[Federal Register Volume 62, Number 63 (Wednesday, April 2, 1997)]
[Notices]
[Pages 15700-15704]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-8388]
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ENVIRONMENTAL PROTECTION AGENCY
[PF-726; FRL-5594-9]
ISK Biosciences Corporation; Pesticide Tolerance Petition Filing
AGENCY: Environmental Protection Agency (EPA).
ACTION: Notice of filing.
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SUMMARY: This notice announces the initial filing of a pesticide
petition proposing the establishment of time-limited tolerances for
residues of the fungicide, chlorothalonil and its metabolite, 4-
hydroxy-2,5,6-trichloroisophthalonitrile in or on non-bell peppers.
This notice includes a summary of the petition that was prepared by the
petitioner, ISK Biosciences Corporation.
DATES: Comments, identified by the docket control number [PF-726], must
be received on or before, May 2, 1997.
ADDRESSES: By mail, submit written comments to: Public Response and
Program Resources Branch, Field Operations Division (7506C), Office of
Pesticide Programs, Environmental Protection Agency, 401 M St., SW.,
Washington, DC 20460. In person, bring comments to Rm. 1132, CM #2,
1921 Jefferson Davis Highway, Arlington, VA.
Comments and data may also be submitted electronically be sending
electronic mail (e-mail) to: [email protected]. Electronic
comments must be submitted as an ASCII file avoiding the use of special
characters and any form of encryption. Comments and data will also be
accepted on disks in WordPerfect 5.1 file format or ASCII file format.
All comments and data in electronic form must be identified by docket
control number [PF-726]. Electronic comments on this notice may be
filed online at many Federal Depository Libraries. Additional
information on electronic submissions can be found in Unit II. of this
document.
Information submitted as a comment concerning this document may be
claimed confidential by marking any part or all of that information as
``Confidential Business Information'' (CBI). CBI should not be
submitted through e-mail. Information marked as CBI will not be
disclosed except in accordance with procedures set forth in 40 CFR part
2. A copy of the comment
[[Page 15701]]
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. All written comments will be available for
public inspection in Rm. 1132 at the address given above, from 8:30
a.m. to 4 p.m., Monday through Friday, excluding legal holidays.
FOR FURTHER INFORMATION CONTACT: By mail: Cynthia Giles-Parker, Product
Manager (PM) 22, Registration Division (7505W), Office of Pesticide
Programs, Environmental Protection Agency, 401 M St., SW., Washington,
DC 20460. Office location, telephone number, and e-mail address: Rm.
229, CM #2, 1921 Jefferson Davis Highway, Arlington, VA, (703) 305-
6226; e-mail: [email protected].
SUPPLEMENTARY INFORMATION: EPA has received a pesticide petition (PP
6F4676) from ISK Biosciences Corporation, 5966 Heisley Road, P.O. Box
8000, Mentor, Ohio 44061-8000 proposing pursuant to section 408(d) of
the Federal Food, Drug, and Cosmetic Act, 21 U.S.C. section 346a(d), to
amend 40 CFR 180.275 by establishing a time-limited tolerance for a
period of 2 years for residues of the fungicide chlorothalonil and its
metabolite, 4-hydroxy-2,5,6-trichloroisophthalonitrile in or on the raw
agricultural commodity non-bell peppers at 5.0 parts per million (ppm).
ISK Biosciences Corporation has committed to providing additional
residue data during this 2-year period from trials conducted in Mexico
in support of a permanent tolerance. The proposed analytical method is
by electron capture gas chromatography.
EPA has determined that the petition contains data or information
regarding the elements set forth in section 408(d)(2); 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.
As required by section 408(d) of the FFDCA, as recently amended by
the Food Quality Protection Act, ISK Biosciences Corporation included
in the petition a summary of the petition and authorization for the
summary to be published in the Federal Register in a notice of receipt
of the petition. The summary represents the views of ISK Biosciences
Corporation. EPA is in the process of evaluating the petition. As
required by section 408(d)(3), EPA is including the summary as a part
of this notice of filing. EPA has made minor edits to the summary for
the purpose of clarity.
I. ISK Biosciences' Petition Summary
A. Residue Chemistry Data
1. Plant/animal metabolism. The nature of the residue of
chlorothalonil in plants and animals, including ruminants, is well
understood. Chlorothalonil is not systemic in plants. Any
chlorothalonil residue found on non-bell peppers occurs as a surface
residue. Chlorothalonil is rapidly metabolized in the ruminant and is
not transferred to meat and milk from the dietary consumption by
animals. Furthermore, chlorothalonil is not stable in meat or milk.
2. Analytical method. An adequate analytical method (gas
chromatography) is available for enforcement purposes. The method is
listed in the Pesticide Analytical Manual, Vol. II (PAM II).
3. Magnitude of the residues. Residue data from studies conducted
with non-bell peppers support a tolerance of 5.0 ppm for combined
residues of chlorothalonil and its metabolite, 4-hydroxy-2,5,6-
trichloroisophthalonitrile in or on the raw agricultural commodity.
B. Toxicological Profile
The following studies on file with the Agency support this
petition:
1. Acute toxicity. Acute toxicity studies include an acute oral rat
study on technical chlorothalonil with an LD50 >10,000 milligrams/
kilograms (mg/kg), an acute dermal toxicity study in the rabbit with an
LD50 >20,000 mg/kg, a 4-hour inhalation study with finely ground
technical chlorothalonil resulting in a LC50 of 0.092 mg/L (actual
airborne concentration), a primary eye irritation study with
irreversible eye effects in the rabbit at 21 days, a primary dermal
irritation study showing technical chlorothalonil is not a dermal
irritant, and a dermal sensitization study showing technical
chlorothalonil is not a skin sensitizer.
2. Genotoxicity. The mutagenic potential of chlorothalonil has been
evaluated in a large number of studies covering a variety of endpoints.
The overall conclusion is that chlorothalonil is not mutagenic.
Mutagenicity studies with chlorothalonil include gene mutation
assays in bacterial and mammalian cells; in vitro and in vivo
chromosomal aberration assays; DNA repair assays in bacterial systems;
and cell transformation assays. All were negative with the following
two exceptions:
Chlorothalonil was positive in an in vitro chromosomal aberration
assay in CHO cells without metabolic activation but was negative with
metabolic activation.
In vivo chromosomal aberration studies in rats and mice were
negative and one study in the Chinese hamster was equivocal. The
results of this study could not be confirmed in a subsequent study at
higher doses. The conclusion was that chlorothalonil does not cause
chromosome aberrations in bone marrow cells of the Chinese hamster. It
can be concluded that chlorothalonil does not have clastogenic
potential in intact mammalian systems.
In bacterial DNA repair tests, chlorothalonil was negative in
Bacillus subtilis, but was positive in Salmonella typhimurium. In an in
vivo DNA binding study in rats with 14C-chlorothalonil, there was
no covalent binding of the radiolabel to the DNA of the kidney, the
target organ for chlorothalonil toxicity in rodents.
3. Developmental and reproductive toxicity. A developmental
toxicity study with rats given gavage doses of 0, 25, 100, and 400 mg/
kg body weight/day from days 6 through 15 of gestation resulted in a no
observed effect level (NOEL) for maternal toxicity of 100 mg/kg/day
based on increased mortality, reduced body weight, and a slight
increase in early resorptions at the highest dose. There were no
developmental effects observed at any dose in this study.
A developmental toxicity study in rabbits given gavage doses of 0,
5, 10, or 20 mg/kg/day on days 7 through 19 of gestation resulted in a
maternal NOEL of 10 mg/kg/day. Effects observed in the dams in the
high-dose group were decreased body weight gain and reduced food
consumption. There were no developmental effects observed in this
study.
A two-generation reproduction study in rats fed diets containing 0,
500, 1,500 and 3,000 ppm resulted in a reproductive NOEL of 1,500 ppm
(equivalent to 115 mg/kg/day) based on lower neonatal body weights by
day 21. There were no effects seen on any other reproductive parameter
at any dose level in this study.
4. Subchronic toxicity. i. A subchronic toxicity study (90 days)
was conducted in rats at doses of 0, 1.5, 3.0, 10, and 40 mg/kg bwt.
Treatment related hyperplasia and hyperkeratosis of the forestomach was
observed at the two highest dose levels. Although the initial
histopathological evaluation did not demonstrate any nephrotoxicity, a
subsequent evaluation observed a treatment-related increase in
hyperplasia of the proximal tubule epithelium at 40 mg/kg bwt in the
male rats but not in the females. The no effect level for renal
histopathology was 10
[[Page 15702]]
mg/kg bwt in males and 40 mg/kg bwt in females.
ii. A 90-day oral toxicity study was conducted in dogs with dose
levels of technical chlorothalonil of 15, 150, and 750, mg/kg bwt/day.
The two highest dosages resulted in lower body weight gain in male
dogs. The no observed adverse effect level (NOAEL) was 15 mg/kg/day.
There were no macroscopic or microscopic tissue alterations related to
chlorothalonil and there were no signs of renal toxicity.
iii. Two 21-day dermal toxicity studies have been conducted with
technical chlorothalonil. In the initial study doses of 50, 2.5, and
0.1 mg/kg bwt/day were administered to rabbits. The NOEL for systemic
effects was greater than 50 mg/kg bwt/day and the NOEL for dermal
irritation was 0.1 mg/kg bwt/day.
A subsequent 21-day dermal study was conducted in male rats, to
specifically evaluate the potential for nephrotoxicity in this
laboratory species following dermal dosing. In this study the doses
were 60, 100, 250, and 600 mg/kg bwt/day. The NOEL for nephrotoxicity
was greater than 600 mg/kg bwt/day.
5. Estrogenic effects. Based upon all of the chronic toxicity,
teratogenicity, mutagenicity, and reproductive studies conducted with
chlorothalonil and its metabolites, there were no results which
indicate any potential to cause estrogenic effects or endocrine
disruption. These effects would have manifested themselves in these
studies as reproductive or teratogenic effects, or by producing
histopathological changes in estrogen sensitive tissues such as the
uterus, mammary glands, or the testes. Thus, it can be concluded based
upon the in-vivo studies, that chlorothalonil does not cause estrogenic
effects.
6. Chronic toxicity.--i. A 12-month chronic oral toxicity study in
Beagle dogs was conducted with technical chlorothalonil at dose levels
of 15, 150, and 500 mg/kg/day. The NOAEL was 150 mg/kg/day based on
lower blood albumin levels at the highest dose. There was no
nephrotoxicity observed at any dose in this study. This study replaced
an old outdated study that was not conducted under current guidelines
and did not use the current technical material.
ii. A chronic feeding/carcinogenicity study with Fischer 344 rats
fed diets containing 0, 800, 1,600 or 3,500 ppm (equivalent to 0, 40,
80, or 175 mg/kg bwt/day) for 116 weeks in males or 129 weeks in
females, resulted in a statistically higher incidence of combined renal
adenomas and carcinomas. At the high dose, which was above the MTD,
there was also a statistically significant higher incidence of tumors
of the forestomach in female rats.
iii. In a second chronic feeding/carcinogenicity study with Fischer
344 rats, designed to define the NOEL for tumors and the preneoplastic
hyperplasia, animals were fed diets containing 0, 2, 4, 15, or 175 mg/
kg/day. The NOEL in this study, based on renal tubular hyperplasia, was
a nominal dose of 2 mg/kg bwt/day. Because of the potential for
chlorothalonil to bind to diet, the 2 mg/kg bwt/day dose, expressed as
unbound chlorothalonil is 1.8 mg/kg bwt/day. The NOEL for hyperplasia
and hyperkeratosis of the forestomach was 4 mg/kg bwt/day or a dose of
3.8 mg/kg bwt/day based on unbound chlorothalonil.
iv. A 2-year carcinogenicity study, conducted in CD-1 mice at
dietary levels of 0, 750, and 1,500 or 3,000 ppm (equivalent to 0, 107,
214, or 428 mg/kg/day), resulted in a statistically higher incidence of
squamous cell carcinomas of the forestomach in both sexes, and a
statistically higher incidence of combined renal adenomas/carcinomas in
only the male mice receiving the low dose. There were no renal tumors
in any female mouse in this study.
v. A 2-year carcinogenicity study in male CD-1 mice for the purpose
of establishing the no effect level for renal and forestomach effects,
was conducted at dietary levels of 0, 10/15, 40, 175, or 750 ppm
(equivalent to 0, 1.4/2.1, 5.7, 25, or 107 mg/kg/day). The NOEL level
for renal effects was 40 ppm and the NOEL for forestomach effects was
15 ppm. This study did not duplicate the results from the previous
study where a statistically higher incidence of renal tumors, when
compared to controls, was observed at 750 ppm.
In 1987, EPA's Office of Pesticide Programs' Toxicology Branch Peer
Review Committee classified chlorothalonil as a B2 (probable human
carcinogen), based on evidence of carcinogenicity in the forestomach
and kidneys of rats and mice. The Agency currently regulates
chlorothalonil as a B2 carcinogen although ISK Biosciences Corporation
has provided a significant amount of mechanistic data indicating that
the tumors result from a threshold mechanism. A potency factor, Q1*, of
0.00766 (mg/kg/day)-1 has been used by the Agency when conducting
mathematical modeling to estimate carcinogenic risk to man. ISK
Biosciences Corporation believes that because the nephrotoxicity seen
in the rat is due to a threshold mechanism, any risk associated with
chlorothalonil can be managed using the margin of safety (exposure)
approach.
Numerous metabolism and toxicology studies indicate that
chlorothalonil is non-genotoxic and produces a species-specific renal
toxicity in the rat that eventually may lead to tumor formation through
an epigenetic mechanism.1 Studies comparing metabolism and
toxicological effects in dogs with those in rats demonstrate that the
renal effects observed in the rat are due to the exposure of the kidney
of the rat to significant levels of nephrotoxic thiol metabolites of
chlorothalonil. In the dog, no thiol metabolites are found and there
are no toxic effects seen in kidneys of dogs dosed with high levels of
chlorothalonil.
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1``Mechanistic Interpretation of the Oncogenicity of
Chlorothalonil in Rodents and an Assessment of Human Relevance,'' by
Drs. C. F. Wilkinson and J. C. Killeen, Regulatory Toxicology and
Pharmacology 24: 69-84 (1996), Article No. 006.
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7. Reference Dose (RfD). The no effect level for chlorothalonil in
the rat is 1.8 mg/kg bwt based on the nephrotoxicity observed in the
chronic rat study. The no effect level in the dog was 15 mg/kg bwt in
the 90-day study and 150 mg/kg bwt based on the one-year study. No
effect levels for maternal toxicity from developmental studies are 10
mg/kg bwt in rabbits and 100 mg/kg bwt in the rat. The no effect level
for pup growth in the reproduction study was 1,500 mg/kg bwt which
would be most conservatively estimated as equating to approximately 75
mg/kg bwt. Data indicate that the nephrotoxicity in the rat is produced
through a mechanism for which there is a clear threshold. In a study
which measured cell turnover in the rat kidney with bromodeoxyuridine
(BRDU) immunohistochemical staining, a NOEL was established at 1.5 mg/
kg bwt. Other chronic studies have established the NOEL for hyperplasia
in the kidney to be 1.8 mg/kg bwt. If all the available toxicity data
in laboratory animals is considered without regards to its
applicability to humans, the lowest NOEL for any adverse effect would
be 1.5 mg/kg bwt/day. Because the mechanism of toxicity which is
related to the tumor formation in the kidney has been shown to have a
threshold, the use of the normal 100 fold safety factor in conjunction
with the 1.5 mg/kg no effect level would produce a RfD which would
provide more than adequate safety for all of the possible effects seen
in any laboratory animal.
In two recent reviews of chlorothalonil by the Joint Meeting of
Pesticide Residue Experts (1990 and 1992), and the review by the World
Heath Organization's International Program for Chemical Safety, these
[[Page 15703]]
esteemed groups concluded that the rat was not the appropriate species
to use in consideration of the risk assessment for man. They concluded
that the dog was the more appropriate species for determination of
subchronic and chronic effects. If the toxicological data for the dog
were used, the NOEL would be at least 15 mg/kg bwt, based on the most
recent 90-day study in the dog.
Therefore, under the most conservative scenario (using the
toxicological data in the rat), the RfD would be 1.8 mg/kg bwt/day
divided by a 100 fold safety factor or 0.018 mg/kg bwt/day with a
threshold model being used for carcinogenic risk assessment. In the
scenario that uses the toxicological data in the dog, the reference
dose would be 15 mg/kg bwt/day, divided by a safety factor of 100 or
0.15 mg/kg bwt/day.
C. Aggregate Exposure
The following is a description of the likelihood of exposure to
chlorothalonil from various routes.
1. Dietary exposure--i. food. ISK Biosciences Corporation has
conducted a dietary exposure analysis for chlorothalonil and its
metabolite, 4-hydroxy-2,5,6-trichloroisophthalonitrile (SDS-3701) in or
on non-bell peppers utilizing EPA's Dietary Risk Evaluation System
(DRES) based on the 1977-78 Food Consumption Survey. The results
demonstrate that the dietary exposure from anticipated residues of 0.5
ppm contributed from non-bell peppers is 0.00000218 mg/kg bwt/day for
the U.S. population or 0.0121% of the RfD.
The Agency had calculated that the exposure of the general
population from existing published tolerances for chlorothalonil is
0.000134 mg/kg bwt/day or 0.744 percent of the RfD.
ii. Drinking water. Chlorothalonil was included for monitoring in
the National Survey of Pesticides in Drinking Water Wells conducted by
EPA. No chlorothalonil residues were detected in any of the 1,300
community water systems and domestic wells (using methodology for
chlorothalonil having a limit of detection [LOD] of 0.06 mg/l and limit
of quantitation of 0.12 mg/l). The absence of chlorothalonil detections
in the National Survey provides adequate information to conclude that
chlorothalonil is not a contaminant in drinking water wells and that
the population is not exposed to chlorothalonil in these water sources.
These findings are consistent with the known physical/chemical
properties of chlorothalonil including low water solubility (0.9 ppm)
and high affinity for organic matter including soil. It has also been
demonstrated that chlorothalonil does not leach into groundwater from
applications made to growing crops.
Aerobic aquatic metabolism studies with chlorothalonil establish a
half-life in natural aquatic habitats of less than 10 hours, depending
on environmental conditions. Considering the short half-life of
chlorothalonil in natural water/sediment systems and that surface water
is filtered and treated prior to consumption, chlorothalonil is not
likely to be present in drinking water obtained from natural surface
water systems.
An exposure estimate, based on surface water concentration recently
cited by EPA, would conclude that the average concentration in surface
water would be less than 0.002 ppb. Assuming that everyone in the U.S.
consumed untreated surface water, the exposure to chlorothalonil of the
general population would be less than 5.8 x 10-7 mg/kg bwt/day.
This would be a worst case scenario, which would greatly overestimate
exposure.
2. Non-dietary exposure. Potential non-dietary exposures to
chlorothalonil may result from the following uses of chlorothalonil. In
each case, the exposure would be from the dermal route and only for an
intermittent duration. The two 21-day dermal studies that have been
conducted in the rabbit and rat indicate that there is no
nephrotoxicity associated with the dermal exposure to chlorothalonil at
dose levels up to 600 mg/kg/day. Therefore, the exposures from the uses
of chlorothalonil listed below, would not be expected to add to the
carcinogenic risk associated with chlorothalonil.
i. Golf course uses. Chlorothalonil products are commonly applied
to golf course tees and greens to control a broad complex of turf
diseases. Application to golf course fairways is much less common.
Golf is not a game played by infants or small children, therefore
no exposure to infants and children would be anticipated.
ii. Residential owner uses. Applications of chlorothalonil products
to home lawns are rare. Thus, there is very little exposure to
chlorothalonil related to use on residential turf. Applications to
roses and other ornamentals in home gardens is also a minor use of
chlorothalonil.
iii. Paint. Chlorothalonil is used in paints and stains for control
of mildew and molds on exterior surfaces of buildings. Chlorothalonil
is also occasionally used for interior paints, but this use represents
only a small proportion of the chlorothalonil used in paints. About 2%
of the chlorothalonil used in paint is used in interior paint; however,
only 0.2% or less of interior paints in the United States contain
chlorothalonil. In paints chlorothalonil is tightly bound within the
paint matrices; thus, effective control of mildew may last for several
years and the potential for exposure is very limited.
iv. Grouts. Chlorothalonil is used in cement tile grouts, also for
control of mildew and molds. Chlorothalonil is bound within the grout
matrices and very little is available for exposure. This is a minor use
of chlorothalonil and non-occupational dermal exposure of humans to
chlorothalonil from this source is extremely low.
v. Wood treatment. Chlorothalonil is not currently used for
pressure-treating wood. It is used for control of sapstain as a surface
treatment on rough-cut, newly-sawn lumber to protect it from molds and
mildews while drying. Being a surface residue, it is removed during the
finishing operations prior to sale of the wood. Chlorothalonil does not
occur in structural wood used for residential or occupational
scenarios.
D. Cumulative Effects
ISK Biosciences has considered the potential for cumulative effects
of chlorothalonil and other substances that have a common mechanism of
toxicity. Chlorothalonil is a halogenated benzonitrile which readily
undergoes displacement of the 2, 4, and 6 chlorines by glutathione and
other thiol containing amino acids and proteins. In the rat, the thiol
metabolites are sufficiently absorbed to produce a nephrotoxic effect.
In dogs where this absorption does not occur, nephrotoxicity does not
occur. ISK Biosciences does not have any information to indicate that
toxic effects observed in rats occur through a mechanism which is
common to any other agricultural chemical. Thus, consideration of
common mechanisms of toxicity is not appropriate at this time.
Chlorothalonil should not be confused with chlorinated hydrocarbon
pesticides which have significantly different chemical and biological
properties.
E. Safety Determination
1. U.S. population. ISK Biosciences Corporation has conducted a
risk assessment for chlorothalonil in or on non-bell peppers using the
1977-78 Food Consumption Survey and a potency factor, Q1*, of 0.00766
(mg/kg/day)-1 and has determined that oncogenic dietary risks
associated with
[[Page 15704]]
potential exposure using an anticipated residue of 0.5 ppm, would 1.7 x
10-8.
The Agency has used a linearized model to estimate the carcinogenic
risk associated with chlorothalonil, whereas ISK Biosciences believes
that a threshold based model is appropriate. Using the overestimated
exposure estimates of EPA, with a threshold based model and using the
conservative RfD of 0.018 mg/kg bwt/day, the margin of safety for the
general population would exceed 10,000 and the margin of safety for
infants and children would exceed 7,000. Using corrected exposure
estimates would obviously yield larger margins of exposure. Using a
conservative RfD of 0.018 mg/kg/day, as the Agency has done in recent
DRES analyses, and incorporating corrections needed in exposure values
for mushrooms and several other lesser corrections, ISK Biosciences
Corporation calculated the overall dietary exposure to ``anticipated
residues'' of chlorothalonil from all registered uses and pending uses
of chlorothalonil to be 0.36% of the RfD for the general U.S.
population.
Because the worst case assumption for human exposure from drinking
water indicate that exposure would be only 1% of the dietary exposure,
the risk assessment is not significantly altered by considering the
exposure from drinking water.
2. Infants and children. There is a complete data base for
chlorothalonil which includes pre- and post-natal developmental
toxicity data as well as mechanistic data related to the rodent
specific nephrotoxicity observed in subchronic and chronic studies. The
toxicological effects of chlorothalonil in rodents are well understood.
Chlorothalonil has a low level of toxicity in dogs.
In a two-generation reproduction study in rats, all reproductive
parameters investigated showed no treatment-related effects except pup
weight gain. Specifically, the weights of pups exposed to
chlorothalonil were comparable to controls at parturition through day 4
of lactation. It was only after day 4 of lactation, when the pups begin
to consume the test diet, that body weight gain lags behind controls.
This only occurred at the highest dose tested; 3,000 ppm. The dose of
chlorothalonil the pups would receive would be far in excess of the
estimated adult dose of 150 mg/kg bwt/day (3,000 ppm divided by 20).
The doses for the pups could have easily exceeded 500 mg/kg bwt/day.
Dose levels of 375 mg/kg bwt and above have been shown to significantly
affect body weight in the rat. Therefore, the reduction of body weight
gain observed in the reproduction study is considered to be comparable
to the effects that have been observed in older rats. The NOEL for this
effect was 1,500 ppm.
In developmental toxicity studies conducted in the rat and the
rabbit, chlorothalonil did not cause any developmental effects even at
dose levels that produced significant maternal toxicity. In the rabbit
a dose level of 20 mg/kg bwt caused maternal toxicity, but there were
no developmental effects and in the rat, a dose level of 400 mg/kg bwt
caused maternal toxicity without developmental toxicity.
The extensive data base that is available for chlorothalonil is
devoid of any indication that chlorothalonil would represent any
unusual or disproportionate hazard to infants or children. Therefore,
there is no need to impose an additional 10x safety factor for infants
or children. The standard uncertainty factor of 100x should be used for
all segments of the human population when calculating risks associated
with chlorothalonil.
F. International Tolerances
There is currently no maximum residue level set for chlorothalonil
on non-bell peppers by the Codex Alimentarius Commission.
II. Public Record
A record has been established for this notice under docket control
number [PF-726] (including comments and data submitted electronically
as described below). A public version of the record, including printed,
paper versions of electronic comments, which does not include any
information claimed as CBI, is available for inspection from 8:30 a.m.
to 4 p.m., Monday through Friday, excluding legal holidays. The public
record is located in Room 1132 of the Public Response and Resources
Branch, Field Operations Division (7506C), Office of Pesticide
Programs, Environmental Protection Agency, Crystal Mall #2, 1921
Jefferson Davis Highway, Arlington, VA.
Electronic comments can be sent directly to EPA at:
[email protected]
Electronic comments must be submitted as an ASCII file avoiding the
use of special characters and any form of encryption.
The official record for this rulemaking, as well as the public
version, as described above will be kept in paper form. Accordingly,
EPA will transfer all comments received electronically into printed,
paper form as they are received and will place the paper copies in the
official rulemaking record which will also include all comments
submitted directly in writing. The official rulemaking record is the
paper record maintained at the address in ADDRESSES at the beginning of
this document.
List of Subjects
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated: March 24, 1997.
Stephen L. Johnson,
Director, Registration Division, Office of Pesticide Programs.
[FR Doc. 97-8388 Filed 4-1-97; 8:45 am]
BILLING CODE 6560-50-F