[Federal Register: April 7, 2004 (Volume 69, Number 67)]
[Rules and Regulations]
[Page 18263-18275]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr07ap04-6]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[OPP-2003-0296; FRL-7339-4]
Fosthiazate; Pesticide Tolerance
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: This regulation establishes a tolerance for combined residues
of
[[Page 18264]]
fosthiazate (O-ethyl S-(1-methylpropyl)(2-oxo-3-
thiazolidinyl)phosphonothioate and its metabolite O-ethyl S-(1-
methylpropyl)[2-(methylsulfonyl)ethyl] phosphoramidothioate (ASC-67131)
in or on tomato. ISK Biosciences requested this tolerance under the
Federal Food, Drug, and Cosmetic Act (FFDCA), as amended by the Food
Quality Protection Act of 1996 (FQPA). This tolerance will support the
use of fosthiazate on tomatoes as a replacement for methyl bromide for
the control of nematodes.
DATES: This regulation is effective April 7, 2004. Objections and
requests for hearings, identified by docket ID number OPP-2003-0296,
must be received on or before June 7, 2004.
ADDRESSES: Written objections and hearing requests may be submitted
electronically, by mail, or through hand delivery/courier. Follow the
detailed instructions as provided in Unit VI. of the SUPPLEMENTARY
INFORMATION.
FOR FURTHER INFORMATION CONTACT: Rita Kumar, Registration Division
(7505C), Office of Pesticide Programs, Environmental Protection Agency,
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone
number: (703) 308-8291; e-mail address: kumar.rita@epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this Action Apply to Me?
You may be potentially affected by this action if you are an
agricultural producer, food manufacturer, or pesticide manufacturer.
Potentially affected entities may include, but are not limited to:
Crop production (NAICS 111)
Animal production (NAICS 112)
Food manufacturing (NAICS 311)
Pesticide manufacturing (NAICS 32532)
This listing is not intended to be exhaustive, but rather provides
a guide for readers regarding entities likely to be affected by this
action. Other types of entities not listed in this unit could also be
affected. The North American Industrial Classification System (NAICS)
codes have been provided to assist you and others in determining
whether this action might apply to certain entities. If you have any
questions regarding the applicability of this action to a particular
entity, consult the person listed under FOR FURTHER INFORMATION
CONTACT.
B. How Can I Get Copies of this Document and Other Related Information?
1. Docket. EPA has established an official public docket for this
action under docket identification (ID) number OPP-2003-0296. The
official public docket consists of the documents specifically
referenced in this action, any public comments received, and other
information related to this action. Although a part of the official
docket, the public docket does not include Confidential Business
Information (CBI) or other information whose disclosure is restricted
by statute. The official public docket is the collection of materials
that is available for public viewing at the Public Information and
Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall 2,
1921 Jefferson Davis Hwy., Arlington, VA. This docket facility is open
from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal
holidays. The docket telephone number is (703) 305-5805.
2. Electronic access. You may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr/ A frequently updated electronic version of 40 CFR part 180 is available at http://.
http://www.access.gpo.gov/nara/cfr/cfrhtml_00/Title_40/40cfr180_00.html, a
beta site currently under development. To access the OPPTS Harmonized
Guidelines referenced in this document, go directly to the guidelines
at http://www.epa.gov/opptsfrs/home/guidelin.htm.
An electronic version of the public docket is available through
EPA's electronic public docket and comment system, EPA Dockets. You may
use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public
comments, access the index listing of the contents of the official
public docket, and to access those documents in the public docket that
are available electronically. Although not all docket materials may be
available electronically, you may still access any of the publicly
available docket materials through the docket facility identified in
Unit I.B.1. Once in the system, select ``search,'' then key in the
appropriate docket ID number.
II. Background and Statutory Findings
In the Federal Register of November 21 2001 (66 FR 58477) (FRL-
6799-1), EPA issued a notice pursuant to section 408 of FFDCA, 21
U.S.C. 346a, as amended by FQPA (Public Law 104-170), announcing the
filing of a pesticide petition (PP 6F4662) by ISK Biosciences
Corporation, 7470 Auburn Road, Suite A, Concord, OH 44077. That notice
included a summary of the petition prepared by ISK Biosciences, the
registrant. There were no comments received in response to the notice
of filing.
The petition requested that 40 CFR part 180 be amended by
establishing a tolerance for combined residues of the insecticide
fosthiazate, (O-ethyl S-(1-methylpropyl)(2-oxo-3-
thiazolidinyl)phosphonothioate) and its metabolite ASC-67131 (O-ethyl
S-(1-methylpropyl)[2-(methylsulfonyl)ethyl] phosphoramidothioate), in
or on tomatoes at 0.02 parts per million (ppm). Fosthiazate is a new
organophosphate (OP) active ingredient (a.i.), that controls a broad
spectrum of nematode species. It may be applied through drip (trickle)
irrigation systems, as a band application under plastic mulch.
Application is made once per season, either prior to or at planting/
transplanting of tomatoes. The United States Department of
Agriculture's Interregional Research Project No. 4 has identified
fosthiazate as a viable alternative to the use of methyl bromide for
control of nematodes infesting tomato fields. Methyl bromide has been
identified as a chemical that depletes the earth's ozone layer, and
thus its use is being phased out. The United States is in the process
of implementing a methyl bromide use reduction strategy leading to a
complete ban for soil fumigation uses by the year 2005. Fosthiazate
will provide growers with a pest management tool for use against
nematode pest pressure.
Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a
tolerance (the legal limit for a pesticide chemical residue in or on a
food) only if EPA determines that the tolerance is ``safe.'' Section
408(b)(2)(A)(ii) of the FFDCA defines ``safe'' to mean that ``there is
a reasonable certainty that no harm will result from aggregate exposure
to the pesticide chemical residue, including all anticipated dietary
exposures and all other exposures for which there is reliable
information.'' This includes exposure through drinking water and in
residential settings, but does not include occupational exposure.
Section 408(b)(2)(C) of the FFDCA requires EPA to give special
consideration to exposure of infants and children to the pesticide
chemical residue in establishing a tolerance and to ``ensure that there
is a reasonable certainty that no harm will result to infants and
children from aggregate exposure to the pesticide chemical residue. . .
.''
EPA performs a number of analyses to determine the risks from
aggregate exposure to pesticide residues. For
[[Page 18265]]
further discussion of the regulatory requirements of section 408 of the
FFDCA and a complete description of the risk assessment process, see
the final rule on Bifenthrin Pesticide Tolerances (62 FR 62961,
November 26, 1997) (FRL-5754-7).
III. Aggregate Risk Assessment and Determination of Safety
Consistent with section 408(b)(2)(D) of the FFDCA, EPA has reviewed
the available scientific data and other relevant information in support
of this action. EPA has sufficient data to assess the hazards of and to
make a determination on aggregate exposure, consistent with section
408(b)(2) of the FFDCA, for a tolerance for combined residues of the
insecticide fosthiazate, (O-ethyl S-(1-methylpropyl)(2-oxo-3-
thiazolidinyl)phosphonothioate) and its metabolite ASC-67131 (O-ethyl
S-(1-methylpropyl)[2-(methylsulfonyl)ethyl] phosphoramidothioate) on
tomatoes at 0.02 ppm. EPA's assessment of exposures and risks
associated with establishing the tolerance follows.
A. Toxicological Profile
EPA has evaluated the available toxicity data and considered its
validity, completeness, and reliability as well as the relationship of
the results of the studies to human risk. EPA has also considered
available information concerning the variability of the sensitivities
of major identifiable subgroups of consumers, including infants and
children. The nature of the toxic effects caused by fosthiazate are
discussed in Table 1 of this unit as well as the no observed adverse
effect level (NOAEL) and the lowest observed adverse effect level
(LOAEL) from the toxicity studies reviewed.
Table 1.--Subchronic, Chronic, and Other Toxicity
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Guideline No. Study Type Results
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870.3100 13-Week feeding study-rat Systemic Toxicity LOAEL: 0.08 and 0.09 mg/
kg/day for males and females,
respectively, based on microscopic lesions
in the adrenals (males) and increased ALT
(females) levels. No NOAEL was
established. At higher doses, the severity
of vacuolation of cells in zona
fasciculata (=1.07 ppm) and
zona glomerulosa (=53.6 ppm) of
the adrenals increased in a dose-dependent
manner; at =53.6 ppm, the brain
cholinesterase inhibition (ChEI) was also
noted. In addition, there was increase in
adrenal gland weight at 429 ppm
LOAEL for ChEI: 10.7 ppm (0.77 and 0.89 mg/
kg/day for males and females,
respectively) based on plasma and RBC
ChEI.
NOAEL: 1.07 ppm (0.08 and 0.09 mg/kg/day
for males and females, respectively)
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-- 4-Week range-finding Systemic LOAEL: 400 ppm (equivalent to
feeding study-rat 40.87 mg/kg/day in males and 43.52 mg/kg/
day in females) based on fur loss, muscle
tremor, enlarged pale spongiocytes in the
adrenals, increased adrenal weights, and
increased alkaline phosphatase and alanine
aminotransferase levels.
Systemic NOAEL: 100 ppm (equivalent to 9.69
mg/kg/day in males and 10.67 mg/kg/day in
females)
LOAEL for ChEI: 5 ppm (equivalent to 0.48
mg/kg/day in males and 0.5 mg/kg/day in
females) based on decreased plasma butyryl-
and acetyl-cholinesterase, and brain
acetyl-cholinesterase in females, and
erythrocyte acetyl-cholinesterase in males
NOAEL: 1 ppm (equivalent to 0.10 mg/kg/day
in males and females
----------------------------------------------------------------------------------------------------------------
-- 28-Day feeding study-rat NOAEL: 1,000 mg/kg/day, the highest dose
with 2-butanesulfonic tested.
acid (BSA)
----------------------------------------------------------------------------------------------------------------
-- 4-Week range-finding LOAEL: 400 ppm (males: 68.99 and females:
feeding study-mice 82.38 mg/kg/day) based on increased
tubular basophilia in the kidney
NOAEL: 100 ppm (equivalent to 17.59 mg/kg/
day in males and 21.43 mg/kg/day in
females)
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870.3150 13-Weeks subchronic Systemic Toxicity
toxicity-dog LOAEL: 0.11 mg/kg/day, based on
histopathological changes in the adrenal
glands
NOAEL: 0.054 mg/kg/day
LOAEL for plasma ChEI: 0.11 mg/kg/day in
females and 0.54 mg/kg/day in males
NOAEL: 0.054 mg/kg/day in females and 0.11
mg/kg/day in males.
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[[Page 18266]]
870.3200 21-Day repeated dermal Systemic LOAEL: 250 mg/kg/day for males and
toxicity-rat females based on mortality, clinical signs
(emaciation, torpor lethargy or dullness,
tremor, hunched posture, hypothermia,
gasping, hypersensitivity to noise, pallor
paleness, tachypnea labored breathing, and
piloerection), decreased body weight
gains, and histopathology of the adrenal
cortex observed in both sexes; increased
food conversion factor and hematology
findings were observed in males only
Systemic NOAEL: 25 mg/kg/day
LOAEL for ChEI: 25 mg/kg/day in males and
2.5 mg/kg/day in females based on
inhibition of plasma, erythrocyte, and
brain cholinesterase (ChE) in both sexes
NOAEL for ChEI: 2.5 mg/kg/day in males and
0.5 mg/kg/day in females
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870.3700 Developmental toxicity-rat Maternal Toxicity
LOAEL = 10 mg/kg/day, based on reduced body
weight gain
NOAEL = 5 mg/kg/day
Developmental Toxicity
LOAEL = Not determined
NOAEL = 10 mg/kg/day
Although data were not provided on clinical
signs in the dams during or after dosing
no cholinergic signs were seen in
neurotoxicity studies at the same dose.
Therefore, the study classification is
upgraded to acceptable/guideline
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870.3700 Developmental toxicity- Maternal
rabbit LOAEL: 2 mg/kg/day based on weight loss,
abortion, and cholinergic clinical signs
noted in the range finding study (MRID
41381110)
NOAEL: 1.5 mg/kg/day.
Developmental toxicity
LOAEL: Not determined
NOAEL: 2 mg/kg/day
No developmental toxicity was observed at
any dose tested in the definitive prenatal
developmental toxicity study. No
developmental toxicity was observed at
doses up to 2.5 mg/kg in a range-finding
study
----------------------------------------------------------------------------------------------------------------
870.3800 2-Generation reproduction- Parental Toxicity
rat LOAEL = 100 ppm (equivalent to 9.32 and
7.21 mg/kg/day in females, and males,
respectively) based on increased
incidences of adrenal zona glomerulosa
hypertrophy, centriacinar hepatocytic
vacuolation and liver inflammation in F0
females and periacinar hepatocytic
hypertrophy in F0 males
NOAEL: 30 ppm (equivalent to 2.6 and 2.09
mg/kg/day) in females and males,
respectively). in F0 females and in males
Reproductive Toxicity
LOAEL = >100 ppm
NOAEL = 100 ppm
Offspring Toxicity
LOAEL = 30 ppm based on decreased litter
size and decreased pup weight and
viability index during lactation
NOAEL = 10 ppm
----------------------------------------------------------------------------------------------------------------
870.4100 1-Year chronic oral Systemic LOAEL: 0.5 mg/kg/day in males
toxicity-dog based on increased alanine
aminotransferase and 5 mg/kg/day in
females based on microscopic lesions in
the adrenal gland
NOAEL: 0.1 mg/kg/day in males and 0.5 mg/kg/
day in females
LOAEL for ChEI: 0.5 mg/kg/day based on
plasma acetyl- and butyryl-cholinesterase
activity in males/females
NOAEL: 0.1 mg/kg/day based on plasma acetyl-
and butyryl-cholinesterase activity
The erythrocyte and brain ChE activity
LOAELs were not observed. The erythrocyte
and brain cholinesterase NOAELs are 5 mg/
kg/day
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[[Page 18267]]
870.4200 Carcinogenicity-mouse Systemic LOAEL: 10.43 mg/kg/day (100 ppm)
for females, based on increased adrenal
cortico-medullary pigmentation and 30.51
mg/kg/day (300 ppm) for males, based on
decreased body weights and non-neoplastic
lesions in the adrenals, pituitary and
kidney. At 300 ppm, increase in
cholinergic signs (ataxia, hunched
posture, tremors) was observed
NOAEL: 3.20 mg/kg/day (30 ppm) and 10.32 mg/
kg/day (100 ppm) for females and males,
respectively. The test material was not
carcinogenic at the doses tested
----------------------------------------------------------------------------------------------------------------
870.4300 Combined chronic/ Systemic
carcinogenicity-rat LOAEL: 50 ppm (2.45 mg/kg/day) for females,
based on decreased RBC parameters (packed
cell volume, hemoglobin, and RBC count),
and increased incidence of atrophy and
foamy interstitial cells in the ovaries
and 200 ppm (8.34 mg/kg/day) for males,
based on increased incidences of retinal
atrophy, skeletal degenerative myopathy
and non-neoplastic lesions in the adrenal
and pituitary glands
NOAEL: 10 ppm (0.50 mg/kg/day) and 50 ppm
(1.94 mg/kg/day) for female and male rats,
respectively. The test material was not
carcinogenic at the doses tested
LOAEL for ChEI: 10 ppm for male rats (0.38
mg/kg/day) and 1 ppm for female rats
(0.051 mg/kg/day) based on inhibition of
plasma and RBC ChE activity
NOAEL: 1 ppm for male rats (0.039 mg/kg/
day) and a NOAEL was not established for
female rats
----------------------------------------------------------------------------------------------------------------
870.5100 Gene mutation salmonella/ Negative in salmonella strains with or
mammalian activation gene without S-9 activation. No cytotoxicity
mutation assay with BSA response up to the limit dose
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870.5265 Gene mutation salmonella/ Negative for mutagenic effects at dose
mammalian activation gene levels up to 5,000 [mu]g/plate with or
mutation assay without metabolic activation
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870.5300 In vitro gene mutation- No evidence of increased mutation frequency
mouse lymphoma assay at the thymidine locus in cells treated
upto cytotoxic concentration with or
without S-9. Cytotoxicity was evident at
=640 [mu]g/ml (-S9) and =160 [mu]g/mL (+S9)
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870.5300 In vitro mammalian gene No evidence of increased mutation frequency
mutation - mouse lymphoma in cells treated up to the limit dose with
assay with BSA or without S-9
----------------------------------------------------------------------------------------------------------------
870.5375 In vitro cytogenetics No effects at concentrations up to 200
(CHO) assay [mu]g/ml (without S9) or 750 [mu]g/mL
(with S9). Cytotoxicity was evident at =50 [mu]g/mL (-S9)and =93.75 [mu]g/mL (+S9)
----------------------------------------------------------------------------------------------------------------
870.5395 In vivo mammalian No evidence of clastogenic or aneugenic
cytogenetics assay effect at doses tested. Negative for
induction of micronuclei at a dose
approaching oral MTD, 50 mg/kg
----------------------------------------------------------------------------------------------------------------
870.5395 In vivo mammalian No evidence of clastogenic or aneugenic
cytogenetics micronucleus effect at doses tested. Negative for
assay with BSA induction of micronuclei
----------------------------------------------------------------------------------------------------------------
870.5500 In vitro DNA repair test Negative in the DNA repair test.
Fosthiazate did not induce any clear
differences in the diameter of growth
inhibitory zones between H17 (rec+) and M
45 (rec-), either in the presence or
absence of metabolic activation
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870.6100 Acute delayed Six hens treated with IKI-1145 (fosthiazate
neurotoxicity (ADNT) technical) died within 6 days; 2 had
study-hen relapses and progressed to moribundity on
days 13 and 26; 9 hens survived. No
abnormal neuropathological changes were
observed except for a minimal case of
focal gliosis in the lumbar sacral area of
one of the two relapsing hens. IKI-1145
did not cause ADNT
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[[Page 18268]]
870.6200 Acute neurotoxicity Neurotoxicity
screening battery LOAEL: 10 mg/kg/day based on decreased
forelimb grip strength in females. No
abnormal neuropathological changes were
observed
NOAEL: 0.4 mg/kg/day
LOAEL for ChEI: 10 mg/kg/day based on
inhibition of plasma. Erythrocyte, and
brain 3 hrs postdosing (plasma ChEI was
reversible)
NOAEL: 0.4 mg/kg/day
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-- Special cholinesterase LOAEL: 4.0 mg/kg/day based on plasma ChEI
inhibition study-rat NOAEL: 0.4 mg/kg/day
Decrease plasma ChE activity was noted in
the male and female rats 3 hours after a
single dose at 4.0 mg/kg body weight.
Brain and RBC ChE activities were
unaffected
----------------------------------------------------------------------------------------------------------------
870.6200 Subchronic neurotoxicity Systemic
screening battery LOAEL: 2.5 mg/kg/day based on decreased
hind limb grip strength (21%; p<0.01) in
females. No abnormal neuropathological
changes were observed
NOAEL: 0.5 mg/kg/day.
LOAEL for ChEI: 0.5 mg/kg/day based on
significant inhibition of plasma,
erythrocyte and brain ChE in females at
weeks 5 and/or 9 and 14
NOAEL: 0.05 mg/kg/day
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870.7485 Metabolism-rat IKI-1145 (fosthiazate technical) was
rapidly absorbed and widely distributed
with only >5% detected in the tissues. No
sex-related differences noted in the
absorption and distribution; absorption
was not dose dependent. Peak concentration
in the blood was at 0.33 hr in both sexes.
Only one metabolite, BESxP, represented
>10% of the administered dose. Test
material was rapidly eliminated primarily
in the urine (57%-72%) within 24 hrs.
Unacceptable/Guideline due to lack of
identification of metabolites in fecal
radioactivity (accounted for 9-15% of the
administered dose). Mean recovery was 95%-
99%. IKI-1145 was metabolized by multiple
processes including hydrolysis, oxidation,
methylation and glutathione conjugation
----------------------------------------------------------------------------------------------------------------
870.7485 Metabolism-rat IKI-1145 was rapidly and extensively
absorbed independent of dose; rapidly
metabolized and excreted in the urine
(>65%), expired air (>10%) and in feces
(<9%). Elimination was biphasic with first
phase elimination half-life (t1/2) of 5-6
hrs and second phase of 85-112 hrs.
Metabolism and excretion was rapid within
24 hrs. IKI-1145 was metabolized by
multiple processes including hydrolysis,
oxidation, methylation and glutathione
conjugation. Female rats tended to excrete
a metabolite containing a
methylsulfinylethyl group while male rats
excreted more containing a sulfoethyl
group
----------------------------------------------------------------------------------------------------------------
870.7485 Metabolism-rat with BSA Recovery was 100-108%. BSA was rapidly
eliminated unchanged following dosing via
the iv (approx. 100% in the urine) or oral
(63%-89% in the urine and 10%-28% in
feces) routes. Tissue burden was low
----------------------------------------------------------------------------------------------------------------
B. Toxicological Endpoints
The dose at which no adverse effects are observed (the NOAEL) from
the toxicology study identified as appropriate for use in risk
assessment is used to estimate the toxicological level of concern
(LOC). However, the lowest dose at which adverse effects of concern are
identified (the LOAEL) is sometimes used for risk assessment if no
NOAEL was achieved in the toxicology study selected. An uncertainty
factor (UF) is applied to reflect uncertainties inherent in the
extrapolation from laboratory animal data to humans and in the
variations in sensitivity among members of the human population as well
as other unknowns. An UF of 100 is routinely used, 10X to account for
interspecies differences and 10X for intraspecies differences. Based on
the weight of evidence presented, the Agency concluded that a
developmental neurotoxicity (DNT) study with comparative cholinestrase
(ChE) measurements in adults and pups is required for fosthiazate. The
available data base confirms that fosthiazate is a ChE inhibitor and
the increased sensitivity for this effect cannot be confirmed until the
results of DNT study are known. Based on the lack of a DNT study, the
Agency also concluded that a Database Uncertainty Factor (UFdb) is
necessary. The available data suggest that results of a DNT study, as
well as additional ChE data, could potentially impact the doses
selected for risk assessment. Therefore, a 10X UFdb is required for
acute dietary risk assessment and a 3X UFdb is required for chronic
dietary risk assessment. Refer to Unit III.D.3 of this document for a
detailed discussion of these uncertainty factors.
For dietary risk assessment (other than cancer) the Agency uses UF
to calculate an acute or chronic reference dose (acute RfD or chronic
RfD) where the RfD is equal to the NOAEL divided by the appropriate UF
(RfD = NOAEL/UF). Where an additional safety factor (SF) is retained
due to concerns unique to the FQPA, this additional factor is applied
to the RfD by dividing the RfD by such additional factor. The acute or
[[Page 18269]]
chronic Population Adjusted Dose (aPAD or cPAD) is a modification of
the RfD to accommodate this type of FQPA SF.
For non-dietary risk assessments (other than cancer) the UF is used
to determine the LOC. For example, when 100 is the appropriate UF (10X
to account for interspecies differences and 10X for intraspecies
differences) the LOC is 100. To estimate risk, a ratio of the NOAEL to
exposures (margin of exposure (MOE) = NOAEL/exposure) is calculated and
compared to the LOC.
The linear default risk methodology (Q*) is the primary method
currently used by the Agency to quantify carcinogenic risk. The Q*
approach assumes that any amount of exposure will lead to some degree
of cancer risk. A Q* is calculated and used to estimate risk which
represents a probability of occurrence of additional cancer cases
(e.g., risk is expressed as 1 x 10-6 or one in a million).
Under certain specific circumstances, MOE calculations will be used for
the carcinogenic risk assessment. In this non-linear approach, a
``point of departure'' is identified below which carcinogenic effects
are not expected. The point of departure is typically a NOAEL based on
an endpoint related to cancer effects though it may be a different
value derived from the dose response curve. To estimate risk, a ratio
of the point of departure to exposure (MOEcancer = point of
departure/exposures) is calculated. A summary of the toxicological
endpoints for fosthiazate used for human risk assessment is shown in
Table 2 of this unit:
Table 2.--Summary of Toxicological Dose and Endpoints for Fosthiazate for Use in Human Risk Assessment
----------------------------------------------------------------------------------------------------------------
Hazard and Exposure
Exposure Scenario Dose (mg/kg/day) UF/MOE Based Special FQPA Study and Toxicological
Safety Factor Effects
----------------------------------------------------------------------------------------------------------------
Dietary risk assessments
-----------------------------------------------------------------------------------------
Acute dietary (general population NOAEL = 0.4 1X Acute oral
including infants and children) UF = 100............... neurotoxicity/rat
UFdb* = 10............. LOAEL = 10 mg/kg/day
based on inhibition of
RBC ChE in males
within 3 hrs post
dosing
---------------------------------------------------
Acute RfD and Acute PAD = 0.0004 mg/kg/day
-----------------------------------------------------------------------------------------
Chronic dietary NOAEL = 0.05 1X Chronic oral toxicity/
UF = 100............... rat
UFdb* = 3.............. LOAEL= 0.38 mg/kg/day
based on inhibition of
plasma and RBC ChE in
males
---------------------------------------------------
Chronic RfD and Chronic PAD = 0.00017 mg/kg/day
----------------------------------------------------------------------------------------------------------------
* UFdb = database uncertainty factors of 10X and 3X are applied for lack of a DNT study and ChE data
C. Exposure Assessment
1. Dietary exposure from food and feed uses. Currently there are no
tolerances established for fosthiazate on any commodity. Risk
assessments were conducted by EPA to assess dietary exposures from
fosthiazate in food as follows:
i. Acute exposure. Acute dietary risk assessments are performed for
a food-use pesticide if a toxicological study has indicated the
possibility of an effect of concern occurring as a result of a one day
or single exposure. The Dietary Exposure Evaluation Model
(DEEMTM) analysis evaluated the individual food consumption
as reported by respondents in the USDA 1994-1996 and 1998 nationwide
Continuing Surveys of Food Intake by Individuals (CSFII) and
accumulated exposure to the chemical for each commodity. The following
assumptions were made for the acute exposure assessments: The acute
dietary risk assessment was based on field trial residues in tomato
(1/89/21/13/23/85/83/8 limit of quantitation (LOQ) parent +
1/89/21/13/23/85/83/8 LOQ ASC-67131) and 100% crop treated
(CT). Risks of concern were considered at the 95th percentile because
field trial data with 1.3X application rate, minimum preharvest
interval (PHI) and 100% CT were used, which are considered conservative
inputs. No detectable residues of either the parent or its metabolite
of concern were found in the edible portion during these field trials
at a limit of detection (LOD) of 0.01 ppm using gas chromatograph/flame
photometric detector (GC/FPD) (phosphorus) as an analytical method.
The Agency believes that the default assumption of
1/89/21/13/23/85/83/8 LOD of the GC/FPD (phosphorus)
analytical method for each of the parent and metabolite significantly
exaggerates actual exposures. Radiolabeled tomato metabolism studies
were done at a 1.3X rate and using an analytical method GC/FPD
(phosphorus) with a much lower LOD of 0.001 ppm (an order of magnitude
lower). No residues were found in the edible fruit following the
radiolabel studies. This means that residues, if present, would be
present at <0.001 ppm at this application rate. Thus, the use of
1/89/21/13/23/85/83/8 LOD of the GC/FPD (phosphorus)
analytical method for both parent and metabolite is a conservative
estimate of exposure (compounded by a 100% CT assumption): Radiolabel
metabolism studies suggest that residues are at least five times lower
than the 1/89/21/13/23/85/83/8 LOD of the GC/FPD (phosphorus)
analytical method assumed in the assessment, and even more if one were
to take into account the 1.3X application rate.
ii. Chronic exposure. In conducting this chronic dietary risk
assessment, the DEEMTM analysis evaluated the individual
food consumption as reported by respondents in the USDA 1994-1996 and
1998 nationwide CSFII and accumulated exposure to the chemical for each
commodity. The following assumptions were made for the chronic exposure
assessments: The chronic dietary risk assessment was based on field
trial residues in tomatoes, 100% CT, and average daily consumption
estimates for each food/food form.
iii. Cancer. In accordance with the EPA Draft Guidelines for
Carcinogen Risk Assessment (July 1999), the Agency has classified
fosthiazate as ``not likely to be carcinogenic to humans.'' This
classification is based on the lack of evidence for carcinogenicity in
studies with mice and rats; therefore, a quantitative cancer dietary
assessment has not been conducted.
[[Page 18270]]
2. Dietary exposure from drinking water. The Agency lacks
sufficient monitoring exposure data to complete a comprehensive dietary
exposure analysis and risk assessment for fosthiazate in drinking
water. Because the Agency does not have comprehensive monitoring data,
drinking water concentration estimates are made by reliance on
simulation or modeling taking into account data on the physical
characteristics of fosthiazate.
The Agency uses the First Index Reservoir Screening Tool (FIRST) or
the Pesticide Root Zone/Exposure Analysis Modeling System (PRZM/EXAMS),
to produce estimates of pesticide concentrations in an index reservoir.
The Screening Concentrations in Groundwater (SCI-GROW) model is used to
predict pesticide concentrations in shallow ground water. For a
screening-level assessment for surface water EPA will use FIRST (a Tier
1 model) before using PRZM/EXAMS (a Tier 2 model). The FIRST model is a
subset of the PRZM/EXAMS model that uses a specific high-end runoff
scenario for pesticides. While both FIRST and PRZM/EXAMS incorporate an
index reservoir environment, the PRZM/EXAMS model includes a percent
crop area factor as an adjustment to account for the maximum percent
crop coverage within a watershed or drainage basin.
None of these models include consideration of the impact processing
(mixing, dilution, or treatment) of raw water for distribution as
drinking water would likely have on the removal of pesticides from the
source water. The primary use of these models by the Agency at this
stage is to provide a coarse screen for sorting out pesticides for
which it is highly unlikely that drinking water concentrations would
ever exceed human health levels of concern.
Since the models used are considered to be screening tools in the
risk assessment process, the Agency does not use estimated
environmental concentrations (EECs) from these models to quantify
drinking water exposure and risk as a %RfD or %PAD. Instead drinking
water levels of comparison (DWLOCs) are calculated and used as a point
of comparison against the model estimates of a pesticide's
concentration in water. DWLOCs are theoretical upper limits on a
pesticide's concentration in drinking water in light of total aggregate
exposure to a pesticide in food, and from residential uses. Since
DWLOCs address total aggregate exposure to fosthiazate, they are
further discussed in the aggregate risk sections in Unit E.
Based on the PRZM/EXAMS and SCI-GROW models, the EECs of
fosthiazate for acute exposures are estimated to be 2.1 parts per
billion (ppb) for surface water and 2.4 ppb for ground water. The EECs
for chronic exposures are estimated to be 0.6 ppb for surface water and
2.4 ppb for ground water. These estimates are based on the assumption
that application will be made by drip irrigation in bands with plastic
mulch. Runoff as a result of this use may be unlikely from the day of
application until the day of harvest (approximately 90 days) when the
field is covered by the plastic mulch, unless an extremely heavy amount
of rain falls immediately after application and causes runoff from
under the mulch into the uncovered area. For this reason, application
is prohibited when heavy rainfall is predicted. Runoff after the
removal of the plastic cover may be possible, however the amount of
fosthiazate remaining in soil and available for runoff would be much
less than the amount applied, due to chemical degradation and
dissipation in soil and to chemical uptake into plants. Assuming that
half of the amount applied is absorbed by plants and the remaining half
dissipates in soil at a rate of 45 days (based on laboratory and field
studies), it is expected that only about one eighth of what was
originally applied would be available for runoff after the cover is
removed (90 days postapplication). Maximum application rate is 1.5 lbs
a.i. per acre with only one application per season. Therefore, the
Agency predicts that the peak estimated drinking water concentrations
(EDWC) would be roughly 2.1 [mu]g/L and the chronic EDWC would be 0.6
[mu]g/L for the maximum application rate. These concentrations were
modeled under the most conservative scenarios and likely exceed the
actual level of contamination in the environment. In actual practice,
the same plastic mulch is left in the field for rotated crops, thus
making the EEC calculations based on the mulch being removed after 90
days even more conservative.
SCI-GROW assumes the pesticide is applied above ground without
cover and the subsequent and heavy amount of water (140% of yearly
average amount of rainfall) leaches some of the pesticide down to
ground water. The plastic mulch cover would minimize volatilization and
runoff, therefore increasing the amount of the chemical available for
leaching. However, with the drip irrigation method, a small amount of
water is slowly dripped into soils precisely where it is needed, thus
lessening the amount of water flowing down through the soil past the
root zone where it cannot be used by the crop. This should greatly
reduce the potential for the chemical to reach ground water systems.
For this reason, the Agency does not expect ground water contamination
from the drip irrigation method under plastic mulch to exceed the
levels calculated by the SCI-GROW model. Terrestrial field dissipation
studies indicate no leaching of fosthiazate residues below the top (0-
15 cm) soil layer.
3. From non-dietary exposure. The term ``residential exposure'' is
used in this document to refer to non-occupational, non-dietary
exposure (e.g., for lawn and garden pest control, indoor pest control,
termiticides, and flea and tick control on pets).
Fosthiazate is not registered for use on any sites that would
result in residential exposure.
4. Cumulative exposure to substances with a common mechanism of
toxicity. Section 408(b)(2)(D)(v) of the FFDCA 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.''
Fosthiazate is an OP pesticide, and has a common mechanism of
toxicity with other OPs. The Agency has completed a Revised Cumulative
Risk Assessment (CRA) for OPs, which can be found on the Agency's web
site http://www.epa.gov/pesticides/cumulative. This assessment examined the
cumulative effects of exposure to the OP pesticides considering
monitoring values for OPs in food and water, and potential residential
exposures. The relative potency factor (RPF) for fosthiazate was
determined using the estimated benchmark dose (BMD)10 for female brain
ChE data from feeding toxicity studies in the rat. The BMD10 is the
estimated dose at which ChE is inhibited 10% compared to background
inhibition. Although fosthiazate was considered in the cumulative
hazard and dose-response assessment, it was not included in the OP
cumulative exposure assessment since this OP pesticide (i) is not
monitored by the USDA's Pesticide Data Program (PDP) or other
monitoring data sets used in the cumulative OP assessment and is not
expected to be present in food as a result of its use on tomatoes at
levels that would be detectable by monitoring; (ii) is not expected to
be present in surface water or ground water to a degree that would have
any impact on the data on drinking water residues of
[[Page 18271]]
OPs used in the cumulative risk assessment; and (iii) has no
residential uses. Residue data are available for fosthiazate from crop
field trials conducted with tomatoes in which maximum (label)
application rates and minimum (label) preharvest intervals were used.
No residues were detected in these field trials (<0.01 ppm). Thus, EPA
concludes that there is reasonable expectation that fosthiazate
residues would not be detected in monitoring data from use on tomato.
Further, fosthiazate would not contribute to the total estimated
cumulative dietary risk in the OP cumulative risk assessment since non-
detectable residues in monitoring data were considered to have a
residue value of ``zero.'' None of the OPs in the CRA made a
significant contribution to overall exposure via the drinking water
pathway, and fosthiazate does not look as though it makes a significant
exposure by the water pathway from the use on tomato because of the low
application rate, only one application per season, application method
of drip irrigation under plastic mulch, and no leaching of the compound
below the top soil layer. Accordingly, after considering the cumulative
effects of the OPs, EPA concludes that the overall cumulative risk has
a limited bearing on this tolerance action because fosthiazate exposure
will have no impact on the estimate of cumulative risk for OPs.
D. Safety Factor for Infants and Children
1.In general. Section 408 of the FFDCA provides that EPA shall
apply an additional tenfold margin of safety for infants and children
in the case of threshold effects to account for prenatal and postnatal
toxicity and the completeness of the data base on toxicity and exposure
unless EPA determines that a different margin of safety will be safe
for infants and children. Margins of safety are incorporated into EPA
risk assessments either directly through use of a MOE analysis or
through using uncertainty (safety) factors in calculating a dose level
that poses no appreciable risk to humans.
2. Prenatal and postnatal sensitivity. In a 2-generation
reproduction study, there is qualitative and quantitative evidence of
increased susceptibility in offspring following prenatal and postnatal
exposure to fosthiazate since the effects on pups are considered to be
severe and occurred at a lower dose than those on parental animals.
Since there is evidence of increased susceptibility of the young
following prenatal and postnatal exposure to fosthiazate in the rat
reproduction study, the Agency performed a Degree of Concern Analysis
to: (i) Determine the level of concern for the effects observed when
considered in the context of all available toxicity data; and (ii)
identify any residual uncertainties after establishing toxicity
endpoints and traditional uncertainty factors to be used in the risk
assessment of this chemical.
In determining the degree of concern for these findings in the
reproduction study, the Agency considered the overall quality of the
study; the dose levels at which the pup effects were observed; the dose
response of the pup effects; and the comparative severity of the
effects seen. It was determined that there is a low degree of concern
and no residual uncertainties for the susceptibility since: (i) The
study was well conducted; (ii) the dose-response in the offspring is
well characterized; (iii) clear NOAEL and LOAEL were established for
the effects on the offspring; (iv) although the decrease in pup
survival seen at the LOAEL is severe, this could be attributed to
exposure to higher levels of the chemical since the mortalities
occurred during early lactation; and (v) although cholinesterase
activity was not measured in this study, cholinergic signs and
cholinesterase inhibition were seen at comparable doses in other
studies and thus could have been a cause for the pup mortality.
3. Conclusion. The toxicological data base for fosthiazate is not
complete and therefore, EPA has retained the FQPA safety factor, in the
form of a UFdb, at the level of 10X for acute risk and 3X for chronic
risk. A 28-day inhalation study in rats is required, in order to better
characterize exposure via the inhalation route. A DNT study in rats
with comparative ChE measurements in adults and pups is also required,
and is currently being conducted by the registrant. The available data
base confirms that fosthiazate is a ChE inhibitor and the increased
sensitivity for this effect cannot be confirmed until the results of a
DNT study are known.
A FQPA safety factor, in the form of a Ufdb, was retained because
the available data suggest that results of a DNT study could
potentially impact the doses selected for risk assessment. ChEI has
been shown to be the most sensitive endpoint for fosthiazate in adults;
it can also be assumed that ChEI may potentially be the most sensitive
endpoint for pups. The regulatory dose level for acute dietary risk
assessment is the NOAEL of 0.4 mg/kg/day selected from the acute
neurotoxicity study in adult rats. The regulatory dose level for
chronic dietary risk assessment is the NOAEL of 0.05 mg/kg/day from the
2-year chronic/carcinogenicity toxicity study in rats. The dose levels
in the reproductive toxicity study are estimated to be 0, 0.21, 0.69,
2.09, and 7.21 mg/kg/day. The offspring NOAEL and LOAEL are 0.69 mg/kg/
day and 2.09 mg/kg/day, respectively, based on decreased pup weight,
viability index, and litter size in the F1 pups.
It can be assumed that doses used in a DNT study may be similar to
those used in the reproductive toxicity study. Although it is not
likely given the effects seen to date in the fosthiazate data base, the
results from the DNT may show severe effects at the lowest dose tested
(estimated at 0.21 mg/kg/day). In such circumstances, EPA may impose up
to a 10X safety factor to project a NOAEL for the DNT which would mean
a projected NOAEL of 0.02 mg/kg/day. Thus, the DNT may result in an
acute ChE NOAEL for pups that is greater than 10X lower than the
established offspring NOAEL of 0.69 mg/kg/day and the NOAEL of 0.4 mg/
kg/day currently used for establishing the acute RfD. Given that the
DNT could impact the level chosen for estimating the acute RfD by 10X
or greater, EPA concludes that reliable data do not support removing
the 10X children's safety factor and thus have retained that factor in
the form of a 10X UFdb for acute dietary risk assessment.
As to the chronic RfD, the projected multi-dosing ChE NOAEL for
pups from the DNT may be lower than the established chronic ChE NOAEL
of 0.05 mg/kg/day from the 2-year chronic/carcinogenicity study and
could be as low as 0.02 mg/kg/day (i.e., 10X lower than the lowest dose
in the reproductive toxicity study). Although the DNT may possibly
impact the level chosen for estimating the chronic RfD, there is
reliable data supporting use of a 3X additional factor for chronic
dietary risk assessment, because, the 0.05 mg/kg/day NOAEL currently
used for risk assessment is approximately 3X higher than the potential
lower NOAEL (0.02 mg/kg/day) that could be attained in the DNT.
Therefore, EPA has chosen a 3X safety factor for the protection of
infants and children, in the form of a 3X UFdb for chronic dietary risk
assessment.
In absence of the 28-day inhalation study, the Agency is assuming
100% absorption for the route to route extrapolation. As the Acute
Toxicity Category for the oral route is II and the Acute Toxicity
Category for the inhalation route is III, it is unlikely that an
inhalation NOAEL would be lower than the oral NOAEL being used
currently. However, in order to better characterize exposure via the
inhalation
[[Page 18272]]
route specifically, this study would provide information on portal of
entry effects specific to the nasal passages and pulmonary tract.
The dietary food exposure assessment is conservative, using field
trial level residues and assuming 100% CT. Dietary drinking water
exposure is based on conservative modeling estimates and there are no
residential uses. These assessments will not underestimate the exposure
and risks posed by fosthiazate.
E. Aggregate Risks and Determination of Safety
To estimate total aggregate exposure to a pesticide from food,
drinking water, and residential uses, the Agency calculates DWLOCs
which are used as a point of comparison against the model estimates of
a pesticide's concentration in water (EECs). DWLOC values are not
regulatory standards for drinking water. DWLOCs are theoretical upper
limits on a pesticide's concentration in drinking water in light of
total aggregate exposure to a pesticide in food and residential uses.
In calculating a DWLOC, the Agency determines how much of the
acceptable exposure (i.e., the PAD) is available for exposure through
drinking water (e.g., allowable chronic water exposure (mg/kg/day) =
cPAD - (average food + residential exposure)). This allowable exposure
through drinking water is used to calculate a DWLOC.
A DWLOC will vary depending on the toxic endpoint, drinking water
consumption, and body weights. Default body weights and consumption
values as used by the USEPA Office of Water are used to calculate
DWLOCs: 2 liter (L)/70 kg (adult male), 2L/60 kg (adult female), and
1L/10 kg (child). Default body weights and drinking water consumption
values vary on an individual basis. This variation will be taken into
account in more refined screening-level and quantitative drinking water
exposure assessments. Different populations will have different DWLOCs.
Generally, a DWLOC is calculated for each type of risk assessment used:
Acute, short-term, intermediate-term, chronic, and cancer.
When EECs for surface water and ground water are less than the
calculated DWLOCs, EPA concludes with reasonable certainty that
exposures to the pesticide in drinking water (when considered along
with other sources of exposure for which EPA has reliable data) would
not result in unacceptable levels of aggregate human health risk at
this time. Because EPA considers the aggregate risk resulting from
multiple exposure pathways associated with a pesticide's uses, levels
of comparison in drinking water may vary as those uses change. If new
uses are added in the future, EPA will reassess the potential impacts
of residues of the pesticide in drinking water as a part of the
aggregate risk assessment process.
1. Acute risk. Using the exposure assumptions discussed in this
unit for acute exposure, the acute dietary exposure from food to
fosthiazate will occupy 12% of the aPAD for the U.S. population, 10% of
the aPAD for females 13-49 years of age, 11% of the aPAD for all
infants <1 year of age and 29% of the aPAD for children 1-2 years of
age. In addition, there is potential for acute dietary exposure to
fosthiazate in drinking water. After calculating DWLOCs and comparing
them to the EECs for surface water and ground water, EPA does not
expect the aggregate exposure to exceed 100% of the aPAD, as shown in
Table 3 of this unit:
Table 3.--Aggregate Risk Assessment for Acute Exposure to Fosthiazate
----------------------------------------------------------------------------------------------------------------
Surface Ground
Population Subgroup aPAD (mg/ % aPAD Water EEC Water EEC Acute DWLOC
kg) (Food) (ppb) (ppb) (ppb)
----------------------------------------------------------------------------------------------------------------
U.S. population 0.0004 12 2.1 2.4 12
----------------------------------------------------------------------------------------
Infants (<1 year) 0.0004 11 2.1 2.4 4
----------------------------------------------------------------------------------------
Children (1-2 years) 0.0004 29 2.1 2.4 3
----------------------------------------------------------------------------------------
Females (13-49 years) 0.0004 10 2.1 2.4 11
----------------------------------------------------------------------------------------------------------------
2. Chronic risk. Using the exposure assumptions described in this
unit for chronic exposure, EPA has concluded that exposure to
fosthiazate from food will utilize 7% of the cPAD for the U.S.
population; 4% of the cPAD for all infants <1 year; 15% of the cPAD for
children 1-2 years; and 6% of the cPAD for females 13-49 years. There
are no residential uses for fosthiazate that result in chronic
residential exposure to fosthiazate. In addition, there is potential
for chronic dietary exposure to fosthiazate in drinking water. After
calculating DWLOCs and comparing them to the EECs for surface water and
ground water, it is noted that the DWLOCs are slightly exceeded by the
estimated ground water EECs for two population subgroups. However,
these concentrations were modeled under the most conservative scenarios
and likely exceed the actual level of contamination in the environment.
SCI-GROW, used to model ground water exposures, is a Tier 1 unrefined
assessment and therefore, highly conservative. Importantly, pesticide-
specific aspects to this use of fosthiazate are likely to significantly
exaggerate the conservativeness of the SCI-GROW estimates. SCI-GROW
assumes the pesticide is applied above ground without cover and a
subsequent and heavy amount of water (140% of yearly average amount of
rainfall) leaches some of the pesticide down to ground water. However,
with the proposed registration using the drip irrigation method, a
small amount of water is slowly dripped into soils precisely where it
is needed, thus lessening the amount of water containing pesticide
residues flowing down through the soil past the root zone where it
cannot be used by the crop. This is expected to reduce the potential
for the chemical to reach into ground water systems, and the actual
ground water EECs would be less than what SCI-GROW predicted. Further,
fosthiazate is required to be applied in fields using plastic mulch
which significantly decreases the effect of rainfall on pesticide
leaching. Finally, terrestrial field dissipation studies submitted to
the Agency indicate no leaching of fosthiazate residues below the top
(0-15 cm) soil layer. Therefore, EPA does not expect the aggregate
exposure to exceed 100% of the cPAD, as shown in Table 4 of this unit:
[[Page 18273]]
Table 4.--Aggregate Risk Assessment for Chronic (Non-Cancer) Exposure to Fosthiazate
----------------------------------------------------------------------------------------------------------------
Surface Ground
Population Subgroup cPAD (mg/kg/ % cPAD Water EEC Water EEC Chronic
day) (Food) (ppb) (ppb) DWLOC (ppb)
----------------------------------------------------------------------------------------------------------------
U.S. population 0.00017 7 0.6 2.4 6
----------------------------------------------------------------------------------------
Infants (< 1 year) 0.00017 4 0.6 2.4 2
----------------------------------------------------------------------------------------
Children (1-2 years) 0.00017 15 0.6 2.4 2
----------------------------------------------------------------------------------------
Females (13-49 years) 0.00017 6 0.6 2.4 5
----------------------------------------------------------------------------------------------------------------
3. Short-term risk. Short-term aggregate exposure takes into
account residential exposure plus chronic exposure to food and water
(considered to be a background exposure level).
Fosthiazate is not registered for use on any sites that would
result in residential exposure. Therefore, the aggregate risk is the
sum of the risk from food and water, which do not exceed the Agency's
level of concern.
4. Intermediate-term risk. Intermediate-term aggregate exposure
takes into account residential exposure plus chronic exposure to food
and water (considered to be a background exposure level).
Fosthiazate is not registered for use on any sites that would
result in residential exposure. Therefore, the aggregate risk is the
sum of the risk from food and water, which do not exceed the Agency's
level of concern.
5. Aggregate cancer risk for U.S. population. Fosthiazate has been
classified into the category ``Not likely to be carcinogenic to
humans.'' This classification is based on the lack of evidence for
carcinogenicity in mice and rats. Therefore, fosthiazate is not
expected to pose a cancer risk.
6. Determination of safety. Based on these risk assessments, EPA
concludes that there is a reasonable certainty that no harm will result
to the general population, and to infants and children from aggregate
exposure to fosthiazate residues.
IV. Other Considerations
A. Analytical Enforcement Methodology
Adequate enforcement methodology is available to enforce the
tolerance expression. The method may be requested from: Chief,
Analytical Chemistry Branch, Environmental Science Center, 701 Mapes
Rd., Ft. Meade, MD 20755-5350; telephone number: (410) 305-2905; e-mail
address: residuemethods@epa.gov.
B. International Residue Limits
There are currently no established Codex, Canadian, or Mexican
maximum residue limits (MRLs) for residues of fosthiazate in/on plant
or livestock commodities.
V. Conclusion
Therefore, the tolerance is established for combined residues of
fosthiazate, (O-ethyl S-(1-methylpropyl)(2-oxo-3-
thiazolidinyl)phosphonothioate) and its metabolite ASC-67131 ((RS)-S-
sec-Butyl O-ethyl N-[2-(methylsulfonyl)ethyl] phosphoramidothioate), in
or on tomato at 0.02 ppm.
VI. Objections and Hearing Requests
Under section 408(g) of the FFDCA, as amended by the FQPA, any
person may file an objection to any aspect of this regulation and may
also request a hearing on those objections. The EPA procedural
regulations which govern the submission of objections and requests for
hearings appear in 40 CFR part 178. Although the procedures in those
regulations require some modification to reflect the amendments made to
the FFDCA by the FQPA, EPA will continue to use those procedures, with
appropriate adjustments, until the necessary modifications can be made.
The new section 408(g) of the FFDCA provides essentially the same
process for persons to ``object'' to a regulation for an exemption from
the requirement of a tolerance issued by EPA under new section 408(d)
of FFDCA, as was provided in the old sections 408 and 409 of the FFDCA.
However, the period for filing objections is now 60 days, rather than
30 days.
A. What Do I Need to Do to File an Objection or Request a Hearing?
You must file your objection or request a hearing on this
regulation in accordance with the instructions provided in this unit
and in 40 CFR part 178. To ensure proper receipt by EPA, you must
identify docket ID number OPP-2003-0296 in the subject line on the
first page of your submission. All requests must be in writing, and
must be mailed or delivered to the Hearing Clerk on or before June 7,
2004.
1. Filing the request. Your objection must specify the specific
provisions in the regulation that you object to, and the grounds for
the objections (40 CFR 178.25). If a hearing is requested, the
objections must include a statement of the factual issues(s) on which a
hearing is requested, the requestor's contentions on such issues, and a
summary of any evidence relied upon by the objector (40 CFR 178.27).
Information submitted in connection with an objection or hearing
request may be claimed confidential by marking any part or all of that
information as CBI. Information so marked will not be disclosed except
in accordance with procedures set forth in 40 CFR part 2. A copy of the
information that does not contain CBI must be submitted for inclusion
in the public record. Information not marked confidential may be
disclosed publicly by EPA without prior notice.
Mail your written request to: Office of the Hearing Clerk (1900C),
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001. You may also deliver your request to the
Office of the Hearing Clerk in Rm. 104, Crystal Mall 2, 1921
Jefferson Davis Hwy., Arlington, VA. The Office of the Hearing Clerk is
open from 8 a.m. to 4 p.m., Monday through Friday, excluding legal
holidays. The telephone number for the Office of the Hearing Clerk is
(703) 603-0061.
2. Tolerance fee payment. If you file an objection or request a
hearing, you must also pay the fee prescribed by 40 CFR 180.33(i) or
request a waiver of that fee pursuant to 40 CFR 180.33(m). You must
mail the fee to: EPA Headquarters Accounting Operations Branch, Office
of Pesticide Programs, P.O. Box 360277M, Pittsburgh, PA 15251. Please
identify the fee submission by labeling it ``Tolerance Petition Fees.''
EPA is authorized to waive any fee requirement ``when in the
judgement of the Administrator such a waiver or refund is equitable and
not contrary to the purpose of this subsection.'' For additional
information regarding the waiver of these fees, you may contact
[[Page 18274]]
James Tompkins by phone at (703) 305-5697, by e-mail at
tompkins.jim@epa.gov, or by mailing a request for information to Mr.
Tompkins at Registration Division (7505C), Office of Pesticide
Programs, Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001.
If you would like to request a waiver of the tolerance objection
fees, you must mail your request for such a waiver to: James Hollins,
Information Resources and Services Division (7502C), Office of
Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania
Ave., NW., Washington, DC 20460-0001.
3. Copies for the Docket. In addition to filing an objection or
hearing request with the Hearing Clerk as described in Unit VI.A., you
should also send a copy of your request to the PIRIB for its inclusion
in the official record that is described in Unit I.B.1. Mail your
copies, identified by docket ID number OPP-2003-0296, to: Public
Information and Records Integrity Branch, Information Resources and
Services Division (7502C), Office of Pesticide Programs, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001. In person or by courier, bring a copy to the location of the
PIRIB described in Unit I.B.1. You may also send an electronic copy of
your request via e-mail to: opp-docket@epa.gov. Please use an ASCII
file format and avoid the use of special characters and any form of
encryption. Copies of electronic objections and hearing requests will
also be accepted on disks in WordPerfect 6.1/8.0 or ASCII file format.
Do not include any CBI in your electronic copy. You may also submit an
electronic copy of your request at many Federal Depository Libraries.
B. When Will the Agency Grant a Request for a Hearing?
A request for a hearing will be granted if the Administrator
determines that the material submitted shows the following: There is a
genuine and substantial issue of fact; there is a reasonable
possibility that available evidence identified by the requestor would,
if established resolve one or more of such issues in favor of the
requestor, taking into account uncontested claims or facts to the
contrary; and resolution of the factual issues(s) in the manner sought
by the requestor would be adequate to justify the action requested (40
CFR 178.32).
VII. Statutory and Executive Order Reviews
This final rule establishes a tolerance under section 408(d) of the
FFDCA in response to a petition submitted to the Agency. The Office of
Management and Budget (OMB) has exempted these types of actions from
review under Executive Order 12866, entitled Regulatory Planning and
Review (58 FR 51735, October 4, 1993). Because this rule has been
exempted from review under Executive Order 12866 due to its lack of
significance, this rule is not subject to Executive Order 13211,
Actions Concerning Regulations That Significantly Affect Energy Supply,
Distribution, or Use (66 FR 28355, May 22, 2001). This final rule does
not contain any information collections subject to OMB approval under
the Paperwork Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose
any enforceable duty or contain any unfunded mandate as described under
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA) (Public Law
104-4). Nor does it require any special considerations under Executive
Order 12898, entitled Federal Actions to Address Environmental Justice
in Minority Populations and Low-Income Populations (59 FR 7629,
February 16, 1994); or OMB review or any Agency action under Executive
Order 13045, entitled Protection of Children from Environmental Health
Risks and Safety Risks (62 FR 19885, April 23, 1997). This action does
not involve any technical standards that would require Agency
consideration of voluntary consensus standards pursuant to section
12(d) of the National Technology Transfer and Advancement Act of 1995
(NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272 note). Since
tolerances and exemptions that are established on the basis of a
petition under section 408(d) of the FFDCA, such as the tolerance in
this final rule, do not require the issuance of a proposed rule, the
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et
seq.) do not apply. In addition, the Agency has determined that this
action will not have a substantial direct effect on States, on the
relationship between the national government and the States, or on the
distribution of power and responsibilities among the various levels of
government, as specified in Executive Order 13132, entitled Federalism
(64 FR 43255, August 10, 1999). Executive Order 13132 requires EPA to
develop an accountable process to ensure ``meaningful and timely input
by State and local officials in the development of regulatory policies
that have federalism implications.'' ``Policies that have federalism
implications'' is defined in the Executive Order to include regulations
that have ``substantial direct effects on the States, on the
relationship between the national government and the States, or on the
distribution of power and responsibilities among the various levels of
government.'' This final rule directly regulates growers, food
processors, food handlers and food retailers, not States. This action
does not alter the relationships or distribution of power and
responsibilities established by Congress in the preemption provisions
of section 408(n)(4) of the FFDCA. For these same reasons, the Agency
has determined that this rule does not have any ``tribal implications''
as described in Executive Order 13175, entitled Consultation and
Coordination with Indian Tribal Governments (65 FR 67249, November 6,
2000). Executive Order 13175, requires EPA to develop an accountable
process to ensure ``meaningful and timely input by tribal officials in
the development of regulatory policies that have tribal implications.''
``Policies that have tribal implications'' is defined in the Executive
Order to include regulations that have ``substantial direct effects on
one or more Indian tribes, on the relationship between the Federal
Government and the Indian tribes, or on the distribution of power and
responsibilities between the Federal Government and Indian tribes.''
This rule will not have substantial direct effects on tribal
governments, on the relationship between the Federal Government and
Indian tribes, or on the distribution of power and responsibilities
between the Federal Government and Indian tribes, as specified in
Executive Order 13175. Thus, Executive Order 13175 does not apply to
this rule.
VIII. Congressional Review Act
The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the
Small Business Regulatory Enforcement Fairness Act of 1996, generally
provides that before a rule may take effect, the agency promulgating
the rule must submit a rule report, which includes a copy of the rule,
to each House of the Congress and to the Comptroller General of the
United States. EPA will submit a report containing this rule and other
required information to the U.S. Senate, the U.S. House of
Representatives, and the Comptroller General of the United States prior
to publication of this final rule in the Federal Register. This final
[[Page 18275]]
rule is not a ``major rule'' as defined by 5 U.S.C. 804(2).
List of Subjects in 40 CFR Part 180
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated: March 26, 2004.
James Jones,
Director, Office of Pesticide Programs.
0
Therefore, 40 CFR chapter I is amended as follows:
PART 180--[AMENDED]
0
1. The authority citation for part 180 continues to read as follows:
Authority: 21 U.S.C. 321(q), 346(a) and 371.
0
2. Section 180.596 is added to subpart C to read as follows:
Sec. 180.596 Fosthiazate; tolerances for residues.
(a) General. Tolerances are established for the combined residues
of Fosthiazate (O-ethyl S-(1-methylpropyl)(2-oxo-3-
thiazolidinyl)phosphonothioate and its metabolite O-ethyl S-(1-
methylpropyl)[2-(methylsulfonyl)ethyl] phosphoramidothioate) (ASC-
67131).
------------------------------------------------------------------------
Parts per
Commodity million
------------------------------------------------------------------------
Tomato..................................................... 0.02
------------------------------------------------------------------------
(b) Section 18 emergency exemptions. [Reserved]
(c) Tolerances with regional registrations. [Reserved]
(d) Indirect or inadvertent residues. [Reserved]
[FR Doc. 04-7864 Filed 4-6-04; 8:45 am]
BILLING CODE 6560-50-S