  SEQ CHAPTER \h \r 1 FILE NAME:   company.wpt   (1/1/2005) (xml)

Template Number P25	

Sugarcane Section 3 - metaconazole

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COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE

(1/1/2005)

EPA Registration Division contact: [insert name and telephone number
with area code]	

		

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TEMPLATE:

[BASF Corporation]

[Insert petition number]

		EPA has received a pesticide petition [insert petition number] from
[BASF Corporation], [26 Davis Drive, P.O. Box 13528, Research Triangle
Park, NC 27709-3528] 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 by establishing a tolerance for residues of
[metconazole,
5-[(4-chlorophenyl)-methyl]-2,2-dimethyl-1-(1H-1,2,4-triazol-1-ylmethyl)
cyclopentanol, measured as the sum of cis- and trans-isomers] in or on
the raw agricultural commodities [Sugarcane, cane at 0.06 parts per
million (ppm), Sugarcane, molasses at 0.08 ppm].

EPA has determined that the petitions contain 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
petitions.  Additional data may be needed before EPA rules on the
petitions.

A. Residue Chemistry                                      

		1. Plant metabolism. [Nature of the residue studies (OPPTS Harmonized
Guideline 860.1300) were conducted in wheat, canola, banana, peas, and
mandarin oranges as representative crops in order to characterize the
fate of metconazole in all crop matrices. Two radiocarbon labeling
positions were studied in each crop. In all crops triazole ring labeling
was used, and the other label was positioned either in the
p-chlorophenyl or the cyclopentyl rings. In all five crops the
metconazole Residues of Concern (ROC) were characterized as parent
metconazole. A confined rotational crop study also determined that
parent metconazole was the residue of concern in the representative
crops of wheat, radish, and lettuce/spinach.] 

		2. Analytical method. [Independently validated analytical methods have
been submitted for analyzing parent metconazole residues with
appropriate sensitivity in the raw crop and processed commodities for
sugarcane for which tolerances are being requested.]  

		3. Magnitude of residues. [Field trials were carried out to determine
the magnitude of the residue in/on sugarcane. The number and locations
of field trials are in accordance with OPPTS Guideline 860.1500. Field
trials were carried out using the maximum label rates, the maximum
number of applications, and the minimum pre-harvest intervals (PHI) for
the crop. Detected residues of metconazole in all the sugarcane crop
commodities support the proposed tolerances.]

B. Toxicological Profile

[A complete, valid and reliable database of mammalian and genetic
toxicology studies supports the proposed tolerance for metconazole on
sugarcane. Two geometric isomers of metconazole exist, with the
fungicidal activity being associated primarily with the cis isomer. The
technical material is a mixture of cis- and trans- isomers in an 85 to
15 ratio (85:15).  Toxicology studies submitted in support of this
petition were conducted on the metconazole technical material composed
of either the 85:15 isomer mixture (AC 900768) or a more purified
(greater than 95%) sample of the cis-isomer (WL 136184).] 

1. Acute Toxicity. [AC 900768 technical is considered to be slightly
toxic (Toxicity Category III) to the rat by the oral route of exposure.
In an acute oral study in rats, the LD50 value of AC 900768 technical
was 727 milligrams per kilogram of body weight (mg/kg b.w.) for males
and 595 mg/kg b.w. for females. The oral LD50 for combined sexes was 660
mg/kg b.w. An oral LD50 study in rats conducted with WL 136184 technical
also supports the classification of metconazole as slightly toxic by the
oral route of exposure. The oral LD50 values of WL 136184 technical were
1,626 mg/kg b.w. for males and 1,312 mg/kg b.w. for females, with an
LD50 value for combined sexes of 1,459 mg/kg b.w.

The 85:15 isomer mixture demonstrates no acute toxicity via the dermal
route of exposure [LD50 value >2000 mg/kg (highest dose tested)]
(Toxicity Category III) or inhalation route of exposure [LC50 >5.6 mg/L]
(Toxicity Category IV).  The material is mildly irritating to the eye
(Toxicity Category III) and is not irritating to the skin (Toxicity
Category IV), nor is it a skin sensitizer.]   

2. Genotoxicity.  [AC 900768 technical (the 85:15 isomer mixture) and WL
136184 technical (greater than 95% cis isomer) were tested in an
extensive battery of in vitro and in vivo genotoxicity assays measuring
several different endpoints of potential genotoxicity. Collective
results from these studies indicate that metconazole does not pose a
genotoxic risk, and therefore, is not likely to be a genotoxic
carcinogen.] 

3. Reproductive and developmental toxicity. [Developmental toxicity
studies in rats conducted with AC 900768 technical and WL 136184
technical showed no evidence of teratogenic effects in fetuses, and no
evidence of developmental toxicity in the absence of maternal toxicity.
Thus, metconazole is neither a selective developmental toxicant nor a
teratogen in the rat. Two rat developmental toxicity studies have been
conducted  with AC 900768 technical. In the first study, the
no-observable-adverse-effect-level (NOAEL) for maternal toxicity was 12
mg/kg b.w./ day, based on decreased body weight gain at 30 mg/kg
b.w./day, the next highest dose tested, and the NOAEL for developmental
toxicity was also 12 mg/kg b.w./day, based on decreased fetal body
weights and an increased incidence of skeletal ossification variations
at 30 mg/kg b.w./day. In the second study, the maternal and fetal NOAEL
was 16 mg/kg/day based on findings similar to the first study at the
next higher dose level of 65 mg/kg/day. In the rat developmental
toxicity study conducted with WL 136184 technical, the NOAEL for
maternal toxicity was 24 mg/kg b.w./day based on decreased body weight
gain at 60 mg/kg b.w./day, the highest dose tested, and the NOAEL for
developmental toxicity was also 24 mg/kg b.w./day, based on an increase
in the total number of resorptions, reductions in fetal body weights and
an increased incidence of skeletal ossification variations at 60 mg/kg
b.w./day. 

Results from a developmental toxicity study in rabbits with the 85:15
isomer mixture also indicated no evidence of teratogenicity or
developmental toxicity in the absence of maternal toxicity. Thus,
metconazole technical is neither a selective developmental toxicant nor
a teratogen in the rabbit. In this rabbit developmental study, the NOAEL
for maternal toxicity was 20 mg/kg b.w./day based on decreased food
consumption and body weight gain, reductions in hemoglobin, hematocrit
and corpuscular volume, increases in platelet counts and alkaline
phosphatase activity, and increased absolute and relative liver weights
at 40 mg/kg b.w./day (the highest dose tested). The NOAEL for
developmental toxicity was also 20 mg/ kg b.w./day, based on an increase
in the total number and mean number of resorptions and decreased fetal
body weight at 40 mg/kg b.w./day. 

Two multi-generation reproduction studies were conducted with
Metconazole Technical -- one with the >95% cis form and one with the
85/15 cis/trans form.  Dose levels and results in both studies were
similar, although the 95% cis study diet was adjusted to maintain a
constant dose.  Dose levels in the >95% cis study were 0, 2, 8, 32 and
48 mg/kg/day and in the 85/15 cis study were 0, 30, 150 and 750 ppm
(approximately 0, 2.1, 10.6 and 52.8 mg/kg/day for pre-mating growth
period).  For the >95% cis study, the results support a NOAEL for
parental toxicity of 8 mg/kg/day based on increased ovarian weight and
increased gestation length at the next highest dose tested (32
mg/kg/day).   The NOAEL for growth and development of the offspring is
also 8 mg/kg/day, based on reductions in live litter size for F2 litters
at 32 mg/kg/day.  The NOAEL for reproductive performance and fertility
was 48 mg/kg/day (the highest dose tested).  In the 85/15 cis/trans
study, the NOAEL identified for parental toxicity, offspring growth and
development and reproductive toxicity was 10.8 mg/kg/day (150 ppm) based
on effects observed at the highest dose tested of 52.8 mg/kg/day (750
ppm).

Results of the pilot and definitive reproduction studies and
developmental toxicity studies conducted with AC 900768 technical and/or
WL 136184 technical show no increased sensitivity to developing
offspring as compared to parental animals, as comparable NOAELs were
obtained for parental toxicity and growth and development of offspring.]


4. Subchronic toxicity.  [Short-term (28-day) dietary toxicity studies
in rats were conducted with AC 900768 and WL 136184 technical materials.
In the 28-day study with AC 900768, the NOAEL was 100 ppm (approximately
9.6 mg/kg b.w./day), based on reductions in body weight, body weight
gain, food consumption, and hemoglobin concentration for males, as well
as increased absolute and relative liver weights, and increased
incidences of hepatic fatty vacuolation and parenchymal hypertrophy for
males and females at 1,000 ppm (the next highest concentration tested).
Similar results were observed in the study conducted with WL 136184
technical. Based on these results, the NOAEL for WL 136184 is 300 ppm
(approximately 28.5 mg/kg b.w./day), supported by decreased body weights
and body weight gains and increased incidences of hepatic fatty
vacuolation for males and females, increased absolute and adjusted liver
weights for females, and decreased food consumption for males at 1,000
ppm (the next highest concentration tested). 

In a 28-day dietary study in dogs conducted with AC 900768 technical
(85:15 isomer mixture), the NOAEL was a dietary concentration of 1,000
ppm (approximately 38.6 mg/kg b.w./day), based on decreased food
consumption, body weight losses, increased alkaline phosphatase
activity, increased spleen and liver weights, and urinalysis changes for
males and females, and increased absolute and relative thyroid gland
weights for females at 7,000 ppm, the highest concentration tested. 

Subchronic (90-day) dietary studies in rats were conducted with AC
900768 technical and WL 136184 technical. In the study conducted with AC
900768, the NOAEL was 100 ppm (approximately 6.8 mg/kg b.w./day) based
on hepatic fatty vacuolation in males at 300 ppm, the next highest
concentration tested. The NOAEL from the study conducted with WL 136184
technical was 450 ppm (approximately 30.9 mg/kg b.w./day) based on
decreased food consumption, body weights, and body weight gains,
clinical chemistry changes, increased absolute and adjusted liver
weights, and histopathological changes in the liver and/or stomach for
males and females, and decreased red blood cell parameters for females
at 1,350 ppm, the highest concentration tested. 

In a 90-day dietary study in mice conducted with AC 900768, the NOAEL
was 30 ppm (approximately 5.5 mg/kg b.w./day), based on increased
aspartate and alanine aminotransferase activities in males, increased
absolute and relative weights of the liver and spleen of females, and
increased incidences of hepatocellular vacuolation and hypertrophy for
males and females at 300 ppm, the next highest concentration tested. 

A 90-day dietary study in beagle dogs with AC 900768 technical supports
a NOAEL of 60 ppm (approximately 2.5 mg/kg b.w./day) based on decreased
body weight gain and food consumption for females, and a slight increase
in reticulocyte count for males at 600 ppm, the next highest
concentration tested.]  

5. Chronic toxicity.  [Findings similar to those observed in the
short-term subchronic studies were also apparent in the long-term
dietary toxicity studies conducted in rats, dogs and mice. 

In a chronic toxicity study, long-term (104-weeks) administration of
metconazole technical to rats supported a NOAEL for systemic toxicity of
100 ppm (approximately 4.8 mg/kg b.w./day), based on increased adjusted
liver weight, clinical chemistry changes, and increased incidences of
hepatocellular lipid vacuolation and centrilobular hypertrophy at
interim sacrifice for males at 300 ppm, the next highest concentration
tested. 

In a 104-week carcinogenicity study in rats fed diets containing 0, 100,
300 or 1000 ppm metconazole technical, the NOAEL for carcinogenicity was
1000 ppm (50 mg/kg/day) the highest dose tested.  The NOAEL for chronic
systemic toxicity was 100 ppm (5.6 mg/kg/day) based on increased
incidences of centrilobular hypertrophy and pigment disposition in the
liver and increased incidences of cortical vacuolation in the adrenal at
300 ppm.

In a one-year dietary study in beagle dogs, the NOAEL was 300 ppm
(approximately 11.1 mg/ kg b.w./day), based on decreased body weight
gain for males during weeks 1 to 13 and increased alkaline phosphatase
activity for males and females at 1,000 ppm, the next highest
concentration tested. 

A 91-week carcinogenicity study in mice with AC 900768 supports a NOAEL
for non-neoplastic effects of 30 ppm (approximately 4.8 mg/kg b.w./
day), based on increased white blood cell count for males, increased
aspartate and alanine aminotransferase activities and increased absolute
and adjusted liver weight for females, and microscopic changes in the
liver, spleen and adrenal gland for males and females at 300 ppm (the
next highest concentration tested). The NOAEL for carcinogenicity was
300 ppm (approximately 48.3 mg/kg b.w./day) based on increased
incidences of hepatocellular adenomas in males and females and
hepatocellular carcinomas in females at 1,000 ppm, the highest
concentration tested. The increased incidences of hepatic adenomas and
carcinomas at the highest concentration tested are considered to occur
through promotional and non-genotoxic secondary mechanisms following
toxicity and induction of mixed function oxidase in mice. Consequently,
metconazole is not likely to be oncogenic in humans at the insignificant
levels of exposure resulting from its use as a fungicide.] 

6. Animal metabolism. [The rat metabolism studies indicate that the
qualitative nature of the residues of metconazole in animals is
adequately understood. In studies conducted with radiolabeled AC 900768
(85:15 isomer mixture) or radiolabeled WL 136184 (greater than 95% cis
isomer) radioactivity was rapidly eliminated in urine and feces within
48 hours of dosing. Biliary excretion was shown to be a prominent route
of elimination. At both high and low doses of AC 900768, male rats
generally excreted statistically significantly lower amounts of
radioactivity in the urine, and greater amounts of radioactivity in the
feces, compared to females. The pattern of metabolites detected was
similar at high and low doses, and little or no parent compound was
found in the feces or urine. Five days following oral dosing of AC
900768 at the higher level, low levels of radioactivity were detected in
the majority of tissues analyzed; however higher concentrations of
radioactivity were found in the adrenal glands, gastro-intestinal tract
and liver. A comparison of radioactivity levels in the adrenal glands
following oral administration of low and high doses indicates that
uptake in the adrenal may be saturable. No differences in tissue levels
were noted between males and females.] 

7. Metabolite toxicology. [The metabolism of metconazole technical is
similar in plants and mammals with extensive hydroxylation being the
predominate reaction.  Due to the similar structural nature of most
metabolites, the toxicity of the plant metabolites is adequately
estimated from the results of studies performed in animals.  EPA concern
for several unique plant metabolites common to most triazole fungicides
is being addressed with research conducted by the US Triazole Task
Force.  On the basis of this research, an interim human health risk
assessment for aggregate exposure to 1, 2, 4-triazole was published in
the Federal Register (40 CFR Part 180, Vol. 69 No. 149 Page 47005,
8/4/04) and will be refined once the research is complete.]

8. Endocrine disruption.  [The toxicology database for metconazole
technical is current and complete.  This includes a thorough evaluation
of the potential effects on reproduction and development, and the
pathology of the endocrine organs following short-term and long-term
exposure.  The battery of tests included as part of this petition fully
characterizes potential endocrine-related in vivo effects, clearly
defines NOAEL/LOAEL values, and indicates no increased sensitivity to
developing offspring.]

C. Aggregate Exposure

		1. Dietary exposure. [Exposure assessments were conducted to evaluate
the potential risk due to acute and chronic dietary exposure to residues
of metconazole. This fungicide considering both the cis and trans
isomers, in or on raw agricultural commodities, was expressed as the
parent compound.  The analysis included all current tolerances for
metconzole (180.617) plus new proposed tolerances for sugarcane.]

		i. Food.  

[Acute Dietary Exposure Assessment

 Acute dietary exposure estimates were based on current and proposed
tolerance values, default process factors, and 100% of all crops
treated.  The consumption data was from the USDA Continuing Survey of
Food Intake by Individuals (CSFII 1994 - 1996, 1998) and the EPA Food
Commodity Ingredient Database (FCID) using Exponent's Dietary Exposure
Evaluation Module (DEEM-FCID) software.  

The result exposure estimates were compared against the metconazole
acute Population Adjusted Dose (aPAD) of 0.12 mg/kg b.w./day for females
13-49 years of age.  This endpoint is based on the NOAEL of 12 mg/kg/day
with an FQPA safety factor of 1 which was proposed by EPA in the most
recent review of metconazole (“Metconazole. FQPA Human Health Risk
Assessment for Proposed New Section 3 Uses on Corn and Cotton and
Section 18 Use on Sugarcane” August 15, 2008).  An acute dietary
exposure assessment is not required for any other sub-population.  The
exposure assessment included residues from food commodities and drinking
water.  Metconazole acute dietary exposure from food and drinking water
is 3.7 % aPAD for females 13-49 years of age.  The results of the acute
dietary assessment are presented in Table 1.

Table 1.	Results for Metconazole Acute Dietary Exposure Analysis
Considering all Current and Proposed Food Tolerances and Exposure from
Drinking Water using DEEM-FCID at the 95th Percentile 

Population	Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)*	 

Females (13-49 years old)	0.00446	3.7



The results of the analysis show that for females 13-49 years of age,
the estimated exposure is well below the Agency's level of concern (<
100% aPAD).  Additional refinements in the dietary risk assessment (i.e.
utilizing anticipated residue values, percent crop treated values) would
further reduce the estimated exposure values.

  Acute Aggregate Exposure and Risk (food and water)

The aggregate acute risk includes residues of metconazole from food and
drinking water (Table 1). Exposures from residential uses are not
included in the acute aggregate assessment.  The results demonstrate
that there are no safety concerns for any subpopulation based on the
proposed uses and the results clearly meet the FQPA standard of
reasonable certainty of no harm.   

Chronic Dietary Exposure Assessment

Chronic dietary exposure estimates were based on current and proposed
tolerance values, default process factors, and 100% crop treated values
for all commodities.  The consumption data was from the USDA Continuing
Survey of Food Intake by Individuals (CSFII 1994 - 1996, 1998) and the
EPA Food Commodity Ingredient Database (FCID) using Exponent's Dietary
Exposure Evaluation Module (DEEM-FCID) software.  

The chronic Population Adjusted Dose (cPAD) used for U.S. population and
all sub-populations is 0.043 mg/kg bw/day. This endpoint is based on the
NOAEL value of 4.3 mg/kg/day with an FQPA safety factor of 1 which was
proposed by EPA in the most recent review of metconazole
(“Metconazole. FQPA Human Health Risk Assessment for Proposed New
Section 3 Uses on Corn and Cotton and Section 18 Use on Sugarcane”
August 15, 2008).  The exposure assessment included residues from food
commodities and drinking water.  The most highly exposure population sub
group was children 1-2 years of age at 10.96% cPAD.   The results of the
chronic dietary assessment are presented in Table 2. 

Table 2. Results for Metconazole Chronic Dietary Exposure Analysis
Considering all Current and Proposed Food Tolerances and Drinking Water
Exposure using DEEM-FCID 

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.002227	5.2

All Infants (< 1 year old)	0.004257	9.9

Children (1-2 years old)	0.004678	10.9

Children (3-5 years old)	0.004475	10.4

Children (6-12 years old)	0.003066	7.1

Youth (13-19 years old)	0.0018	4.2

Females (13-49 years old)	0.001972	4.6

Adults (20-49 years old)	0.001672	3.9

Adults (50+ years old)	0.00169	3.9



 The results of the analysis show that for all sub-populations, the
exposures are below a level of concern (< 100% cPAD).  Additional
refinements in the chronic dietary risk assessment (i.e. utilizing
anticipated residue values and percent crop treated values) would
further reduce the estimated exposure values. 

Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes residues of metconazole from food
and drinking water (Table 2). Exposures from residential uses are not
included in the chronic aggregate assessment.  The results demonstrate
there are no safety concerns for any subpopulation based on the proposed
uses and the results clearly meet the FQPA standard of reasonable
certainty of no harm.]   

		ii. Drinking water. [The drinking water concentrations used in the
assessment are from the most recent analysis by EPA.  The EPA acute
drinking water value is 45.48 ug/L and the EPA chronic drinking water
value is 31.25 ug/L.  These water concentration were included in the
dietary assessment conducted for metconazole (Tables 1 and 2).]

  		2. Non-dietary exposure. [HERE Metconazole is currently registered
for use on residential and recreational turf.   The US EPA has
determined that the quantification of dermal exposure and risk is not
required due to lack of systemic or dermal toxicity observed at the
limit dose in the 21-day dermal toxicity study in rat and the lack of
target organ toxicity, neurotoxicity, developmental or reproductive
toxicity (“Metconazole. FQPA Human Health Risk Assessment for Proposed
New Section 3 Uses on Corn and Cotton and Section 18 Use on Sugarcane”
August 15, 2008).  The US EPA also stated in their recent assessment
that post-application inhalation exposure is insignificant and does not
need to be assessed.  The only exposure which needs to be assessed is
toddler post-application incidential oral exposure.   The results shown
in Table 3 are from the US EPA’s evaluation of toddler
post-application incidental oral exposure.   The exposure values in
Table 3 are for the total incidental oral exposure including,
hand-to-mouth, object-to-mouth, and soil ingestion.  

Table 3.  Toddler Incidental Oral Post-Application Exposure and MOE
values.  

Population	Total Exposure (mg/kg bw-day)	MOE1 

Subgroup	Short term	Int. Term	Short term	Int. Term

Children 1-6 years old	0.0112	0.0064	810	995

1Short Term NOAEL = 9.1 mg/kg bw-day, Intermediate Term NOAEL = 6.4
mg/kg bw-day.  MOE = NOAEL / total exposure.  

The MOE level of concern is 100.  The MOE values for toddler incidental
post-application oral exposure exceed the level of concern which
indicates that the total exposure is below the level of concern.  

Short-Term and Intermediate Term Aggregate Exposure.

Short-term and intermediate term aggregate exposure includes exposure
from food, drinking water, and residential exposure.  The most highly
dietary exposure children sub-group was children 1-2 years old,
therefore, this group was used in the aggregate assessment.   The
aggregate exposures for children 1-2 years old are shown in Table 4.  

Table 4.  Short-Term and Intermediate-Term Aggregate Exposure for
Children 1-2 Years Old.  

Population	Exposure Term	Aggregate Exposure

(mg/kg bw-day	Aggregate Exposure (mg/kgbw-day)	Aggregate MOE1



Food+ Drinking water	Incidental Oral



Children 1 – 2 years old	Short– Term	0.004678	0.0112	0.01588	572

	Int. - Term	0.004678	0.0064	0.01108	576

1Short Term NOAEL = 9.1 mg/kg bw-day, Intermediate Term NOAEL = 6.4
mg/kg bw-day.  MOE = NOAEL / total exposure.  

The MOE level of concern is 100.  The MOE values for aggregate exposure
for children 1-2 years old exceed the level of concern which indicates
that the total exposure is below the level of concern.] 

D. Cumulative Effects

	[Metconazole is a triazole fungicide. There are several triazole
fungicides registered for use within the United States. Although
metconazole and other triazole fungicides may have similar modes of
action, no data are available to determine if these compounds have
common mechanisms of mammalian toxicity or information on how to include
metconazole in a cumulative risk assessment.  Therefore, for the
purposes of this tolerance petition no assumption has been made with
regard to cumulative exposure with other compounds having a common mode
of action. Further, triazole fungicides, including metconazole, have a
common primary metabolite, 1,2,4-triazole, with secondary metabolites
triazolylalanine and triazolacetic acid. EPA’s concern with these
common metabolistes is being addressed with research conducted by the US
Triazole Task Force.  On the basis of this research, an interim human
health risk assessment for aggregate exposure to 1, 2, 4-triazole was
published in the Federal Register (40 CFR Part 180, Vol. 69 No. 149 Page
47005, 8/4/04) and will be refined once the research is complete.]	

		

E. Safety Determination

		1. U.S. population. [Based on this risk assessment, BASF concludes
that there is a reasonable certainty that no harm will result to the
general population from the aggregate exposure to metconazole from the
pending and proposed uses.]

		2. Infants and children. [Based on this risk assessment, BASF
concludes that there is a reasonable certainty that no harm will result
to infants or childeren from the aggregate exposure to metconazole from
the pending and proposed uses.]

F. International Tolerances

	[There are no CODEX maximum residue levels established or proposed for
residues of metconazole in sugarcane.]

