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 (RH7592) 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 μg/g and 0.003 μg/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 (μg/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)-1is 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 subgroups. 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)-1in 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 95th 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 10-6for 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 preand 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.]