[Federal Register Volume 61, Number 238 (Tuesday, December 10, 1996)]
[Notices]
[Pages 65043-65047]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 96-31303]


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ENVIRONMENTAL PROTECTION AGENCY
[PF-676; FRL-5575-8]


Merck Co., Inc.; Notice of Pesticide Petition Filing

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice of Filing.

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SUMMARY: This notice announces the filing of a pesticide petition 
proposing the renewal/reissuance of regulations establishing tolerances 
for residues of the pesticide chemical abamectin (avermectin B1) 
in or on various agricultural commodities. This notice includes a 
summary of the petition that was prepared by the petitioner, Merck Co., 
Inc.
DATES: Comments, identified by the docket number PF-676, must be 
received on or before January 9, 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 Hwy., Arlington, VA 22202.
    Comments and data may also be submitted electronically by 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 in 5.1 file format or ASCII file 
format. All comments and data in electronic form must be identified by 
the docket number PF-676. No Confidential Business Information (CBI) 
should be submitted through e-mail. Electronic comments on this 
proposed rule 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 notice may be 
claimed

[[Page 65044]]

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. No CBI should be submitted 
through e-mail. A copy of the comment 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.

FOR FURTHER INFORMATION CONTACT: George LaRocca (PM-13), Rm. 204, 
Crystal Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA 22202. Mail 
address: Registration Division (7505C), Environmental Protection 
Agency, Washington, DC 20460. Telephone (703) 305-6100; e-mail 
[email protected].
SUPPLEMENTARY INFORMATION: EPA has received a pesticide petition from 
Merck Co., Inc., Agricultural Research and Development, Hillsborough 
Rd., Three Bridges, NJ 08487. The petition proposes amending 40 CFR 
180.449 to renew/reissue the regulations that established tolerances 
for the insecticide abamectin (avermectin B1) and its delta-8,9-
isomer in or on cottonseed at 0.005 parts per million (ppm); citrus, 
whole fruit, at 0.02 ppm; citrus oil, at 0.1 ppm; citrus dried pulp, at 
0.1 ppm; cattle, meat, at 0.02 ppm; cattle, meat byproducts, at 0.02 
ppm; cattle, fat, at 0.015 ppm; milk, at 0.005 ppm; and hops, dried, at 
0.5 ppm. These tolerances were originally established in response to 
pesticide petitions 7F3500, 8F3592, 4E04419, and food additive petition 
8H5550. The petition also proposes to establish a tolerance in or on 
the raw agricultural commodity potatoes at 0.005 ppm. As required by 
section 408(d) of FFDCA, as recently amended by the Food Quality 
Protection Act, Merck 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 Merck; 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. Merck Co., Inc.'s Petition Summary

    This is a petition by Merck Co., Inc. (Merck), under section 408 of 
the Federal Food, Drug, and Cosmetic Act (FFDCA), as most recently 
amended by the Food Quality Protection Act (FQPA), asking that the 
Environmental Protection Agency (EPA) issue permanent tolerances 
without time limits for pesticide chemical residues consisting of the 
insecticide abamectin (avermectin B1) and or its delta 8,9-isomer 
in or on the following food items: cottonseed; citrus, whole fruit; 
citrus, oil; citrus, dried citrus pulp; hops, dried; milk; cattle, 
meat; cattle, meat byproducts; cattle, fat; and potatoes. These 
tolerances were originally requested in petitions 7F3500, 8F3592, 
4E04419, and 5F04508, and food additive petition 8H5550.
    On April 30, 1996, the time-limited tolerances for abamectin use on 
cottonseed, citrus food and feed items, milk, and cattle food items 
expired. A proposal by EPA to extend the tolerances was published in 
the Federal Register; no public comments were received in response. 
However, the Agency did not publish a final rule prior to the enactment 
of FQPA. On October 21, 1996, in response to procedural guidance from 
EPA, Merck submitted to EPA a request for reissuance of the tolerances. 
With one exception (potatoes), the requested tolerances would replace 
the time-limited abamectin tolerances that have been issued in the past 
by EPA and that recently expired or will soon expire. Merck requested 
that EPA issue permanent tolerances for these commodities, saying that 
the time limitations associated with these earlier tolerances were a 
result of aquatic exposure issues, and that it understood that the 
Agency no longer imposes time limitations on tolerances because of non-
dietary issues.

A. Residue Data

    Abamectin (also known as avermectin B1) is an effective 
miticide/insecticide that is used on various crops at the maximum use 
rate of 0.025 pounds active ingredient per acre. Residue data covering 
all the uses associated with the tolerances requested by this petition 
have been previously submitted to EPA for review and have been found by 
EPA to support the requested tolerances and preharvest intervals. See 
54 FR 23209, May 31, 1989 (cottonseed); 54 FR 31836, Aug. 2, 1989 
(citrus food and feed items, cattle food items, and milk); and 60 FR 
47529, Sept. 13, 1995 (hops). Merck has submitted practical analytical 
methods (high density liquid chromatography--fluorescence, with crop-
specific cleanup methods) for detecting and measuring levels of 
abamectin and its delta 8,9-isomer in or on food with residues at or 
above the proposed tolerance levels. EPA has provided information on 
these methods to EPA, and the methods are available to anyone 
interested in pesticide residue enforcement at the address listed under 
``FOR FURTHER INFORMATION CONTACT'' above.

B. Abamectin Safety Data

    To date Merck has submitted approximately 78 toxicology studies, 
including the following principal studies, to support the tolerances 
for abamectin (studies conducted with the delta 8,9-isomer of abamectin 
are noted):
    1. Acute studies. A rat acute oral study with a LD50 of 4.4 to 
11.8 mg/kg (males) and 10.9 to 14.9 mg/kg (females).
    A rabbit acute dermal study with a LD50 >2,000 mg/kg. A rat 
acute inhalation study with a LC50 >5.73 mg/L.
    A primary eye irritation study in rabbits which showed irritation.
    A primary dermal irritation study in rabbits which showed no 
irritation.
    A primary dermal sensitization study in guinea pigs which showed no 
skin sensitization potential.
    An acute oral toxicity study in monkeys with a no observed adverse 
effects level (NOAEL) of 1.0 mg/kg based upon emesis at 2.0 mg/kg.
    2. Subchronic studies. A rat 8-week feeding study with a NOAEL of 
1.4 mg/kg/day based upon tremors.
    A rat 14-week oral toxicity study with a NOAEL of 0.4 mg/kg/day, 
the highest dose tested.
    A dog 12-week feeding study with a NOAEL of 0.5 mg/kg/day based 
upon mydriasis.
    A dog 18-week oral study with a NOAEL of 0.25 mg/kg/day based upon 
mortality.
    A CD-1 mouse 84-day feeding study with a NOAEL of 4 mg/kg/day based 
upon decreased body weights.
    3. Chronic studies. A rat 53-week oncogenicity feeding study, 
negative for oncogenicity, with a NOAEL of 1.5 mg/kg/day based upon 
tremors.
    A CD-1 mouse 94-week oncogenicity feeding study, negative for 
oncogenicity, with a NOAEL of 4 mg/kg/day based upon decreased body 
weights.
    A dog 53-week chronic feeding study, with a NOAEL of 0.25 mg/kg/day 
based upon mydriasis.
    4. Developmental toxicity studies. An oral teratology study in the 
CF-1 mouse with a maternal NOAEL of 0.05 mg/kg/day based upon decreased 
body weights and tremors. The fetal NOAEL was 0.20 mg/kg/day based upon 
cleft palates.
    An oral teratology study with the delta 8,9-isomer in CF-1 mice 
with a maternal NOAEL of 0.10 mg/kg/day based upon decreased body 
weights. The fetal NOAEL was 0.06 mg/kg/day based upon cleft palate.
    An oral teratology study in rabbits with a maternal NOAEL of 1.0 
mg/kg/

[[Page 65045]]

 day based upon decreased body weights and tremors. The fetal NOAEL was 
1.0 mg/kg/day based upon clubbed feet.
    An oral teratology study in rats with a maternal and fetal NOAEL at 
1.6 mg/kg/day, the highest dose tested.
    An oral teratology study with the delta 8,9-isomer with a maternal 
NOAEL in CF-1 mice that expressed P-glycoprotein greater than 1.5 mg/
kg/day, the highest and only dose tested. No cleft palates were 
observed in fetuses that expressed normal levels of P-glycoprotein, but 
fetuses with low or no levels of P-glycoprotein had increased incidence 
of cleft palates.
    5. Reproductive effects study. A two-generation study in rats with 
a NOAEL of 0.12 mg/kg/day in pups based upon retinal folds, decreased 
body weight, and mortality. The NOAELs for systemic and reproductive 
toxicity were 0.4 mg/kg/day.
    6. Mutagenicity studies. The Ames assays conducted with and without 
metabolic activation were both negative.
    The V-79 mammalian cell mutagenesis assays conducted with and 
without metabolic activation did not produce mutations. In an alkaline 
elution/rat hepatocyte assay, abamectin was found to induce single 
strand DNA breaks without significant toxicity in rat hepatocytes 
treated in vitro at doses greater than 0.2 mM. This in vitro dose of 
0.2 mM is biologically unobtainable in vivo, due to the toxicity of the 
compound. However, at these potentially lethal doses, in vivo treatment 
did not induce DNA single strand breaks in hepatocytes. In the mouse 
bone marrow assay, abamectin was not found to induce chromosomal 
damage. Merck has also conducted many studies and accumulated a great 
deal of clinical and follow-up experience with regard to ivermectin, a 
closely similar human and animal drug.

C. Toxicity Issues

    1. Acute toxicity. Typical symptoms of classical CNS abamectin/
ivermectin acute toxicity include mydriasis (dilated pupils, a marker 
effect occurring at relatively low exposure levels); fatigue or 
lethargy; and tremors. At sufficiently high exposure levels, coma and 
sometimes death may result. Once exposure ceases, recovery in affected 
living animals is rapid (typically within a few days).
    Some species of animals are more sensitive generally to this 
classical pattern of abamectin toxicity than other species. In 
particular, a subpopulation of CF-1 mice and the neonatal rat have been 
observed to be sensitive to abamectin/ivermectin toxicity. Merck 
research has attributed the sensitivity of the subpopulation of CF-1 
mice to the absence of P-glycoprotein, a major component of the blood-
brain barrier. Neonatal rat sensitivity has been attributed in part to 
the lack of a fully developed blood-brain barrier. The neonatal blood-
brain barrier is not complete until after 2 weeks following birth, 
while the blood-brain barrier in humans is completed pre-natally. The 
extensive human use of ivermectin has not identified a subpopulation of 
humans with deficient P-glycoprotein. Furthermore, the animal and human 
data bases do not indicate increased concerns for infants and children.
    2. Developmental effects. Tests of abamectin and ivermectin have 
been conducted in a variety of species, and ivermectin is widely used 
as a human and animal drug. In livestock species there is no suggestion 
that ivermectin is a developmental toxicant. In mice and rabbits there 
is evidence that dosing with either abamectin or ivermectin may produce 
malformations, but only at doses that are clearly maternally toxic as 
well. However, the delta 8,9-isomer of abamectin has been shown to 
produce cleft palate malformations in the CF-1 mouse at dose levels 
that are not maternally toxic and that are much lower than the dose 
levels that show any indication of developmental toxicity in other 
species or in other mouse strains. Merck research has shown that the 
subpopulation of CF-1 mice with these malformations have inherited a 
genetic deficiency that prevents or severely limits their production of 
a P-glycoprotein which is a principal factor of the blood-brain barrier 
and which Merck hypothesizes may perform a protective function in fetal 
development as well, perhaps by playing a role in the blood-placenta 
barrier. Based upon extensive use of ivermectin in humans without 
observed adverse effects, this deficiency is not expected to occur in 
humans.
    3. Other toxicity issues. There are no nonthreshold effects and no 
other toxic endpoints of concern. The oncogenicity assays and chronic 
feeding studies revealed no indication of carcinogenic potential. 
Abamectin was found to be non-mutagenic.

D. Exposure Analysis for Threshold Effects

    1. Chronic exposure assessments. EPA's chronic dietary exposure 
assessments for abamectin currently use a reference dose (RfD) of 
0.0004 mg/kg/day based upon a NOAEL of 0.12 mg/kg/day from effects on 
neonatal pups in the rat multigeneration reproduction study and an 
uncertainty factor of 300 (including an additional modifying factor of 
3 to account for the severity of the effects).
    As noted above, this acute toxicity in rat pups results solely from 
their exposure to abamectin in the milk they ingest. It is well 
understood that abamectin concentrates in fat and that rat milk has 
considerably more fat content than that of most other species 
(including humans), so that the exposure level for the rat dams 
considerably understates the exposure level of the affected rat pups. 
As discussed earlier, the blood-brain barrier of the neonatal rat pup 
is not fully formed until a week or more after birth, while in humans 
the barrier is complete well before birth. Due to these differences 
between rats and humans, using the neonatal rat to model risks to 
infants arguably is inappropriate; certainly use of the 0.0004 mg/kg/
day RfD derived from the abamectin level in the rat dams' diet 
introduces additional conservative safety factors. Additional assurance 
comes from the absence of adverse effects in studies using neonatal and 
juvenile monkeys and from the absence of adverse effects in nursing 
human infants whose mothers have been treated with ivermectin.
    Notwithstanding these issues, Merck has calculated chronic exposure 
estimates and compared them to this RfD. Using mean anticipated 
residues, adjusted for percent crop treated with abamectin, the chronic 
exposure for the overall U.S. population was estimated to be 0.000005 
mg/kg/day, which is approximately 1.4% of the RfD. For infants, 
exposure was similarly estimated to be 0.000005 mg/kg/day (1.4% of the 
RfD). The exposure estimates for the two most highly exposed population 
subgroups, children 1 to 6 years old and children 7 to 12 years old, 
were 0.000013 mg/kg/day (3.2% of the RfD) and 0.000008 mg/kg/day (2.1) 
of the RfD), respectively.
    2. Acute exposure assessments. In evaluating the potential hazard 
of abamectin acute exposure for women of childbearing age, EPA 
currently uses a NOAEL of 0.05 mg/kg/day for maternotoxic effects of 
abamectin in CF-1 mice and a NOAEL of 0.06 mg/kg/day for developmental 
effects of the delta 8,9-isomer in CF-1 mice. To assess the potential 
hazard of acute exposure of infants and children, EPA uses the rat 2-
generation reproduction study NOAEL of 0.12 mg/kg/day based upon the 
toxicity observed in the nursing pups.
    The relevance of the neonatal rat model has already been discussed. 
As to the relevance of the CF-1 mouse studies, Merck research has shown 
that both the induction of cleft palate in fetuses and the induction of 
maternal

[[Page 65046]]

toxicity at low dose levels result from a heritable genetic deficiency 
that precludes some animals of that strain from producing P-
glycoprotein. In a recent study, where dams that expressed P-
glycoprotein were treated with the delta 8,9-isomer of abamectin and 
mated to males with and without P-glycoprotein, every fetus that did 
not inherit the ability to express P-glycoprotein developed cleft 
palate while every fetus that inherited the ability to express P-
glycoprotein fully was free of the malformation. Additionally, in the 
dams (all of whom were chosen because they possessed the ability to 
express the P-glycoprotein) no effects were seen at the 1.5 mg/kg/day 
dose (the only dose tested), in contrast to the much lower 
maternotoxicity NOAELs (as low as 0.05 mg/kg/day) seen in comparable 
studies using abamectin or its delta 8,9-isomer in CF-1 mice that had 
not been tested for ability to express P-glycoprotein. Epidemiological 
studies of humans treated with ivermectin, as well as breeding-animal 
studies on ivermectin conducted to obtain its approval as animal drug 
and surveys of adverse reaction reports (billions of treatments have 
been administered to animals) all indicate a lack of a human population 
susceptible to the induction of birth defects by ivermectin or 
abamectin. Accordingly, the CF-1 mouse is not an appropriate model to 
assess the toxicity of the avermectins.
    Despite these issues, Merck has incorporated these toxicity 
endpoints from the CF-1 mouse into acute exposure assessments. (For 
purposes of simplification, Merck has used the NOAEL of 0.05 mg/kg/day 
for acute exposure assessments for the overall U.S. population and also 
for women of childbearing age.) These assessments show that the margins 
of exposure (MOEs) at the 95th percentile of exposure (using a Monte 
Carlo analysis conducted in accordance with Tier 3 of EPA' June 1996 
``Acute Dietary Exposure Assessment''guidance document) are 
significantly greater than the EPA standard of 100 for all 
subpopulations. The 95th percentile of exposure for the overall U.S. 
population was estimated to be 0.000023 mg/kg/day (MOE of 2,146), while 
that for women greater than 13 years of age was 0.000017 mg/kg/day (MOE 
of 2,970). For children 1 to 6 years old, the 95th percentile of 
exposure was estimated to be 0.000042 mg/kg/day (MOE of 2,863), while 
that for children 7 to 12 years old was 0.000030 mg/kg/day (MOE of 
3,965). For infants, the 95th percentile of exposure was estimated to 
be 0.0028 mg/kg/day (MOE of 4,244).

E. Aggregate Exposure

    The dietary assessments (both acute and chronic) accounts for all 
anticipated dietary exposure for tolerances that are subject to this 
request (citrus and derivatives, cottonseed, meat, meat byproducts, 
milk, and hops), and all other active and pending tolerances for 
abamectin. The other active tolerances are for tomatoes, strawberries, 
celery, lettuce, cucurbits, peppers, apples, pears, almonds, and 
walnuts. The tolerance petition for potatoes is pending. The 
assessments also take into account the use on grapes under an emergency 
exemption.
    Additional uses of abamectin include a bait for fire ants, an 
indoor crack and crevice treatment, and a roach bait; however, 
significant exposure from these products is not likely. The fire ant 
bait contains approximately 0.011% abamectin and is used primarily in 
the southern portion of the United States, where the fire ant is most 
prevalent. Post application exposure resulting from mound-directed 
treatment is considered unlikely, and significant exposure from the 
broadcast treatment is also unlikely since the treatment rate is very 
low (1.0 lb of bait, containing only 50 mg of abamectin, per acre). In 
a recent exposure study using the crack and crevice treatment, no 
measurable air or surface residues were detected. Significant exposure 
is not expected from the roach bait because of the child resistant 
safety packaging and the essentially non-existent vapor pressure of 
abamectin.
    Based upon the available studies of abamectin's fate in the 
environment, there is no reason to expect human exposure to residues of 
abamectin in drinking water. It has been clearly demonstrated that 
abamectin does not leach.
    The typical therapeutic dose of ivermectin as a human drug is 200 
g/kg (0.2 mg/kg). Merck is in the process of quantitatively 
assessing the total dietary exposure resulting from abamectin and 
ivermectin uses. Generally, use of ivermectin in food-producing animals 
is only once per year and the ivermectin residues in most treated 
animals are below the level of detection.

F. Endocrine Effects

    There is no evidence that abamectin is an endocrine disrupter. 
Evaluation of the rat multigenerational study demonstrated no effect on 
the time to mating or on the mating and fertility indices, suggesting 
no effects on the estrous cycle, on mating behavior, or on male or 
female fertility at doses up to 0.4 mg/kg/day, the highest dose tested. 
Furthermore, the range finding study demonstrated no adverse effect on 
female fertility at doses up to 1.5 mg/kg/day, the highest dose tested. 
Similarly, chronic and subchronic toxicity studies in mice, rats, and 
dogs did not demonstrate any evidence of toxicity to the male or female 
reproductive tract, or to the thyroid or pituitary (based upon organ 
weights and gross and histopathologic examination). In the 
developmental studies, the pattern of toxicity observed does not seem 
suggestive of any endocrine effect. Finally, experience with ivermectin 
in breeding animals, including sperm evaluations in multiple species, 
shows no adverse effects suggestive of endocrine disruption.

G. International Tolerances

    The U.S. tolerances for pears and citrus are greater than the Codex 
proposals, reflecting the differences in how the United States and 
Codex CCPR treat the highest residue values from field studies. The 
differences in tolerances for cottonseed and milk are the result of 
differences in the limits of detection of the analytical methods 
accepted by the two organizations. Assuming label directions are 
followed, actual anticipated residues in foods in commerce should not 
be affected by the different tolerances, since the same residue 
database has been used to set both the Codex and U.S. tolerances.

H. Safety to Infants and Children

    Merck's petition notes that EPA has evaluated abamectin repeatedly 
since its introduction in 1985 and has found repeatedly that the level 
of dietary exposure is sufficiently low to provide ample margins of 
safety to guard against any potential adverse effects of abamectin. The 
FQPA authorizes the employment of an additional safety factor of up to 
10X to guard against the possibility of prenatal or postnatal toxicity, 
or to account for an incomplete database on toxicity or exposure. Merck 
states that the database for abamectin is complete and argues that 
there is no need for an additional safety factor because of the 
conservatism in the end points selected for risk assessment. 
Additionally, there is much more information regarding human risk 
potential than is the case with most pesticides, because of the 
widespread animal-drug and human-drug uses of ivermectin, the closely 
related analog of abamectin.
    It is the opinion of Merck that the use of an additional safety 
factor to address

[[Page 65047]]

risks to infants and children is not necessary. The established 
endpoints for abamectin in the CF-1 mouse and the neonatal rat have 
been shown by Merck to be overly conservative. Similar endpoints for 
ivermectin are not used by the Food and Drug Administration to support 
the allowable daily intake for ivermectin residues in food from treated 
animals.
    No evidence of toxicity was observed in neonatal rhesus monkeys 
after 14 days of repeated administration of 0.1 mg/kg/day (highest dose 
tested) and in juvenile rhesus monkeys after repeated administration of 
1.0 mg/kg/day (highest dose tested). The comparative data on abamectin 
and ivermectin in primates also clearly demonstrate the dose response 
for exposure to either compound is much less steep than that seen in 
the neonatal rat. Single doses as high as 24 mg/kg of either abamectin 
or ivermectin in rhesus monkeys did not result in mortality; however, 
this dose was more than two times the LD50 in the adult rat and 
more than 20 times the LD50 in the neonatal rat. The absence of a 
steep dose-response curve in primates provides a further margin of 
safety regarding the probability of toxicity occurring in infants or 
children exposed to avermectin compounds. The significant human 
clinical experience and widespread animal drug uses of ivermectin 
without systemically toxic, developmental, or postnatal effects 
supports the safety of abamectin to infants and children.''

II. Administrative Matters

     A record has been established for this notice of filing under 
docket number PF-677 (including comments and data submitted 
electronically as described below). A public version of this 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 4:00 p.m., Monday through Friday, excluding legal 
holidays. The public record is located in Room 1132 of the Public 
Response and Program 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 notice of filing, 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 record which will also include all comments 
submitted directly in writing. The official record is the paper record 
maintained at the address in ``ADDRESSES'' at the beginning of this 
document.

List of Subjects

    Environmental protection, Agricultural commodities, Pesticides and 
pests, Reporting and recordkeeping.

    Authority: 7 U.S.C. 136a.

    Dated: December 3, 1996.

Stephen L. Johnson,
Acting Director, Office of Pesticide Programs.

[FR Doc. 96-31303 Filed 12-09-96; 8:45 am]
BILLING CODE 6560-50-F