occur by way of 
consumption of canola oil can be estimated by taking the average annual 
consumption of canola oil in the U.S. (includes both domestically 
produced and imported canola oils) and dividing it by the approximate 
U.S. population of 266.3 million people. This gives a per-capita 
consumption estimate for the general population. To calculate exposure, 
this number is divided by the average number of days in a year and the 
average body weight of a person (60 kg). (This weight is the same that 
was used by EPA as part of their ``Food Factor'' system that predated 
the current Tolerance Assessment System). This value 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 (70 kg), and 
assuming that an average person lives to be 69-years old (Review Draft 
of the Exposure Factors Handbook, U.S. EPA). Using these assumptions, 
canola oil consumption was calculated to be 0.088 g/kg bw/day.
    While this method provides a useful estimate of exposure, it is 
clearly a conservative estimate for risk assessment purposes, since 
this estimate assumes that all the canola oil used in the U.S. is 
indeed ingested. In reality some percentage of any commodity is lost 
between production and consumption. In addition, oil may be used in 
cooking activities such as deep-fat frying where most of the oil is not 
actually eaten but is discarded or recycled. With the understanding 
that the dietary analysis will be very conservative, the consumption 
data for canola used in the DRES analysis for all population subgroups 
was set at 0.088 g/kg bw/day. This was done by entering a consumption 
estimate of 0.088 for ``rapeseed'' for all population subgroups (there 
is no agricultural commodity in TAS for canola oil).
    When a tolerance for canola (1.0 ppm) was added to the current 
tolerances, the TMRC was 0.000376 mg/kg/day for the U.S. population (48 
states) and 0.000847 mg/kg/day for the highest population subgroup 
(non-nursing infants >1-yrs. old). When expressed as a percentage of 
the RfD, the U.S. population (48 states) was approximately 4.2% and the 
highest population subgroup was approximately 9.4%. These results 
indicate that predicted chronic exposure after the addition of a canola 
tolerance is well below the RfD even with the conservative (high) 
nature of the assumptions that were made in calculating consumption.
    3. Drinking water. Another potential source of dietary exposure to 
pesticides is residues in drinking water. There is no established 
Maximum Concentration Level (MCL) for quizalofop ethyl in water. Based 
on the low use rate of quizalofop ethyl, and a use pattern that is not 
widespread (since the current and proposed uses are on minor crops), 
DuPont does not anticipate residues of quizalofop in drinking water and 
exposure from this route is unlikely.
    4. Non-dietary exposure. Quizalofop ethyl is not registered for any 
use which could result in non-occupational, non-dietary exposure to the 
general population.

D. Cumulative Effects

    There is no evidence to indicate or suggest that quizalofop p-ethyl 
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 
0.9 mg/kg and a reference dose (RfD) of 0.009 mg/kg/day, the existing 
tolerances and proposed use of quizalofop ethyl on canola are expected 
to utilize 4.2% of the RfD for the general U.S. population. Generally, 
exposures below 100% 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, there is a 
reasonable certainty that no harm will result from aggregate exposure 
to quizalofop ethyl 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 quizalofop ethyl, 
data were considered from developmental toxicity studies in the rat and 
rabbit, and a multi-generation reproduction study in rats. There were 
no developmental effects observed in the absence of maternal toxicity 
in the rat and rabbit developmental studies. Minimal adaptive or 
physiological effects were observed in livers of weanlings in the 2-
generation rat reproduction study described earlier. However, this 
effect was only observed at a dose that far exceeds any expected human 
exposure. Further, the NOEL of 0.9 mg/kg/day from the 2-year rat study 
with quizalofop ethyl which was used to calculate the RfD (discussed 
above), is already lower than any of the NOEL's defined in the 
developmental and reproductive toxicity studies with quizalofop ethyl.
    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 indicates 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 U.S. 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 this 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 grams canola oil/kg 
body weight. If we use the additional conservative assumptions that all 
the canola oil consumed contains

[[Page 66083]]

quizalofop ethyl residues at tolerance levels of 1.0 ppm, we calculate 
that the TMRC in the infants' and children's diets would be 0.000847 
mg/kg/day or 9.4% of the RfD.
    As indicated above, infants and children have a low potential for 
quizalofop ethyl exposure because of both the low levels of canola oil 
in the diet, and the absence of detectable residues in field-treated 
canola. The toxicology profile of quizalofop ethyl demonstrates low 
mammalian toxicity. Because there was no evidence that offspring were 
uniquely susceptible to the toxic effects of quizalofop ethyl, an 
additional 10-fold uncertainty factor should not be required to protect 
infants and children. Therefore, the RfD of 0.009 mg/kg/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 quizalofop ethyl.

F. International Tolerances

    Harmonization of Tolerances: Since there are no Mexican or Codex 
MRLs/tolerances, compatibility is not a problem at this time. 
Compatibility cannot be achieved with the Canadian negligible residue 
type limit at 0.1 ppm at the USA use pattern, which had findings of 
real residues above 0.1 ppm.                    (James Tompkins)

[FR Doc. 97-32935 Filed 12-16-97; 8:45 am]
BILLING CODE 6560-50-F