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

Template Number P25	

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COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE

(1/1/2005)

EPA Registration Division contact: 

[Cynthia Giles-Parker, 

Registration Division (7505C), 

Office of Pesticide Programs, 

Environmental Protection Agency, 

1200 Pennsylvania Ave., NW.

Washington, DC 20460–0001; 

Telephone number: (703) 305–7740; 

e-mail address: giles-parker.cynthia@epa.gov.]

	

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TEMPLATE:

 by establishing a tolerance for residues of [Boscalid (BAS 510F);
[3-pyridinecarboxamide,2-chloro-N-(4'-chloro(1,1'-biphenyl)-2-yl]] in or
on the raw agricultural commodities, cotton, undelinted seed at [1.0]
part per million and cotton, gin byproducts at [55.0] parts per million
(ppm). EPA has determined that the petition contains data or information
regarding the elements set forth in section 408(d)(2) of the FFDCA;
however, EPA has not fully evaluated the sufficiency of the submitted
data at this time or whether the data supports granting of the petition.
 Additional data may be needed before EPA rules on the petition.

                                      

.  [Based on available acute toxicity data boscalid (BAS 510F) and its
formulated products do not pose acute toxicity risks.  The acute
toxicity studies place technical Boscalid (BAS 510F) in toxicity
category IV for acute oral; category III for acute dermal and category
IV for acute inhalation.  BAS 510F is category IV for both eye and skin
irritation, and it is not a dermal sensitizer.  For Cotton foliar and
seed treatment use, the formulated end use product proposed is as
follows: a water dispersible granule (WG), BAS 516 02/04F, containing a
2:1 mixture of boscalid (BAS 510F) and pyraclostrobin (BAS 500F).  BAS
516 02F, the basic formulation, has an acute oral toxicity category of
III, acute dermal of category III, acute inhalation of category IV, eye
irritation of category III, skin irritation of category IV, and is not a
dermal sensitizer.

.  [Ames Test (1 Study; gene point mutation): Negative; In Vitro
CHO/HGPRT Locus Mammalian Cell Mutation Assay (1 Study; point gene
mutation): Negative; In Vitro V79 Cell Cytogenetic Assay (1 Study;
Chromosome Damage): Negative; In Vivo Mouse Micronucleus (1 Study;
Chromosome Damage): Negative; In Vitro Rat Hepatocyte (1 Study; DNA
damage and repair): Negative. BAS 510F has been tested in a total of 5
genetic toxicology assays consisting of in vitro and in vivo studies. 
It can be stated that BAS 510F did not show any mutagenic, clastogenic
or other genotoxic activity when tested under the conditions of the
studies mentioned above.  Therefore, BAS 510F does not pose a genotoxic
hazard to humans.]

.  [The reproductive and developmental toxicity of BAS 510F was
investigated in a two-generation rat reproduction study as well as in
rat and rabbit teratology studies.  There were no adverse effects on
reproduction in the two-generation study at any dose tested.  The
reproductive NOAEL is 10,000 ppm (1165 and 1181 for males and females,
respectively), the highest dose tested. Pup effects were observed, at
the highest dose tested only. In males of the F1 generation, reduced
body weight and reduced body weight gain were observed at 10,000 ppm.
Additionally, hepatocyte degeneration was observed in males in animals
of both the F0 and F1 generations at 10,000 ppm.  The parental systemic
NOAEL is 1000 and 10,000 (113 and 1181 mg/kg b.w./day) for males and
females, respectively.  Toxicity to the offspring was seen at 1,000 ppm
in the form of decreased pup weights in the F2 males, and at 10,000 ppm
in the form of decreased pup weights for both males and females of both
the F1 and F2 generations.  The offspring NOAEL is 100 and 1000 ppm (12
and 116 mg/kg b.w./day) for males and females, respectively. 

The Agency concluded that there are no residual uncertainties for pre-
and postnatal toxicity as the degree of concern is low for the
susceptibility seen in the above studies, and the dose and endpoints
selected for the overall risk assessments will address the concerns for
the body weight effects seen in the offspring.  Although the dose
selected for overall risk assessments (21.8 mg/kg b.w./day) is higher
than the NOAELs in the 2-generation reproduction study (10.1 mg/kg
b.w./day) and the developmental neurotoxicity study (14 mg/kg b.w./day),
these differences are considered to be an artifact of the dose selection
process in these studies.  For example, there is a 10-fold difference
between the LOAEL (106.8 mg/kg b.w./day) and the NOAEL (10.1 mg/kg
b.w./day) in the two generation reproduction study.  A similar pattern
was seen with regard to the developmental neurotoxicity study, where
there is also a 10-fold difference between the LOAEL (147 mg/kg
b.w./day) and the NOAEL (14 mg/kg b.w./day).  There is only a 2-3-fold
difference between the LOAEL (57 mg/kg b.w./day) and the NOAEL (21.8
mg/kg b.w./day) in the critical study used for risk assessment.  Because
the gap between the NOAEL and LOAEL in the 2-generation reproduction and
developmental neurotoxicity studies was large and the effects at the
LOAELs were minimal, the true no-observed-adverse-effect-level was
probably considerably higher.  Therefore, the selection of the NOAEL of
21.8 mg/kg b.w./day from the 1-year dog study is conservative and
appropriate for the overall risk assessments.  In addition, the
endpoints for risk assessment are based on thyroid effects seen in
multiple species (mice, rats and dogs) and after various exposure
durations (subchronic and chronic exposures) which were not observed at
the LOAELs in either the 2-generation reproduction or the developmental
neurotoxicity studies.  Based on these data, the Agency concluded that
there are no residual uncertainties for pre- and post-natal toxicity.

No teratogenic effects were noted in either the rat or rabbit
developmental studies. In the rat study, evidence of maternal or
developmental toxicity was not observed at any dose (highest dose tested
of 1,000 mg/kg b.w./day).  Neither a maternal nor developmental LOAEL
were found since the highest dose tested was the NOAEL in both studies. 
In the rabbit teratology study, maternal toxicity observed at the mid
dose of 300 milligrams/kilogram of body weight (mg/kg b.w./day)
consisted of discolored/reduced feces in one dam and an abortion in one
dam.  This finding is not necessarily indicative of a definitive test
substance related adverse effect.  The dam which displayed the fecal
alterations and abortion also displayed decreased body weight and body
weight gain - compared to the group mean - during gestation.  These
decreases occurred even prior to compound administration.  Food
consumption was also dramatically decreased in this dam compared to the
other animals in the group.  Every day from gestation day (GD) 1–12,
this dam had food consumption values which were less than half the mean
for the group (compound administration began on GD 7).  From GD 13 to 26
(when the animal aborted and was sacrificed) this dam ate essentially
nothing (food consumption during this time period was less than or equal
to 1.5 grams food/day).  These decreases in body weight, body weight
gain, and food consumption, prior to compound administration, all
indicate an animal in poor health and this poor state of health, rather
than compound exposure, was likely the reason for the fecal alterations
and abortion.

At the high dose of 1,000 mg/kg b.w./day a maternal body weight gain
decrease compared to controls of 81% was observed during the treatment
period.  Reduced food consumption, reduced body weight and abortions in
three dams, were also seen at 1,000 mg/kg b.w./day.  Evidence of
developmental toxicity was not seen at any dose tested. 

Developmental neurotoxicity was not observed at any dose in the
developmental neurotoxicity study.  No maternal toxic effects were noted
at any dose in this study.  No developmental toxicity was seen at the
low dose of 12 mg/kg b.w./day (100 ppm).  Reduced body weights and body
weight gains were seen at 118 mg/kg b.w./day (1,000 ppm) during post
natal day (PND) 1–4.  Reduced body weights and body weight gains were
seen at 1,183 mg/kg b.w./day (10,000 ppm) as well as decreased absolute
pup brain weight at day PND 11 (both sexes) and decreased brain length
(males only) at PND.  The reduced pup brain weights and decreased brain
length go hand-in-hand and both are due to the decreased pup weights
seen at this dose.  In this respect, it should be noted that pup brain
weights relative to body weight at PND 11 were not significantly
different from controls at this dose. Though no maternal toxicity was
seen in this study, other studies using similar doses of BAS 510F
resulted in maternal toxicity.  A dose of 118 mg/kg b.w./day in female
rats of the same strain in the multigeneration study, resulted in an
increased incidence of hepatic centrilobular hypertrophy - a parameter
which could not have been detected in the developmental neurotoxicity
(DNT) study as liver histopathology on parental animals was not
performed in the DNT study.]

[The subchronic toxicity of BAS 510F was investigated in a 90–day
feeding studies with rats, mice and dogs, and in a 28–day dermal
administration study in rats.  Additonally a 90–day neurotoxicity
study in rats was performed.  Generally, mild toxicity was observed.  At
high dose levels (doses above the LOAELs) in feeding studies, all three
species displayed alterations in various clinical chemistry parameters. 
These clinical chemistry alterations were likely secondary to general
toxicity.  Statistically significant increased absolute and relative
thyroid weights were observed in male rats only at doses at and above
the LOAEL.  Increased absolute and relative liver weights were observed
in both sexes at doses above the LOAEL in rats and dogs.  Increased
absolute and relative liver weights were seen in both sexes of the mouse
at lower doses.  However, the increases in liver weights at these lower
doses in the mouse were not deemed to be compound related due to the
unusually low concurrent control liver weight values.  At doses above
the LOAELs, liver weight increases were supported by histopathology
alterations in the rat and mouse, but not in the dog.  Overall, only
mild toxicity was observed in oral subchronic testing.

In the 28–day repeat dose dermal study, no systemic effects were noted
up to the highest dose tested of 1,000 mg/kg b.w./day.

In a 90–day rat neurotoxicity study, there was no mortality, signs of
clinical toxicity, or adverse effects on food consumption or body weight
at any dose level in either sex.  No signs of neurotoxicity were
observed during clinical observations, functional observation batteries,
motor activity measurements of neuropathology.  Therefore, there were no
selective neurotoxic effects.  Adverse effects were not seen even at the
highest dose level tested.  A LOAEL was not found and the NOAEL is the
highest tested of 15,000 ppm (1,050 mg/kg b.w./day in males; 1,272 mg/kg
b.w./day in females).]

. [Based on review of the available data, the Reference Dose (RfD) for
BAS 510F will be based on a 1-year feeding study in dogs with a  NOAEL
of  21.8 mg/kg b.w./day.  Using an uncertainty factor of 100, the RfD is
calculated to be 0.218 mg/kg b.w./day.  The following are summaries of
chronic toxicity studies submitted to EPA. 

The chronic toxicity/oncogenicity studies with BAS 510F include a
12–month feeding study with Beagle dogs, an 18–month B63CF1 mouse
feeding study, a 24–month Wistar rat chronic feeding study and a
24–month Wistar rat oncogenicity study. 

At the highest dose tested in dogs, effects observed consisted primarily
of increased liver and thyroid weights and some serum clinical chemistry
changes.  The NOAEL was 800 ppm (21.8 mg/kg b.w./day males; 22.1 mg/kg
b.w./day females).

Decreased body weights were seen in males in the mouse chronic study at
doses of 8000 ppm (1804 mg/kg b.w./day) and above.  Decreased female
body weight was seen at doses of 2,000 ppm (331 mg/kg b.w./day) and
above.  The target organ in this study was the liver.  The NOAEL was 65
and 443 mg/kg b.w./day (8000 and 2000 ppm) for male and female mice,
respectively.  In both the rat chronic and oncogenicity studies, the
highest dose tested of 15,000 ppm exceeded a maximum tolerated dose
(MTD) and was discontinued after 17 months.  Effects observed at the
next highest dose of 2,500 ppm primarily centered around the thyroid and
liver.  The NOAEL was 23 and 30 mg/kg b.w./day (2500 ppm) for male and
female rats, respectively.

Overall, mild toxicity was observed with chronic exposure to BAS 510F. 
No evidence of treatment-induced oncogenicity was observed in the mouse
or dog studies.  A slight increase in thyroid follicular cell adenomas
was seen in both sexes at the high dose when the data from both rat
bioassays are combined.

	A mode of action (MOA) for the thyroid follicular cell adenomas has
been proposed. This MOA is based on the EPA publication “Assessment of
Thyroid Follicular Cell Tumors,” March 1998, EPA/630/R–97/002.  This
document describes the criteria which must be met in order for a
compound to be considered under the MOA described in that

publication.  BASF Corporation believes that BAS 510F has met the cited
criteria.

Threshold effects.  Based on a review of the available chronic toxicity
data, BASF believes EPA will establish the RfD for BAS 510F at 0.281
mg/kg b.w./day.  This RfD for BAS 510F is based on the 2–year chronic
and 2–year oncogenicity studies in rats and the 1 year dog study with
a the lowest threshold NOAEL of 21.8 mg/kg b.w./day for males.  Using an
uncertainty factor of 100, the RfD is calculated to be 0.218 mg/kg
b.w./day.  Based on the acute toxicity data, BASF believes that BAS 510F
does not pose any acute dietary risks.

BAS 510F was shown to be noncarcinogenic in mice and dogs.  There was a
slight increase in thyroid follicular cell ademonas at the high dose in
both sexes in the rat.  A threshold based MOA for these tumors based on
the EPA publication “Assessment of Thyroid Follicular Cell Tumors”
(EPA/630/R–97/002, March, 1998), has been proposed.  BASF believes the
data to support this proposed mode of action are strong, and that the
thyroid tumors seen in the rat following BAS 510F exposure have a
threshold.  In addition, a battery of genotoxicity studies demonstrated
that BAS 510F has no genotoxic or clastogenic potential.  Therefore,
BASF believes that the threshold approach to regulating BAS 510F is
appropriate.  Also, it should be noted that, while the Agency has in the
past considered tumors of this type to be potential human carcinogens,
the European Union has published a policy which considers these tumor
types, when they occur at low incidence rates in the rat, to not be
relevant to man.  (The publication: European Commission, European
Chemicals Bureau, ECBI/49/99 – Add. 1 Rev. 2; “Draft Summary Record,
Commission Group of Specialized Experts in the fields of
Carcinogenicity, Mutagenicity and Reprotoxicity” Meeting at Arona,
1– 2 September 1999), Therefore, BASF believes that these tumors are
not likely relevant to humans and, if these tumors are to be considered
relevant to humans, the threshold approach to cancer risk assessment is
appropriate.]

. [In the rat, the predominant route of excretion of BAS 510F is fecal
with urinary excretion being minor.  The half-life of BAS 510F is less
than 24 hours.  Saturation of absorption appears to be occurring at the
high dose level. BAS 510F is rapidly and intensively metabolized to a
large number of biotransformation products.  The hydroxylation of the
diphenyl moiety was the quantitatively most important pathway.  Second
most important was the substitution of the Cl of the 2-chloropyridine
part against SH by conjugation with glutathione.  No major differences
were observed.  In hens and goats the residues of concern were
determined to be parent, the hydroxylated metabolite M510 F01
(2-chloro-N-(4'chloro-5-hydroxy-biphenyl-2-yl)nicotinamide), and the
glucuronic acid of the metabolite M510 F02.]

. [No additional studies were required for metabolite toxicology.]

.  [No specific tests have been conducted with BAS 510F to determine
whether the chemical may have an effect in humans that is similar to an
effect produced by a naturally occurring estrogen or other endocrine
effects. However, there were no significant findings in other relevant
toxicity studies (i.e., subchronic and chronic toxicity, teratology and
multi-generation reproductive studies) which would suggest that BAS 510F
produces endocrine related effects.] 

. An assessment was conducted to evaluate the potential risk due to
chronic dietary exposure of the U.S. population and sub-populations to
residues of boscalid.  Tolerance values for boscalid (BAS 510F) have
previously been established and are listed in U.S. 40 CFR § 180.589.   

This analysis included all crops with established boscalid tolerance
values, crops pending tolerance assignment (Belgian Endive 12 ppm),
increased tolerance values (berries, crop group 13 at 8 ppm; cotton,
undelinted seed 1.0 ppm; cotton, gin byproducts 55 ppm) and proposed
tolerances (herbs, fresh at 60 ppm; avocado at 1.5 ppm; mango, papaya,
black sapote, mamey sapote, canistel, sapodilla, star apple at 1.5 ppm).

.  

Acute Dietary Exposure Assessment

An acute assessment was not needed since the U.S. EPA Toxicological
Endpoint Selection (TES) Committees had previously evaluated the
boscalid toxicity data and determined there were no toxic effects
attributable to a single dose.  Therefore, a quantitative acute dietary
exposure and risk assessment were not required. 

Chronic Dietary Exposure Assessment

A Tier 1 chronic dietary exposure assessment was conducted assuming
tolerance level residues, default processing factors, 100% crop treated
factors for all crops and consumption data 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.  Residues in animal
commodities (i.e. meat, meat byproducts, fat, milk, eggs) were included
at the tolerance levels currently established and listed in U.S. 40 CFR
§ 180.589.  

Dietary exposure estimates were compared against the established
boscalid chronic Population Adjusted Dose (cPAD) of 0.218 mg/kg b.w./day
for all populations.  Results of the chronic dietary assessments are
listed in the Table 1.  The estimated chronic dietary exposure from
crops and animal commodities was less than 32 % of the cPAD for all
subpopulations.  Additional refinements such as the use of anticipated
residues and adjusted crop treated factors would further reduce the
estimated chronic dietary exposure.  The results in Table 1 demonstrate
there are no safety concerns for any subpopulation based on established
and new uses, and the results clearly meet the FQPA standard of
reasonable certainty of no harm.

 

Table 1.  Summary of Chronic Dietary Exposure Assessment 

Considering Crops with Established and Proposed Tolerances

for Boscalid

Population

Subgroups	Exposure Estimate

(mg/kg b.w./day)	%cPAD

U.S. Population	0.020205	9.3

All Infants	0.046646	21.4

Children 1-2 years	0.067399	30.9

Children 3-5 years	0.047358	21.7

Children 6-12 years	0.024632	11.3

Youth 13-19 years	0.013956	6.4

Females 13-49 years	0.015654	7.2

Adults 20-49 years	0.015436	7.1

Adults 50+ years	0.016902	7.8

%cPAD = percent of chronic population adjusted dose 

Exposure estimates based on tolerance values, default processing 

	

.  

Based on PRZM/EXAMS and SCI-GROW models, the estimated drinking water
exposure concentrations of boscalid for chronic exposure were 26 ppb for
surface water and 0.63 ppb for ground water.  Drinking water
contributions were assessed based on the maximum estimated boscalid
water concentrations (26 ug/L), and water consumption and body weights
reported in CSFII, using DEEM-FCID software.  The chronic estimated
water exposure values are summarized in Table 2.  Minimal exposure of
boscalid occurs through drinking water with < 1.0% cPAD for all
subpopulations.

Table 2. 	Results for Boscalid Chronic Water Exposure Analysis
Considering the Maximum Estimated Chronic Drinking Water Concentration
using 

DEEM-FCID 

Population	Water Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.000548	0.3

All Infants (< 1 year old)	0.001797	0.8

Children (1-2 years old)	0.000814	0.4

Children (3-5 years old)	0.000762	0.3

Children (6-12 years old)	0.000525	0.2

Youth (13-19 years old)	0.000396	0.2

Females (13-49 years old)	0.000510	0.2

Adults (20-49 years old)	0.000512	0.2

Adults (50+ years old)	0.000538	0.2

cPAD = chronic  population adjusted dose

Based on estimated acute surface water value of 26 ug/L

Acute Aggregate Exposure and Risk (Food and water)

Since the U.S. EPA Toxicological Endpoint Selection (TES) Committees has
evaluated the Boscalid toxicity data and determined there was no
toxicological endpoints for acute dietary exposure, the determination of
an acute aggregate exposure and risk evaluation was not required.  

Short- and Intermediate Term Aggregate Exposure and Risk (food,water,
and residential)

Short- and intermediate-term aggregate exposure takes into account
residential exposure plus chronic exposure from food and water. 
Residential exposure is used to refer to non-occupational and
non-dietary exposure.  No new residential uses are currently being
registered for boscalid that would increase non-dietary exposure.  The
residential exposure value used in this risk assessment was previously
determined by the EPA (Federal Register, Volume 68, No 146, July 30,
2003) and considers dermal exposure to adults from the golf course use. 
 The MOE presented in the Table 3 is considered to be representative for
youth playing golf because youth and adults possess similar body surface
area to weight rations and because the dietary exposure for youth (13-19
years old) is less than that of the general US population.    

Table 3. 	Estimated Short/Intermediate Term Aggregate Exposure and Risk
of Boscalid  

Population	NOAEL (mg/kg/day)	Target MOE1	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Residential Exposure2 (mg/kg/day)	Total Exposure
(mg/kg/day)	MOE3

US	21.8	100	0.020205	0.000548	0.0008	0.021553	1011

1 Target MOE is 100.

2  Residential Exposure = Exposure to adult while playing golf.

3 Aggregate MOE = (NOAEL / (Food + Water + Residential Exposure)

 Chronic Aggregate Exposure and Risk (food and water) 

The aggregate chronic risk includes residues of boscalid from food and
water (Table 4). 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 established and new uses,
and that the results clearly meet the FQPA standard of reasonable
certainty of no harm. 

  Table 4. 	Estimated Chronic Aggregate Exposure and Risk of Boscalid 

Population Subgroup	cPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% cPAD

U.S. Population	0.218	0.020205	0.000548	0.020753	9.52

All Infants (< 1 yr old)	0.218	0.046646	0.001797	0.048443	22.22

Children 1-2 years	0.218	0.067399	0.000814	0.068213	31.29

Children 3-5 years	0.218	0.047358	0.000762	0.04812	22.07

Children 6 – 12 years	0.218	0.024632	0.000525	0.025157	11.54

Youth 13-19 years	0.218	0.013956	0.000396	0.014352	6.58

Females 13-49 years	0.218	0.015654	0.00051	0.016164	7.41

Adults 20-49 years	0.218	0.015436	0.000512	0.015948	7.32

Adults + 50	0.218	0.016902	0.000538	0.01744	8.00



	Section 408(b)(2)(D)(v) requires that, when considering whether to
establish, modify, or revoke a tolerance, the Agency consider
‘‘available information’’ concerning the cumulative effects of a
particular pesticide’s residues and ‘‘other substances that have a
common mechanism of toxicity.’’ BAS 510F510F is a foliar fungicide
chemically belonging to the carboxin class of fungicides. BAS 510F510F
acts in the fungal cell by inhibiting mitochondrial respiration through
inhibition of the succinate-ubiquinone oxidase reductase system in
Complex II of the mitochondrial electron transport chain. BAS 510F510F
shares this mode of action with only one other currently registered U.S.
pesticide - carboxin. 

The EPA is currently developing methodology to perform cumulative risk
assessments. At this time, there is no available data to determine
whether BAS 510F510F has a common mechanism of toxicity with other
substances or how to include this pesticide in a cumulative risk
assessment. Unlike other pesticides for which EPA has followed a
cumulative risk approach based on a common mechanism of toxicity, BAS
510F510F does not appear to produce a toxic metabolite produced by other
substances.

E. Safety Determination

.  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 pyraclostrobin residues.

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