Document ID: EPA-HQ-OPP-2012-0520-0003
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2012-09-28T04:00Z

COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE  
                                                          (8/7/2007)

EPA Registration Division contact: [Erin Malone, (703) 347-0253; PM Team 20 Fungicide Branch]

Dow AgroSciences

Petition # 2F8034

	EPA has received a pesticide petition (2F8034) from Dow AgroSciences LLC, 9330 Zionsville Road  - Indianapolis, Indiana 46268 proposing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180.381.

   	1. by amending an established tolerance for residues of
   
   fenbuconazole, alpha - [2 - (4 - chlorophenyl) -  ethyl] - alpha - phenyl - 3 - (1H - 1,2,4 - triazole) -  1 - propanenitrile, and its metabolites RH - 9129, cis - 5 - (4 - chlorophenyl) -  dihydro - 3 - phenyl - 3 - (1H - 1,2,4 -  triazole - 1 - ylmethyl) - 2 - 3 H - furanone, and RH - 9130, trans - 5 - (4 -  chlorophenyl)-dihydro - 3 - phenyl - 3 -  (1H - 1,2,4 - triazole - 1 - ylmethyl) - 2 - 3 H -  furanone  in or on the raw agricultural commodity pepper at 1.0 ppm. EPA has determined that the petition contains data or information regarding the elements set forth in section 408 (d)(2) of the FDDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data supports granting of the petition.

A. Residue Chemistry

	1. Plant metabolism  [The qualitative nature of fenbuconazole residues in plants is adequately understood based on acceptable metabolism studies on wheat, peaches, sugarbeets and peanuts.  The metabolism of fenbuconazole was qualitatively similar in all crops and proceeded via three pathways.  Based on these metabolism studies, the residue of concern for dietary exposure and tolerance setting purposes in pepper is the combined residues of the parent compound, fenbuconazole and its metabolites, RH-9129 and RH-9130 [cis and trans-5-(4-chlorophenyl)-dihydro-3-phenyl-3-(1H-1,2,4-triazole-1-ylmethyl)-2-3H-furanone)].  The total residue is expressed as fenbuconazole.] 

	2. Analytical method. [Adequate analytical methods are available to enforce the tolerances of fenbuconazole residues in plant commodities.  The analytical methods vary depending on the matrices being analyzed.  These methods had undergone successful independent laboratory validation.

For pepper, samples from the residue trials were analyzed for fenbuconazole (RH-7592) and its lactone metabolites, RH-9129 and RH-9130, using Rohm & Haas analytical method Technical Report Number  34-90-47 or Technical Report Number 34-90-47R.  The method had undergone an independent method validation and was also successfully accepted by EPA with minor modifications suggested by the Agency that included procedure for the standardization of the silica gel and Florisil column clean-up elution pattern (TR-34-90-47R).  The limits of quantitation and detection of the method are 0.01 ug/g and 0.003 ug/g, respectively.]

	3. Magnitude of residues.[The magnitude of residues of fenbuconazole and its two metabolites, RH-9129 and RH-9130, in was determined following four foliar broadcast applications of either ENABLE 2F at 12 fl oz/A or INDAR 75 WSP at 4 oz/A per application, in side-by-side treatments.  The active ingredient in both test substances was fenbuconazole.  Target rates were 0.188 lb ai/A per application with a total treatment rate of 0.752 lb ai/A.  The applications were made with a nominal 10-day retreatment interval, approximately 37, 27, 17 and 7 days prior to harvest.  Application rates ranged from 98% to 104% of the target rate and spray volumes ranged from 30 to 47 gal/A.  Non-ionic surfactant was used for all applications. This study contained six RAC (raw agricultural commodity) trials, including one decline trial to obtain residue data to satisfy EPA regulatory requirements for fenbuconazole.

A total of six trials were conducted.  Residues of fenbuconazole and two metabolites in bell peppers were determined using gas chromatography with a NP-specific detector.  The limit of quantitation (LOQ) of the method was 0.01 ppm and limit of detection (LOD) was 0.003 ppm for each analyte.

Residue data show fenbuconazole residues in bell pepper to be similar when treated with either of the two formulations used in this study.  Fenbuconazole residues, in the individual samples, range from 0.029 to 0.668 ppm (ug/g).  The highest fenbuconazole residues were found in trial A conducted in Alabama where pepper maturity was delayed by weather a month beyond normal growth.  There were no metabolite residues (<0.01 ppm) found in any of the 7-day pepper samples collected.

Average fenbuconazole residues in peppers from the decline trial are calculated.  The difference in residue levels was minimal in bell peppers treated with the two formulations while residues in both treated plots showed fairly rapid degradation for both Enable and Indar formulations, respectively.  Metabolites residues were found only in the 0-day pepper samples in this trial with the highest residue level of 0.017 ppm.] 

B. Toxicological Profile

	1. Acute toxicity.[Fenbuconazole is practically non-toxic after administration by the oral and dermal routes, and was not significantly toxic to rats after a 4 hour inhalation exposure. Fenbuconazole is classified as not irritating to skin and inconsequentially irritating to the eyes. It is not a skin sensitizer.

The toxicological profile and endpoints for fenbuconazole which supports this petition to establish tolerances were previously published in the Federal Register of July 20, 2005 (70 FRL-7702-7).  For acute dietary risk assessments, EPA has established a reference dose (acute RfD) of 0.3 mg/kg/day for females 13-49 years old, the population sub-group of concern.  The aRfD is based on the developmental toxicity study in the rat with a maternal and developmental NOAEL of 30 mg/kg/day and an uncertainty factor of 100.  A decrease in maternal body weight, an increase in post-implantation loss and a significant decrease in the number of live fetuses per dam were observed at the LOAEL of 75 mg/kg/day.  No appropriate endpoint was available for analyzing the acute exposure of the overall U. S. 
population.  

	2. Genotoxicty. [Fenbuconazole was negative (non-mutagenic) in an Ames assay with and without hepatic enzyme activation.  Fenbuconazole was negative in a hypoxanthine guanine phosphoribosyl transferase (HGPRT) gene mutation assay using Chinese hamster ovary (CHO) cells in culture when tested with and without hepatic enzyme activation.  In isolated rat hepatocytes, fenbuconazole did not induce unscheduled DNA synthesis (UDS) or repair.  Fenbuconazole did not produce chromosome effects in rats in vivo.  On the basis of the results from this battery of tests, it is concluded that, fenbuconazole is not mutagenic or genotoxic.]

	3. Reproductive and developmental toxicity. [i. Developmental toxicity in the rat. In the developmental study in rats, the maternal (systemic) no observed adverse effect level (NOAEL) was 30 mg/kg/day based on decreases in body weight and body weight gain at the lowest observed adverse effect level (LOAEL) of 75 mg/kg/day.  The developmental (fetal) NOAEL was 30 mg/kg/day based on an increase in post implantation loss and a significant decrease in the number of live fetuses per dam at the LOAEL of 75 mg/kg/day.  
    ii. Developmental toxicity in the rabbit. In the developmental study in rabbits, the maternal (systemic) NOAEL was 10 mg/kg/day based on decreased body weight gain at the LOAEL of 30 mg/kg/day.  The developmental (fetal) NOAEL was 30 mg/kg/day based on increased resorptions at the LOAEL of 60 mg/kg/day.
    iii. Reproductive toxicity.  In the 2-generation reproduction toxicity study in rats, the maternal (systemic) NOAEL was 4 mg/kg/day based on decreased body weight and food consumption, increased number of dams delivering nonviable offspring, and increases in adrenal and thyroid weights at the LOAEL of 40 mg/kg/day.  The reproductive (pup) NOAEL was 40 mg/kg/day, the highest dose tested.]

	4. Subchronic toxicity. [ i. Rat 90-day oral study. A Subchronic feeding study in rats conducted for 13-weeks resulted in a NOAEL of 80 parts per million (ppm) (5.1 and 6.3 mg/kg/day in males and females, respectively).  The only effect observed at 80 ppm was minimal centrilobular hypertrophy (seen in one male) and hepatocytic centrilobular vacuolation (3 males) with no concomitant increase in liver weight or clinical chemistry correlates and no analogous effects in females.  As such, these observations are not considered to be adverse.  Increased liver weight, hepatic hypertrophy, thyroid hypertrophy, and decreased body weight were observed at the higher doses of 400 and 1,600 ppm.

    ii. Dog 90-day oral study. A subchronic feeding study in dogs conducted for 13-weeks resulted in a NOAEL of 100 ppm (3.3 and 3.5 mg/kg/day in males and females, respectively).  At the LOAEL of 400 ppm, increased liver weight, clinical chemistry parameters, and liver hypertrophy (males) were observed.

    iii. Rat 4-week dermal study. In a 21-day dermal toxicity in the rat study, the NOAEL was greater than 1,000 mg/kg/ day, with no effects seen at this limit dose.]  

	5. Chronic toxicity. [ i. Dog. A 1-year feeding study in dogs resulted in a NOAEL of 15 ppm (0.62 mg/kg/day) for females and 150 ppm (5.2 mg/kg/day) for males.  Decreased body weight, increased liver weight, liver hypertrophy, and pigment in the liver were observed at the LOAEL of 150 and 1,200 ppm in females and males, respectively.

    ii. Mouse. A 78-week chronic/oncogenicity study was conducted in male and female mice at 0, 10, 200 (males only), 650, and 1,300 ppm (females only). The NOAEL was 10 ppm (1.4 mg/kg/day), and the LOAEL was  200 ppm (26.3 mg/kg/day) for males and 650 ppm (104.6 mg/kg/day) for females based on increased liver weight and histopathological effects on the liver, which were consistent with chronic enzyme induction.  There was no statistically significant increase of any tumor type in males. However, there was a statistically significant increase in combined liver adenomas and carcinomas in females at the high dose only (1,300 ppm; 208.8 mg/kg/day).  There were no liver tumors in the control females, and liver tumor incidences in the high-dose females just exceeded the historical control range. In ancillary mode-of-action studies in female mice, the increased tumor incidence was associated with changes in several parameters in mouse liver following high doses of fenbuconazole, including an increase in P450 enzymes (predominately of the CYP 2B type), an increase in cell proliferation, an increase in hepatocyte hypertrophy, and an increase in liver weight.  Changes in these liver parameters, as well as the occurrence of the low incidence of liver tumors, were non-linear with respect to dose (i.e., effects were observed only at high dietary doses of fenbuconazole). Similar findings have been shown with several pharmaceuticals, including phenobarbital, which is not carcinogenic in humans. The non-linear dose response relationship observed with respect to liver changes (including the low incidence of tumors) in the mouse indicates that these findings should be carefully considered in deciding the relevance of high-dose animal tumors to human dietary exposure.

    iii. Rat. A 24-month chronic/oncogenicity study in male and female rats was conducted at 0, 8, 80, and 800 ppm fenbuconazole, and a second 24-month chronic/oncogenicity study was conducted in male rats at 0, 800, and 1,600 ppm. The NOAEL was 80 ppm (3 and 4 mg/kg/day in males and females, respectively), and the LOAEL was 800 ppm (31 and 43 mg/kg/day in males and females, respectively) based on decreased body weight, increased liver and thyroid weights, and liver and thyroid hypertrophy.  Fenbuconazole produced a minimal but statistically significant increase in the incidence of combined thyroid follicular cell benign and malignant tumors.  These findings occurred only in male rats following life-time ingestion of very high levels (800 and 1,600 ppm in the diet) of fenbuconazole.

For chronic dietary risk assessments, EPA has established the chronic reference dose (cRfD) for fenbuconazole at 0.03 mg/kg/day.  The cRfD is based on the 2-year combined chronic feeding-carcinogencity study in rats with a NOAEL of 3.0 and 4.0 mg/kg/day in males and females, respectively, and uncertainty factor of 100 accounting for both interspecies extrapolation (10x) and intraspecies variability (10x).  The FQPA safety factor is 1X.  In general, the primary organs for toxicity were the liver (hepatocellular enlargement in females and hispathological lesions in both sexes) and thyroid (histopathological lesions and thyroid weight increase in both sexes).

    iv. Carcinogenicity. The Agency has concluded, that the available data provide limited evidence of the carcinogenicity of fenbuconazole in both mice and rats and has classified fenbuconazole as a Group C carcinogen (possible human carcinogen) in accordance with Agency guidelines, published in the Federal Register (51 FR 33992, September 24, 1986), and recommended that for the purpose of risk characterization a low-dose extrapolation model applied to the experimental animal tumor data should be used for quantification of human risk (Q1*).  EPA's 26 Feb 1998 Hazard Identification Assessment Review Committee (HIARC) report concluded that 0.00359 (mg/kg/day)-1 is the appropriate Q1* for fenbuconazole; this Q1* is based on the fenbuconazole mouse liver tumor data, along with a power surface area scaling factor.]

	6. Animal metabolism. [The absorption, distribution, excretion, and metabolism of fenbuconazole in rats, goats, and hens were investigated.  Following oral administration, fenbuconazole was completely and rapidly absorbed, extensively metabolized by oxidation/hydroxylation and conjugation, and rapidly and essentially completely excreted, predominately in the feces.  Fenbuconazole did not accumulate in tissues.]

	7. Metabolite toxicology. [There are no toxicological concerns for fenbuconazole based on differential metabolic pathways in plants and animals.  Triazole fungicides are known to produce three common metabolites, 1,2,4-triazole, triazolylalanine and triazole acetic acid.  To support the extension of existing parent triazole-derivative fungicide tolerances, EPA conducted an interim human health assessment for aggregate exposure to 1,2,4-triazole.  This interim assessment was summarized in the Federal Register notice dated August 4, 2004 and titled Propiconazole; Time-Limited Pesticide Tolerances.  EPA concluded, that for all exposure durations and population subgroups, aggregate exposures to 1,2,4-triazole are not expected to exceed its level of concern.]

	8. Endocrine disruption. [The mammalian endocrine system includes estrogen and androgens as well as other hormonal systems.  Fenbuconazole is not known to interfere with reproductive hormones; thus, fenbuconazole should not be considered to be estrogenic or androgenic.  There are no known instances of proven or alleged adverse reproductive or developmental effects to people, domestic animals, or wildlife as a result of exposure to fenbuconazole or its residues.]

C. Aggregate Exposure

	1. Dietary exposure. [The exposure and risk resulting from agricultural uses of fenbuconazole was considered for the U.S. population and special sub-populations.  There are two direct sources of exposure to humans considering fenbuconazole's uses across all labels:  from food intake and from consuming drinking water.  The exposure and risk are estimated in this report for different durations of both routes of exposure and their aggregated contribution.  In an aggregate assessment, exposures from food residues were combined with conservative estimates of potential water residues.  The current approach of the EPA Office of Pesticide Programs (OPP) is to use a tiered approach for acute dietary risk assessment that proceeds from very conservative assumptions about food residues, to inclusion of more realistic residue values measured closer to the point of consumption.]

	i. Food. [The process of dietary risk assessment of pesticides considers chronic and acute exposures to the U.S. population and sensitive population sub-groups.  Additional exposures from potential residues in drinking water were also estimated.

The Dietary Exposure Evaluation Model (DEEM-FCID, version 2.14), a commercially available software package, was used to estimate exposure to fenbuconazole via food consumption by the general U.S. population and certain subgroups.  The model combined the consumption data and residue data for a given pesticide to analyze dietary risk.  

Food consumption data from the USDA Continuing Survey of Food Intakes by Individuals (CSFII) conducted from 1994 through 1998 including the children's supplemental survey were used in this assessment.  The food consumption data, i.e., foods as consumed, were translated into raw agricultural commodities and their food forms using recipe translation files contained within the DEEM software.  For chronic assessments, exposure assessment was conducted that is more refined because it uses average residues from field trials.]

a.  Acute dietary exposure.  Although, no acute adverse effect was observed as a result of exposure to a single dose, EPA has established an acute reference dose (aRfD) for the purpose of the acute dietary assessment. This aRfD was set at 0.3 mg/kg/day for females 13-49 years old, the population sub-group of concern.  This was based on the developmental rat toxicity study with a NOAEL of 30 mg/kg/day and an uncertainty factor of 100.  The 100-fold safety factor includes intraspecies and interspecies variations.  Exposures from all existing and proposed residues result in very low acute exposures.  Using the above assumptions for Tier 1 assessment, the food exposure to fenbuconazole for females 13-49 years old at the 95th percentile was estimated to be 0.009159 mg/kg/day that utilized 3.1% of the aRfD.

b.  Chronic dietary exposure. EPA has established a chronic reference dose (cRfD) for fenbuconazole at 0.03 mg/kg/day for all population subgroups.  The cRfD is based on the 2-year combined chronic feeding-carcinogenicity study in rats with a NOAEL of 3.03 and 4.02 mg/kg/day in males and females respectively, and an uncertainty factor of 100.  The 100-fold safety factor includes intraspecies and interspecies variations.  No additional FQPA safety factor is required.  The food exposure for the overall U.S. population was estimated for the Tier 2 assessment to be 0.000739 mg/kg/day that utilized 2.5% of the cRfD using the refined Tier 2 conservative exposure assumptions of 100% crop treated and average residues from field trials.  The population subgroup with the highest potential for exposure was All Infants (< 1 year old) with food + water exposure of 0.002032 mg/kg/day that represented 6.8% of the cRfD.  

c.  Cancer dietary exposure. EPA has classified fenbuconazole as a Group C carcinogen (possible human carcinogen) and has established a Q1* of 0.00359 (mg/kg/day)[-1] in human equivalents.  The group used in this analysis was the general U. S. population.  A Tier 3 cancer dietary assessment used the same food residue inputs as those used in the chronic non-cancer assessment.  The cancer analysis is further refined in that it makes use of average percent crop treated estimates.  The cancer risk estimate using these food residue inputs and a worst case use pattern assumption for water is 1.9 x 10[-6].  Typically, HED is concerned when the risk estimate associated with food and drinking water exceeds 3 x 10[-6].  As a result, cancer risk to the general U.S. population is below HED's level of concern.]
 
	ii. Drinking Water. [Direct measurements of fenbuconazole in drinking water were not available.  Estimates of potential water concentrations resulting from agricultural use of fenbuconazole were estimated using three environmental models, assuming certain environmental degradation properties for fenbuconazole and modeled dynamics of ground water and surface water bodies.  The acute drinking water estimates were estimated using PRZM/EXAMS and SCI-GRO models and are known to overestimate potential water residues.  These three models provide conservative, screening level estimates of water concentrations.  PRZM/EXAMS is used for surface water while SCI-GROW is used to give estimates of ground water concentrations.  Such water estimates are very sensitive to the input parameters; however, they can still serve as a screening estimate for exposure considerations. Based on the PRZM/EXAMS and SCI-GROW models the US EPA estimated EECs of fenbuconazole for acute exposures to be 24.1 parts per billion (ppb) for surface water and 0.031 ppb for ground water.  The EECs for chronic (non-cancer) and for cancer exposures are estimated to be 16.5 ppb for surface water and 0.031 ppb for groundwater.  Finally, the 30-year annual mean surface water value of 11.7 ppb is greater than the groundwater value of 0.031 ppb.  As a result, the surface water value was used in the cancer dietary analysis.

The potential, acute, aggregate exposures from food and drinking water for females of child bearing age is approximately 0.009159 mg/kg-bw/day or 3.1 % of the acute reference dose (aRfD) for the upper 95th %tile of the population using a Tier 1 assessment.

Potential chronic exposure to water residues was estimated using 16.5 ppb for the two commodities, i.e., "water, direct, all sources" and "water, indirect, all sources" for input to DEEM-FCID for chronic water (Tier II) analysis.  After considering all existing and proposed uses, the exposure to fenbuconazole residues is 6.8 % of the chronic reference dose for the most exposed population sub-group, All Infants (< 1 year old).  

Cancer dietary exposure with water was also calculated.  Incorporation of water at 11.7 ppb into the Tier 3 assessment resulted in an estimated exposure of 0.000522 mg/kg/day including pepper use with a cancer risk estimate of 1.9 x 10[-6].]

	2. Non-dietary exposure. [Fenbuconazole is not currently registered for use on any sites that would result in residential exposure.  Thus, the risk from non-dietary exposure would be considered negligible.]

D. Cumulative Effects. [Fenbuconazole is a member of the triazole class of fungicides.  There is currently no evidence to indicate that conazoles share common mechanisms of toxicity, and EPA is not following a cumulative risk approach based on a common mechanism of toxicity for the conazoles.]

	
E. Safety Determination

	1. U.S. population. [Using the above conservative exposure assumptions and taking into account the completeness and reliability of the toxicity data, chronic dietary food exposure to fenbuconazole from pepper using refinement (Tier 2) of the tolerance residues by adjusting for the average residues from field trials resulted in risk estimates of 2.5% of cRfD for the general U. S. population when amended pepper tolerances were included in the assessment with all existing uses of fenbuconazole.  Generally, EPA has no concern for exposures below 100% of the chronic reference dose (cRfD) because the cRfD represents the level at or below which daily dietary exposures over a lifetime will not pose appreciable risks to human health.  

Likewise, the acute dietary food exposure for pepper use at 95[th] percentile (Tier 1) for females 13-49 years old, the population sub-group of concern is 3.1 % of acute reference dose (aRfD).  Therefore, there is no concern for exposure because the acute RfD represents the level at or below which a single daily exposure will not pose appreciable risks to human health.

Using refined assessment (Tier 3), the cancer risk estimate is when pepper use was included in the assessment with all existing uses of fenbuconazole, including water, the cancer risk estimate was 1.9 x 10[-6].  Generally, the Agency has no concern for exposures that result in a cancer risk estimate below 3 x 10[-6].  Considering the conservative assumptions of this assessment and the screening level exposure from drinking water, the cancer risk is not expected to exceed 1 x 10[-6] for the U.S. population as a whole; therefore exposure to fenbuconazole would not result in unacceptable levels of aggregate human health risk for cancer.

Short-term and intermediate-term risks are considered to be negligible because of lack of significant toxicological effects.  Therefore, based on these risk assessments, Dow AgroSciences concludes that there is reasonable certainty that no harm will result to the U. S. population from aggregate exposure to fenbuconazole residues.]

	2. Infants and children. [EPA uses a weight evidence approach in determining what safety factor is appropriate for assessing risks to infants and children.  This approach takes into account the nature and severity of the effects observed in pre- and post-natal studies and other information such as epidemiological data.  The completeness and adequacy of the toxicity database is also considered.

Toxicity database and exposure data for fenbuconazole are complete.  No indication of increased susceptibility of rats or rabbits to in utero and/or postnatal exposure was noted in the acceptable developmental toxicity studies in rats and rabbits as well as in a 2-generation reproductive toxicity study in rats.  EPA has previously determined that no additional safety factor to protect infants and children is necessary for fenbuconazole and that the RfD at 0.03 mg/kg/day is appropriate for assessing risk to infants and children.

Using the conservative assumptions described above, the chronic dietary exposure to fenbuconazole will utilize 6.8 % of the cRfD for All Infants (<1 yr old), 6.2 % of the cRfD for children 1-2 yrs old and 4.9 % of the cRfD for children 3-5 yrs old.
In assessing the potential for additional sensitivity of infants and children to residues of fenbuconazole, data from developmental toxicity studies in rats and rabbits and a 2-generation reproduction study in the rat are considered.  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 from exposure to the pesticide on the reproductive capability and potential systemic toxicity of mating animals and on various parameters associated with the well-being of offspring.  The completeness and adequacy of the toxicity data base is also considered.  No indication of increased susceptibility to infants and children was noted in these studies for fenbuconazole.  EPA has previously determined that no additional safety factor to protect infants and children is necessary for fenbuconazole and that the RfD of 0.03 mg/kg/day is appropriate for assessing risk to infants and children.

Therefore, based on the completeness and reliability of the toxicity data and the conservative exposure assessment, Dow AgroSciences concludes with reasonable certainty that no harm will result to infants and children from the aggregate exposure to fenbuconazole from all current and proposed ending uses.]   

F. International Tolerances

	[MRLs for residues of fenbuconazole have been established by EPA, Codex, Canada, and Mexico.  The residue definition for both Codex and Mexico is fenbuconazole, per se.  The USA and Canadian residue definition, however, is the combined residues of fenbuconazole and its metabolites, RH-9129 and RH-9130, each expressed as parent (i.e., the same as the U.S. tolerance definition).  US tolerance was previously set by EPA at 0.4 ppm.  However, new residue data has shown probability of residue increase when plant paturation might be delayed by weather conditions and therefore a tolerance increase to 1,0 ppm is deemed necessary.  As there are no established or proposed Canadian, Mexican, or Codex MRLs for fenbuconazole on peppers, there are no international harmonization issues for the pepper tolerance petition.]