[Federal Register Volume 62, Number 92 (Tuesday, May 13, 1997)]
[Notices]
[Pages 26305-26313]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-12472]


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ENVIRONMENTAL PROTECTION AGENCY

[PF-731; FRL-5714-3]


Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: This notice announces the initial filing of pesticide 
petitions proposing the establishment of regulations for residues of 
certain pesticide chemicals in or on various food commodities.
DATES: Comments, identified by the docket control number PF-731, must 
be received on or before June 12, 1997.
ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch, Information Resources and Services Division 
(7506C), Office of Pesticides 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 by following 
the instructions under ``SUPPLEMENTARY INFORMATION.'' No confidential 
business information should be submitted through e-mail.
    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 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: Philip Errico, Product 
Manager (PM-25), Registration Division (7505C), Office of Pesticide 
Programs, Environmental Protection Agency, 401 M St., S.W., Washington, 
D.C. 20460.

[[Page 26306]]

 Office Location, telephone number, and e-mail address: Rm. 241 Crystal 
Mall #2, 1921 Jefferson Davis Highway, Arlington, VA 22202, (703) 305-
6800; e-mail: [email protected].
SUPPLEMENTARY INFORMATION: EPA has received pesticide petitions as 
follows proposing the establishment and/or amendment of regulations for 
residues of certain pesticide chemicals in or on various food 
commodities under section 408 of the Federal Food, Drug, and Comestic 
Act (FFDCA), 21 U.S.C. 346a. EPA has determined that these petitions 
contain 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 grantinig of 
the petition. Additional data may be needed before EPA rules on the 
petition.
    The official record for this notice of filing, as well as the 
public version, has been established for this notice of filing under 
docket control number [PF-731] (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 p.m., Monday through Friday, excluding legal 
holidays. The official record is located at the address in 
``ADDRESSES'' at the beginning of this document.
    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. Comment 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 the docket number (insert docket number) and appropriate 
petition number. Electronic comments on this proposed rule may be filed 
online at many Federal Depository Libraries.

List of Subjects

    Environmental protection, Agricultural commodities, Food additives, 
Feed additives, Pesticides and pests, Reporting and recordkeeping 
requirements.

    Dated: April 30, 1997.

James Jones,

Acting Director, Registration Division, Office of Pesticide Programs.

Summaries of Petitions

    Petitioner summaries of the pesticide petitions are printed below 
as required by section 408(d)(3) of the FFDCA. The summaries of the 
petitions were prepared by the petitioners and represent the views of 
the petitioners. EPA is publishing the petition summaries verbatim 
without editing them in any way. The petition summary announces the 
availability of a description of the analytical methods available to 
EPA for the detection and measurement of the pesticide chemical 
residues or an explanation of why no such method is needed.

1. DowElanco

PP 4F4412

    EPA has received a pesticide petition (PP 4F4412) from DowElanco 
9330 Zionsville Road Indianapolis, IN 46254 proposing pursuant to 
section 408(d) of the Federal Food, Drug and Cosmetic Act, 21 U.S.C. 
346a(d), to amend 40 CFR part 180 by establishing a tolerance for 
inadvertent residues of the herbicide picloram in or on the raw 
agricultural commodity grain sorghum grain, forage, and stover at 0.3, 
0.2, and 0.5 ppm, respectively. The proposed analytical method is ACR 
73.3.S2. Pursuant to the sect 408(d)(2)(A)(i) of the FFDCA, as amended, 
Company has submitted the following summary of information, data and 
arguments in support of their pesticide petition. This summary was 
prepared by DowElanco and EPA has not fully evaluated the merits of the 
petition. EPA edited the summary to clarify that the conclusions and 
arguments were the petitioner's and not necessarily EPA's and to remove 
certain extraneous material.
    Picloram provides control of deep rooted perennial weeds either in 
grainland, fallowland or on CRP acres. With the addition of the 
proposed tolerance, grain sorghum could be considered as a rotational 
crop option for the producer. The Agency has completed the 
reregistration review of picloram, culminating in publication of the 
Reregistration Eligibility Decision (RED) for picloram which was 
received on October 5, 1995. The RED concludes that picloram and its 
derivatives can be used without causing unreasonable adverse effects to 
humans or the environment. Therefore, all uses of products containing 
picloram acid and its derivatives were judged eligible for 
reregistration. In view of this comprehensive regulatory review, as 
well as the lack of human dietary consumption of grain sorghum and the 
negligible dietary impact on livestock associated with this proposed 
use, establishment of these tolerances will not cause exposure to 
exceed the levels at which there is an appreciable risk.

A. Residue Chemistry

    1. Plant metabolism. The qualitative nature of the residue in 
plants is understood based on a wheat metabolism study. The residue of 
concern in wheat forage, straw and grain is conjugated picloram, which 
is hydrolyzable by acid, base and B-glucosidase. The minor metabolites 
that were identified in grain and straw were 4-amino-6-hydroxy-3,5-
dichloropicolinic acid and 4-amino-2,3,5-trichloropyridine.
    2. Analytical method. The analytical portions of the magnitude of 
residue studies were performed at DowElanco in Midland, MI. The 
analytical method utilized for the determination of picloram residue 
levels in the submitted studies was ACR 73.3.S2. There is a practical 
analytical method for detecting and measuring levels of picloram in or 
on food with a limit of quantitation that allows monitoring of food 
with residues at or above the levels set in these tolerances. EPA has 
provided information on this method to FDA. The method is available to 
anyone who is interested in pesticide residue enforcement.
    3. Magnitude of residues.

  Table --Summary Of Residues Of Picloram (ppm) Found In Grain Sorghum  
------------------------------------------------------------------------
                  Matrix                                Range           
------------------------------------------------------------------------
Grain                                       NDa0.23                     
Forage                                      ND-0.17                     
Fodder                                      ND-0.44                     
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aND = less than one-half of the validated lower limit of quantitation of
  0.05 g/g in grain and 0.1 g/g in forage and fodder. 

B. Toxicological Profile

    1. Acute toxicity. Studies for acute toxicity indicate that 
picloram is classified as category III for acute oral toxicity, 
category III for acute dermal toxicity, category I/II (depending on 
whether acid or salts) for acute inhalation toxicity, category IV for 
skin irritation potential, and category III for eye irritation 
potential. The potassium salt is classified as a skin sensitizer. In 
addition, picloram has a low vapor pressure.
    Picloram potassium salt has low acute toxicity. The rat oral 
LD50 is 3,536

[[Page 26307]]

milligrams per kilogram (mg/kg) or greater for males and females. The 
rabbit dermal LD50 is >2,000 mg/kg and the rat inhalation 
LC50 is >1.63 mg/L air (the highest attainable 
concentration). Picloram potassium salt is a positive skin sensitizer 
in guinea pigs but is not a dermal irritant. Technical picloram 
potassium salt is a moderate ocular irritant but ocular exposure to the 
technical material would not normally be expected to occur to infants 
or children or the general public. End use formulations of picloram 
have similar low acute toxicity profiles plus low ocular toxicity as 
well. Therefore based on the available acute toxicity data, picloram 
does not pose any acute dietary risks.
    2. Genotoxicity. Picloram acid was evaluated in the Ames test using 
Salmonella typhimurium. Doses ranged up to 5,000 ug/plate, with and 
without metabolic activation. The test substance did not produce a 
mutagenic response either in the presence or absence of activation.
    Picloram acid was evaluated for gene mutation in mammalian cells 
(HGPRT/CHO). As evaluated up to toxic levels (750 ug/ml without 
metabolic activation; 1,250 ug/ml with metabolic activation), the 
compound was found to be negative for inducing forward mutation in 
Chinese hamster ovary (CHO) cells.
    Picloram acid was evaluated for cytogenetic effects on bone marrow 
cells of rats via intragastric administration at dosage levels of 0 
(vehicle), 20, 200 or 2,000 mg/kg. The test material did not produce 
cytogenetic effects in the study.
    Picloram acid was evaluated for genotoxic potential as administered 
to primary rat hepatocyte cultures at concentrations of 0 (vehicle), 
10, 33.3, 100, 333.3 or 1,000 ug/ml. The test material was negative for 
unscheduled DNA synthesis (UDS, a measure of DNA damage/repair) treated 
up to cytotoxic levels of (1,000 ug/ml).
    3. Reproductive and developmental toxicity. The HED RfD Peer Review 
Committee concluded that there was no evidence, based on the available 
data, that picloram and its salts were associated with significant 
reproductive or developmental toxicity under the testing conditions.
    In the following developmental toxicity studies, the dose levels 
that appear in parenthesis are picloram acid equivalents where the 
conversion factor employed was 0.86 as applied to doses of potassium 
salt.
    Picloram potassium salt was administered to New Zealand rabbits by 
oral Savage at dosage levels of 0, 40, 200 and 400 milligram per 
kilogram per day (mg/kg/day) (picloram acid equivalents) during days 6 
to 18 of gestation. The maternal NOEL is 40 (34) mg/kg/day, where the 
LOEL is 200 (172) mg/kg/day based on reduced maternal weight gain 
during gestation. The developmental NOEL is 400 mg/kg/day and the LOEL 
was not determined.
    The potassium salt of picloram was administered to CD rats by 
gastric intubation at dosage levels of 0, 35 (30), 174 (150) and 347 
(298) mg/kg/day during day 6-15 of gestation: The test vehicle was 
distilled water. There was no evidence of developmental toxicity at 
doses up to and including the high dose of 347 (298) mg/kg/day. The 
maternal LOEL is 347 (298) mg/kg/day based upon excessive salivation in 
the dams of the high dose group. Hence, the developmental toxicity NOEL 
is greater than or equal to 347 (298) mg/kg/day. The maternal toxicity 
LOEL is 347 (298) mg/kg/day and NOEL is 174 (150) mg/kg/day.
    Picloram acid was evaluated in a 2-generation reproduction study in 
the CD rat. Dosage levels employed were 0, 20, 200 or 1,000 mg/kg/day. 
The parental LOEL is 1,000 mg/kg/day based on histopathological lesions 
in the kidney of males of both generations and some females. In males 
of both generations, blood in the urine, decreased urine specific 
gravity, increased absolute and relative kidney weight, and increased 
body weight gain was observed at the high dose. The parental LOEL is 
1,000 mg/kg/day and the NOEL is 200 mg/kg/day. The reproductive LOEL 
was not identified and the NOEL is 1,000 mg/kg/day.
    4. Subchronic toxicity. In a 90-day oral toxicity study, picloram 
acid was administered via the diet to groups of 15 F344 rats/sex/dose 
at dosage levels of 0, 15, 50, 150, 300 or 500 mg/kg/day. Based upon 
liver weight changes and minimal microscopic changes in the liver, the 
systemic LOEL is 150 mg/kg/day. The NOEL is 50 mg/kg/day.
    In a 1982 6-month dog dietary study, picloram acid was evaluated at 
dosage levels of 0, 7, 35 or 175 mg/kg/day. The systemic NOEL is 35 mg/
kg/day and the LOEL is 175 mg/kg/day based on decreases in the 
following: body weight gain, food consumption, liver weights 
(relative), alkaline phosphatase and alanine transaminase. Increased 
liver to body weight ratios and absolute weights were observed in only 
two males at the 35 mg/kg/day dosage level.
    In a 21-day dermal toxicity study, the potassium salt of picloram 
was administered dermally to groups of five New Zealand white rabbits 
of each sex at doses of 0 (vehicle control), 75.3, 251 or 753 mg/kg/day 
(O. 65, 217 or 650 mg/kg/day picloram acid equivalents) for a total of 
15 applications over the 21-day period. The NOEL is greater than or 
equal to 753 mg/kg/day for both sexes: hence, a LOEL was not 
established for either sex. Although the limit dose of 1,000 mg/kg/day 
was not achieved, practical difficulties precluded administering more 
test material. The study revealed the non-systemic effects of dermal 
irritation and very slight to well defined edema and/or erythema in 
both sexes at all dose levels.
    5. Chronic toxicity. In a 1988 1-year chronic feeding study in the 
dog, picloram acid was administered orally via the diet at dosage 
levels of 0, 7, 35 or 175 mg/kg/day The LOEL is 175 mg/kg/day based on 
increased liver weight (absolute and relative). The NOEL is 35 mg/kg/
day.
    In a chronic toxicity/carcinogenicity feeding study conducted in 
the F344 rat, picloram acid (technical grade 93% containing 197 ppm 
hexachlorobenzene as an impurity) was evaluated at 0, 20, 60 or 200 mg/
kg/day for 2 years. The chronic toxicity LOEL was 60 mg/kg/day as 
evidenced by altered size and tinctorial properties of centrilobular 
hepatocytes and increased absolute and/or relative liver weights in 
both sexes. The NOEL was 20 mg/kg/day. The study was negative for 
carcinogenicity, but due to concerns that a MTD may not have been 
achieved and the fact that the test material contained 197 ppm 
hexachlorobenzene impurity, the study was not considered to fulfill 
adequately the carcinogenicity testing requirement.
    In response to the deficiencies cited in the study above, an 
additional 2-year dietary chronic/carcinogenicity study was conducted 
(in 1992) using F344 rats administered picloram acid at dosage levels 
of 0, 250 or 500 mg/kg/day for 104 weeks. Chronic toxicity was observed 
at 250 mg/kg/day among males only (increased incidence and severity of 
glomerulonephritis, blood in urine, decreased specific gravity of 
urine, increased size of hepatocytes that often had altered staining 
properties). Among females there were chronic effects only at 500 mg/
kg/day (increased glomerulonephropathy, increased absolute and relative 
kidney weight). There was no evidence of carcinogenicity in this study. 
It should be noted that use of the Osborne-Mendel rat was waived due to 
lack of availability of the strain of rat. In addition, the level of 
hexachlorobenzene in the test material employed in this study was 12 
ppm. These two studies fulfill the guidelines 83-l(a) and 83-2(a) for 
rats.
    In a 1992 2-year dietary carcinogenicity study in B6C3F1 mice,

[[Page 26308]]

picloram acid was evaluated at doses of 0, 100, 500 or 1,000 mg/kg/day. 
The systemic NOEL in this study is 500 mg/kg/day based on a significant 
increase in absolute and relative kidney weights in males (at the high 
dose level). No histopathological lesions were found to corroborate 
these changes. There was no evidence of carcinogenicity.
    The dose levels tested in the 1992 carcinogenicity studies in rats 
and mice were considered adequate for carcinogenicity testing. The 
treatment did not alter the spontaneous tumor profile in mice or 
different strains of rats tested under the testing conditions. The 
chemical was classified as a ``Group E - Evidence of Non-
Carcinogenicity for humans.'' This classification applies to the 
picloram acid and potassium salt forms for which acceptable 
carcinogenicity studies were available for review by the HED 
Carcinogenicity Peer Review Committee (5/26/88).
    Using its Guidelines for Carcinogen Risk Assessment published 
September 24, 1986 (51 FR 33992), picloram is classified as Group ``E'' 
for carcinogenicity (no evidence of carcinogenicity) based on the 
results of the carcinogenicity studies. The dose levels tested in the 
1992 carcinogenicity studies in rats and mice were considered adequate 
for carcinogenicity testing. The treatment did not alter the 
spontaneous tumor profile in mice or different strains of rats tested 
under the testing conditions. The chemical was classified as a ``Group 
E - Evidence of Non-Carcinogenicity for humans.'' This classification 
applies to the picloram acid and potassium salt forms for which 
acceptable carcinogenicity studies were available for review by the HED 
Carcinogenicity Peer Review Committee (5/26/88). Thus, a cancer risk 
assessment would not be appropriate.
    6. Animal metabolism. The absorption, distribution, metabolism and 
excretion of picloram acid was evaluated in female rats administered a 
single i.v. or oral gavage dose of 10 mg/kg, an oral gavage dose of 
1,000 mg/kg 14C-picloram, or 1 mg/kg/day unlabeled picloram 
by gavage for 14 days followed by a single oral gavage dose of 10 mg/kg 
14C-picloram on day 15. The study demonstrates that 
14C-picloram is rapidly absorbed, distributed and excreted 
following oral and i.v. administration. This study alone is not 
adequate; however, this study is acceptable when considered in 
conjunction with a male rat metabolism study which yielded similar 
results.

C. Aggregate Exposure

    1. Dietary exposure-- i. Food. For purposes of assessing the 
potential dietary exposure under these tolerances, aggregate exposure 
is estimated based on the TMRC from the existing and future potential 
tolerances for picloram on food crops. The TMRC is obtained by 
multiplying the tolerance level residues (existing and proposed) by the 
consumption data which estimates the amount of those food products 
eaten by various population subgroups. Exposure of humans to residues 
could also result if such residues are transferred to meat, milk, 
poultry or eggs. The following assumptions were used in conducting this 
exposure assessment: 100% of the crops were treated, the RAC residues 
would be at the level of the tolerance, and certain processed food 
residues would be at anticipated (average) levels based on processing 
studies (see attached Dietary Risk Evaluation for Picloram). This 
results in an overestimate of human exposure and a conservative 
assessment of risk. As mentioned previously, 0.9% of the RfD is 
utilized using these assumptions.
    The chronic dietary exposure/risk estimates for picloram are 
extremely low. For the United States population as a whole, the 
Theoretical Maximum Residue Contribution (TMRC) is 0.001845 milligrams 
per kilogram of body weight per day (mg/kg bw/day), only 0.9% of the 
RfD. For this same group, the Anticipated Residue Contribution (ARC) is 
0.001053 mg/kg bw/day, only 0.5% of the RfD. The subgroup with the 
greatest routine chronic exposure/risk is non-nursing infants (less 
than 1 year old), which has a TMRC of 0.004753 mg/kg bw/day (2.4% of 
the RfD) and an ARC of 0.003805 mg/kg bw/day (1.9% of the RfD).
    There is currently no form of sorghum observed in human consumption 
surveys utilized by EPA in their DRES assessments. Therefore, sorghum 
tolerances will have no effect on the human dietary consumption of 
picloram, and the proposed action, as well as existing tolerances, pose 
no concern with regards to chronic dietary exposure to food residues of 
picloram.
    ii. Drinking water. An additional potential source of dietary 
exposure to residues of pesticides are residues in drinking water. The 
Maximum Contaminant Level for residues of picloram in drinking water 
has been established at 500 g/L and a 1-10 day Health Advisory 
of 20,000 g/L. Monitoring data available from the Pesticides 
in Ground Water Database indicate that picloram has been detected in 
ground water at concentrations ranging up to 30 g/L. Results 
reported in this database typically were focused on highly vulnerable 
areas and in many cases, the database reports information from poorly 
constructed or damaged wells. These wells are at high risk because of 
the potential for surface residues to be carried directly down the 
casing into the ground water. Recognizing these high risk situations, 
an analysis of this database shows that less than 3% of the wells 
sampled were found to contain picloram. No distinction has been made 
between point and non point sources of material. Many of the 
detection's are known to be related to point source contamination 
including spills at mixing/loading sites, near wells and back siphoning 
events. Of the detection's which may have resulted from non-point 
sources, none are documented to occur on sites where application would 
be recommended based on current labeling. Nearly 99% of the ground 
water detection's are at levels of less than 1% of the Maximum 
Contaminant Level ( i.e., < 5 g/L) established for human 
consumption by the EPA Office of Drinking Water. The STORET database 
maintained by the USEPA Office of Drinking Water indicates that 
picloram has been reported in surface water samples before 1988. Of 
these detections, 85% were at concentrations 0.13 g/L or lower 
and the maximum was 4.6 g/L. The maximum concentration 
reported was 4.6 g/L.
    The impact of potential residues of picloram in drinking water on 
the aggregate risk of the herbicide is minimal. If it is assumed that 
all of the drinking water in the U.S. contains 30 g/L of 
picloram, the maximum observed in the groundwater data base, its 
contribution to the TMRC would be 0.000280 mg/kg bw/day for the general 
U.S. population, or 0.14% of the RfD. For the most sensitive population 
subgroup, Non-nursing Infants (<1 yr. old), the contribution to the 
TMRC would be 0.002855 mg/kg bw/day, or 1.4% of the RfD. In reality, 
the likelihood of drinking water being contaminated with picloram is 
extremely remote, and actual contribution to the dietary exposure of 
picloram is virtually nil.
    In summary, these data on potential water exposure indicate 
insignificant additional dietary intake and risk for picloram.
    2. Non-dietary exposure. This is a restricted use chemical that has 
no residential uses at this time; therefore, there are no human risks 
associated with residential uses.
    Entry into a treated area soon after the application of picloram is 
expected to be rare given the cultural practices typically associated 
with the use-sites (rights-of-way, forestry, pastures, range

[[Page 26309]]

lands, and small grains) defined by the picloram labels at this time. 
Furthermore, if entry should occur, the potential exposures are 
expected to be minimal due to the characteristics of those use-sites

D. Cumulative Effects

    The potential for cumulative effects of picloram and other 
substances that have a common mechanism of toxicity was considered. The 
mammalian toxicity of picloram is well defined. However, the 
biochemical mechanism of toxicity of this compound is not well known. 
No reliable information exists to indicate that toxic effects produced 
by picloram would be cumulative with those of any other chemical 
compounds. Therefore, consideration of a common mechanism of toxicity 
with other compounds is not appropriate. Thus only the potential risks 
of picloram are considered in the aggregate exposure assessment.

E. Safety Determination

    1. U.S. population. In the meeting of September 30, 1993, the OPP 
RfD Peer Review Committee recommended that the RfD for this chemical be 
based on a NOEL of 20 mg/kg/day for a dose-related increase in size and 
altered tinctorial properties of centrilobular hepatocytes in males and 
females at 60 and 200 mg/kg/day in a chronic toxicity study in rats. An 
uncertainty factor (UF) of 100 was used to account for the inter-
species extrapolation and intra-species variability. On this basis, the 
RfD was calculated to be 0.20 mg/kg/day. The theoretical maximum 
residue contribution (TMRC) from existing tolerances is 0.001845 mg/kg/
day. Existing tolerances utilize 0.9% of the RfD. It should be noted 
that no regulatory value has been established for this chemical by the 
World Health Organization (WHO) up to this date. The committee 
classified picloram as a ``Group E'' chemical, no evidence of 
carcinogenicity for humans.
    Using the conservative exposure assumptions described above and 
based on the completeness and reliability of the toxicity data, it is 
concluded that aggregate exposure to picloram will utilize 
approximately 1 percent of the RfD for the U.S. population. Generally, 
exposures below 100 percent of the RfD are of no concern because the 
RfD represents the level at or below which daily aggregate dietary 
exposure over a lifetime will not pose appreciable risk to human 
health. Thus, there is a reasonable certainty that no harm will result 
from aggregate exposure to picloram residues.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of picloram, data from 
developmental toxicity studies in the rat and rabbit and a 2-generation 
reproduction study in the rat were considered. The developmental 
toxicity studies are designed to evaluate adverse effects on the 
developing organism during prenatal development resulting from 
pesticide exposure to one or both parents. Reproduction studies 
provide: (1) Information relating to effects from exposure to the 
pesticide on the reproductive capability of mating animals and (2) data 
on systemic toxicity.
    Developmental toxicity was studied using rats and rabbits. The 
developmental study in rats resulted in a developmental NOEL of >298 
mg/kg/day and a maternal toxicity NOEL of 280 mg/kg/day. A study in 
rabbits resulted in a maternal NOEL of 34 mg/kg/day and a developmental 
NOEL of 344 mg/kg/day. Based on all of the data for picloram, there is 
no evidence of developmental toxicity at dose levels that do not result 
in maternal toxicity.
    In a 2-generation reproduction study in rats, The NOEL for parental 
systemic toxicity is 200 mg/kg/day. There was no effect on reproductive 
parameters at 1,000 mg/kg/day nor was there an adverse effect on the 
morphology, growth or viability of the offspring; thus, the 
reproductive NOEL is 1,000 mg/kg/day.
    FFDCA section 408 provides that EPA may apply an additional safety 
factor for infants and children in the case of threshold effects to 
account for pre- and post-natal toxicity and the completeness of the 
database. Based on the current toxicological data requirements, the 
database relative to pre- and post-natal effects for children is 
complete. Therefore, it is concluded that an additional uncertainty 
factor is not warranted and that the RfD at 0.2 mg/kg/day is 
appropriate for assessing aggregate risk to infants and children.
    Using the conservative exposure assumption previously described, it 
is concluded that the percent of the RfD that will be utilized by 
aggregate exposure to residues of picloram will be less than 4 percent 
of the RfD for all populations and subgroups. Since this estimate 
represents the ``worst case'' exposure for a given population (non-
nursing infants, <1 year old), exposures will be less for all other 
sub-populations e.g. children, 1-6 years. Therefore, based on the 
completeness and reliability of the toxicity data and the conservative 
exposure assessment, it is concluded that there is a reasonable 
certainty that no harm will result to infants and children from 
aggregate exposure to picloram residues.

Other Considerations

F. International Tolerances

    There are no Codex maximum residue levels established for residues 
of picloram.
    1. Endocrine effects. An evaluation of the potential effects on the 
endocrine systems of mammals has not been determined; However, no 
evidence of such effects were reported in the chronic or reproductive 
toxicology studies described above. There was no observed pathology of 
the endocrine organs in these studies. There is no evidence at this 
time that picloram causes endocrine effects.
    2. Data gaps. Data gaps currently exist for residue data for 
sorghum aspirated grain fractions. Based on the toxicological data and 
the levels of exposure, EPA has determined that the proposed tolerances 
will be safe.

2. Novartis Crop Protection

PP 6F4688

    EPA has received a pesticide petition (PP 6F4688) from Novartis 
Crop Protection, Inc., P. O. Box 18300, Greensboro, North Carolina 
27419, proposing pursuant to section 408(d) of the Federal Food, Drug 
and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR part 180 by 
establishing a tolerance for residues of the herbicide CGA-277476, 
Benzoic acid, 2-[[[[4,6-dimethyl-2-pyrimidinyl)-
amino]carbonyl]amino]sulfonyl]-,3-oxetanylester in or on the raw 
agricultural commodity soybeans at 0.01 ppm. The proposed analytical 
method involves homogenization, filtration, partition and cleanup with 
analysis by high performance liquid chromatography using UV detection. 
EPA has determined that the petition contains data or information 
regarding the elements set forth in section 408(d)(2) of the FFDCA; 
however, EPA has not fully evaluated the sufficiency of the submitted 
data at this time or whether the data supports granting of the 
petition. Additional data may be needed before EPA rules on the 
petition.
    As required by section 408(d) of the FFDCA, as recently amended by 
the Food Quality Protection Act (FQPA) Pub.L. 104-170, Novartis Crop 
Protection 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 Novartis Crop Protection. EPA is in the process of evaluating 
the petition. As

[[Page 26310]]

required by section 408(d)(3) of the FFDCA, 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.

A. Metabolism

    The qualitative nature of the metabolism of CGA-277476 in plants 
and animals is well understood for the purposes of the proposed 
tolerance. Metabolism proceeds through hydrolysis of the oxetane ring 
with subsequent cleavage of the oxetane ester and the sulfonylurea 
bridge. Metabolic pathways in plants (soybeans), rats, ruminants 
(goats), and poultry are similar. Parent CGA-277476 is the residue of 
concern.

B. Analytical Methodology

    Novartis Crop Protection, Inc. has submitted a practical analytical 
method involving homogenization, filtration, partition and cleanup with 
analysis by high performance liquid chromatography using UV detection. 
The methodology accounts for residues of CGA-277476. The limit of 
quantitation (LOQ) for the method is 0.01 ppm for CGA-277476. This 
method has undergone a successful method trial and is available for 
enforcement.

C. Residue

    Twenty field trials were conducted in typical soybean growing areas 
across the U.S. Either a single preplant or preemergence application 
(57 grams ai/A) or a split application made preemergence followed by a 
post broadcast application (total of 81 grams ai/A) was made. No 
residues (<0.01 ppm) were found in the dry beans (1X) and no residues 
were found in the processed commodities at rates up to 5X. No residues 
(<0.01 ppm) were found in rotational crops treated at the 1X rate. A 
prohibition against grazing forage, hay and silage will be placed in 
the label, as will a 60 day preharvest interval.

D. International MRL's

    There are no Codex Alimentarius Commission (CODEX) maximum residue 
levels (MRL's) established for residues of CGA-277476 in or on raw 
agricultural commodities.

E. Toxicological Profile

    1. Acute toxicity. CGA-277476 has a low order of acute toxicity. 
The rat oral LD50 is > 5,000 mg/kg, the acute rabbit dermal 
LD50 is > 2,000 mg/kg and the rat inhalation LC50 
is > 5.08 mg/L. CGA 277476 is moderately irritating to the skin but not 
irritating to the eye. It is not a skin sensitizer in guinea pigs. The 
commercial formulation (75WG) of CGA-277476 has a similar acute 
toxicity profile, with both technical and formulated product carrying a 
Category III CAUTION Signal Word.
    2. Genotoxicity. Assays for genotoxicity were comprised of tests 
evaluating the potential of CGA-277476 to induce point mutations 
(Salmonella assay and a Chinese hamster V79 lung tissue assay), 
chromosome aberrations (mouse micronucleus and a Chinese hamster ovary 
study) and the ability to induce either scheduled or unscheduled DNA 
synthesis in rat hepatocytes. The results indicate that CGA-277476 is 
not mutagenic or clastogenic and does not induce unscheduled DNA 
synthesis.
    3. Developmental/reproductive effects. The developmental and 
teratogenic potential of CGA-277476 was investigated in rats and 
rabbits. The results indicate that CGA-277476 was not maternally or 
developmentally toxic in the rabbit. Minimal developmental toxicity was 
observed at the limit dose (1,000 mg/kg) in the rat; the developmental 
no observed effect level in the rat was 300 mg/kg/day. No evidence of 
teratogenicity was observed at the limit dose of 1,000 mg/kg in either 
the rat or rabbit.
    A 2-generation reproduction study was conducted with CGA-277476 at 
feeding levels of 0, 20, 200, 5,000 or 20,000 ppm (0, 1, 10, 250 or 
1,000 mg/kg/day). The reproductive NOEL was established at a feeding 
level of 5,000 ppm (equivalent to approximately 250 mg/kg/day). Reduced 
fertility observed at the highest dose tested (20,000 ppm) was 
associated with degenerative changes in the seminiferous tubules and 
atypical spematogenesis in males and severe effects on kidneys in 
females. The NOEL for parental toxicity was established at the 200 ppm 
feeding level based on slight effects on body weight parameters at the 
next highest dose tested (i.e. 5,000 ppm).
    4. Subchronic toxicity. The subchronic toxicity of CGA-277476 was 
evaluated in studies in the rat, mouse and dog at high doses. Target 
organs included the liver, spleen, blood, kidney, urogenital tract, 
testes, epididymis and peripheral nerves and muscles. No observable 
effect levels have been established for all end-points in subchronic 
studies. The dog appears to be the most sensitive species (NOEL = 40 
ppm; 1 mg/kg) with treatment related effects on testes, peripheral 
nerve and muscle appearing at doses  5,000 ppm ( 125 mg/kg/
day).
    5. Chronic effects. The chronic toxicity of CGA-277476 was 
investigated in long term studies in the rat, mouse and dog. Target 
organs included the central and peripheral nervous systems, skeletal 
muscle, liver, kidney, gallbladder, testes, and blood. No observed 
effect levels (NOELS) have been established in each study. The dog is 
the most sensitive species with a NOEL = 40 ppm (1.3 mg/kg/day). Based 
on these data, it is expected the EPA will establish a RfD for CGA-
277476 at 0.01 mg/kg/day using the NOEL of 1.3 mg/kg/day and an 
uncertainty factor of 100.
    6. Carcinogenicity. The carcinogenicity studies conducted with CGA- 
277476 showed no evidence of an oncogenic response in either mouse or 
rat at doses that did not exceed the maximum tolerated dose. Dose 
levels in the mouse study were 2.25, 150, 525, and 1,050 mg/kg/day. In 
the rat study, dose levels were 1, 10, 100, 500, 750 (females), and 
1,000 (males) mg/kg/day. At the end of the chronic rat study, a 
statistically significant increased incidence of schwannomas was found 
in the heart of the 1,000 mg/kg/day male rats (7/59) compared to the 
control group (0/60). Based on the Guidelines for Carcinogenic Risk 
Assessment published by EPA September 24, 1986 (51 FR 33992), Novartis 
Crop Protection believes that CGA-277476 should be classified as Class 
E because the neoplastic response (marginal increased incidence of 
schwannomas) was observed only in male rats at a dose exceeding the 
maximum tolerated dose of 500 mg/kg/day. No effect was observed at 
doses  500 mg/kg/day.

F. Threshold Effects

    1. Chronic effects. Based on the available chronic toxicity data, 
it is expected the EPA will establish a RfD for CGA-277476 at 0.01 mg/
kg/day based on the results obtained in the 1-year feeding study in 
dogs using the No-Observed Effect Level (NOEL) of 1.3 mg/kg/day and an 
uncertainty factor of 100.
    2. Acute toxicity. Based on the available acute toxicity data, 
Novartis Crop Protection believes CGA-277476 does not pose any acute 
dietary risks.

G. Nonthreshold Effects.

     Carcinogenicity. Based on the Guidelines for Carcinogenic Risk 
Assessment published by EPA September 24, 1986 (51 FR 33992), Novartis 
Crop Protection believes that CGA-277476 should be classified as Class 
E because the neoplastic response (marginal increased incidence of 
schwannomas) was observed only in male rats at a dose exceeding the 
maximum tolerated dose of 500 mg/kg/day. No effect was observed at 
doses  500 mg/kg/day.

[[Page 26311]]

H. Endocrine Effects.

    CGA-277476 belongs to the sulfonylurea class of chemicals, one not 
known or suspected of having adverse effects on the endocrine system. 
Reduced fertility observed in high dose females (20,000 ppm) in the rat 
reproduction study was associated with degenerative changes in the 
seminiferous tubules and a typical spermatogenesis observed in high 
dose males. Evidence of impaired spermatogenesis was also observed at 
high doses ( 125 mg/kg/day) in the subchronic dog study.

I. Aggregate Exposure

    1. Dietary exposure. For purposes of assessing the potential 
dietary exposure to CGA-277476, Novartis Crop Protection has estimated 
aggregate exposure based on the Theoretical Maximum Residue 
Contribution from the use of CGA-277476 in or on raw agricultural 
commodities for which tolerances have been proposed (0.01 ppm on 
soybeans). In conducting this exposure assessment, Novartis has 
conservatively assumed that 100% of soybeans will contain CGA-277476 
residues at the proposed level of 0.01 ppm. No residues are anticipated 
in animal commodities and therefore, tolerances in meat, meat 
byproducts, milk, poultry and eggs are not proposed.
    2. Drinking water exposure. Another potential source of exposure of 
the general population to residues of pesticides are residues in 
drinking water. The potential for CGA-277476 to enter surface or ground 
water sources of drinking water is limited because of the low use rate. 
This is supported by the results of two small-scale prospective ground 
water monitoring studies which did not show any quantifiable residues 
of CGA-277476 in ground water samples. The Maximum Contaminant Level 
Guideline (MCLG) calculated for CGA-277476 according to EPA's procedure 
leads to an exposure value (7 ppb) substantially greater than any level 
expected to reach ground water based on study results.
    3. Non-occupational exposure. Novartis Crop Protection has 
evaluated the estimated non-occupational exposure to CGA-277476 and 
concludes that the potential for non-occupational exposure to the 
general population is unlikely because CGA-277476 is not planned to be 
used in or around the home, including home lawns, schools, recreation 
facilities or parks.

J. Cumulative Risk.

    Novartis Crop Protection has also considered the potential for 
cumulative effects of CGA-277476 and other chemicals belonging to this 
chemical class (sulfonylureas) that may have a common mechanism of 
toxicity. It is concluded that consideration of a common mechanism of 
toxicity is not appropriate at this time because there is no reliable 
data to establish whether a common mechanism exists.

K. Safety Determinations.

    1. U.S. general population. Using the conservative exposure 
assumptions described above, based on the completeness and reliability 
of the toxicity data, Novartis Crop Protection has concluded that 
aggregate exposure to CGA-277476 will utilize 0.07 percent of the RfD 
for the U.S. population based on chronic toxicity endpoints. Because 
EPA generally has no concern for exposures below 100 percent of the 
RfD, it is concluded that there is a reasonable certainty that no harm 
to the general population will result from aggregate exposure to CGA-
277476.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of CGA-277476, Novartis 
Crop Protection has considered data discussed above from developmental 
toxicity studies conducted with CGA-277476 in the rat and rabbit and a 
2-generation rat reproduction study. The developmental toxicity studies 
are designed to evaluate adverse effects on the developing organism 
resulting from chemical exposure during prenatal development to one or 
both parents. Reproduction studies provide information relating to 
effects from exposure to a chemical on the reproductive capability of 
mating animals and data on systemic toxicity.
    FFDCA section 408 provides that EPA may apply an additional safety 
factor for infants and children in the case of threshold effects to 
account for pre- and post-natal toxicity and the completeness of the 
database. Based on the current toxicological data requirements, the 
database relative to pre- and post-natal effects for children is 
complete. Further, for CGA-277476, the NOEL of 1.3 mg/kg/day from the 
chronic dog study, which was used to calculate the RfD (discussed 
above), is at least an order of magnitude lower than the developmental 
NOEL of 300 mg/kg/day from the rat teratogenicity study or the 
reproductive NOEL of 250 mg/kg/day from the multigeneration 
reproduction study. There is no evidence to suggest that developing 
organisms are more sensitive to the effects of CGA-277476 than are 
adults.
    However, Novartis Crop Protection has determined that when an 
additional tenfold safety margin is used, the percent of the RfD that 
will be utilized by aggregate exposure to residues of CGA-277476 is 0.8 
percent for nursing infants less than 1 year old, 3.5 percent for non-
nursing infants, 1.4 percent for children 1 to 6 years old and 1.1 
percent for children 7 to 12 years old. Therefore, based on the 
completeness and reliability of the toxicity data and the conservative 
exposure assessment, it is concluded that there is a reasonable 
certainty that no harm to infants and children will result from 
aggregate exposure to CGA-277476 residues.

3. Siemer and Associates

PP 6F4789

    EPA has received a pesticide petition (PP 6F4789) from Siemer & 
Associates, Inc. on behalf of National Chelating, 4672 West Jennifer, 
Suite 103, Fresno, CA 93722, proposing pursuant to section 408(d) of 
the Federal Food, Drug and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 
CFR part 180 by establishing an exemption from the requirements for a 
tolerance for ammonium thiosulfate when used for blossom thinning on 
apples.
    Pursuant to the section 408(d)(2)(A)(i) of the FFDCA, as amended, 
Siemer & Associates, Inc. on behalf of National Chelating has submitted 
the following summary of information, data and arguments in support of 
their pesticide petition. This summary was prepared by Siemer & 
Associates, Inc. and EPA has not fully evaluated the merits of the 
petition. EPA edited the summary to clarify that the conclusions and 
arguments were the petitioner's and not necessarily EPA's and to remove 
certain extraneous material.
    On August 30, 1996 Siemer & Associates on behalf of National 
Chelating petitioned the EPA, under pesticide petition 6F4789, for a 
permanent exemption from the requirements of a tolerance for ammonium 
thiosulfate on apples.
    Section 408(b)(2)(A) of the amended Federal Food, Drug, and 
Cosmetic Act allows the EPA to establish an exemption from the 
requirements for a tolerance only if the Administrator determines that 
there is a ``reasonable certainty that no harm will result from the 
aggregate exposure to the pesticide chemical residue, including all 
anticipated dietary exposures and all other exposures for which there 
is reliable information.''
    The available information indicates that there is a reasonable 
certainty that no harm will result from various types of exposure. 
Requests for waivers from the requirements of performing studies for 
known chemistry are presented and

[[Page 26312]]

substantiated. The following is a summary of the information submitted 
to the EPA to support the establishment, under Section 408(b)(2)(D) of 
the amended FFDCA, of a tolerance for ammonium thiosulfate on apples.

A. Residue Chemistry

    1. Plant metabolism. The qualitative nature of the residues of 
ammonium thiosulfate in apple is adequately understood. The requirement 
for residue studies was waived by EPA based on the knowledge that 
ammonium thiosulfate has been used as a soil applied and foliar applied 
fertilizer for many years. Prior experience and numerous publications 
teach that ammonium thiosulfate ionizes when placed into water, forming 
an ammonium ion and a thiosulfate ion which further degrades to form 
elemental sulfur and a sulfate ion. The sulfur is further oxidized to 
form a sulfate ion. The ammonium and sulfate ions thus formed are 
absorbed into the growing plant and moved into the naturally occurring 
nitrogen and sulfate pools that occur naturally in growing plants. Once 
applied to the plant, without isotope identification, it is not 
possible to separate the ammonium and sulfate ions that will occur from 
those that already occur naturally in the plant. On this basis, an 
exemption from the requirements of a tolerance is justified. There is 
no analytical method needed since there is no practical way to separate 
the ammonium and sulfate ions from those that naturally occur.
    2. Analytical method. The need for an analytical method is waived 
on the basis that there is no need for analyzing for the component of 
ammonium and sulfate ion applied for blossom thinning purposes.
    3. Magnitude of residues. No residues of ammonium thiosulfate will 
be identified separately from those ammonium and sulfate ions naturally 
occurring. This result supports the proposed exemption from the 
requirements for a tolerance.

B. Toxicological Profile

    A request to waive the battery of mammalian toxicity studies for 
ammonium thiosulfate is based on and justified by the following:
    1. Acute toxicity. Based on EPA criteria, ammonium thiosulfate 
previously registered for a non-food use as an ornamental herbicide has 
been shown to be relatively non-toxic and has been registered for non-
food use purposes as a Category III herbicide. These data have 
previously been supplied to the agency.
    2. Genotoxicity. A request for a waiver from the following 
requirements is made on the basis that sodium thiosulfate is on the FDA 
Generally Recognized as Safe (GRAS) list at 21 CFR 184.1807, and 
ammonium thiosulfate is already exempted from the requirements of a 
tolerance when used in accordance with good agricultural practices as 
inert (or occasionally active) ingredients in pesticide formulations 
applied to growing crops or to raw agricultural commodities after 
harvest (at 40 CFR 180.1001(c)). Ammonium thiosulfate ionizes to form 
ammonium ion and thiosulfate ion in water with neither of these ions 
being mutagenic or genotoxic. On that basis the following tests are 
requested to be waived.
    i. Gene Mutation - Ames.
    ii. In vitro Structural chromosomal aberration assay.
    iii. In vitro CHO/HGPRT assay.
    iv. In vivo micronucleus aberration assay.
    3. Reproductive and developmental toxicity. A request for waiving 
the data requirements for the following is made on the basis listed 
above for ``B''. In addition, all of the tests listed below rely on 
feeding the test substance, to animals that have acidic stomachs. 
Placing ammonium thiosulfate into an acidic environment will cause near 
instantaneous ion formation giving rise to ammonium and thiosulfate 
ions, which ultimately breaks down to elemental sulfur and sulfite. 
These sulfur forms will be quickly oxidized under acidic conditions to 
sulfate, which will be incorporated into the normal sulfate pool that 
exists within the metabolic system of the various animal test systems. 
The ammonium ion will react with the acidic component, most likely 
forming ammonium chloride which will be metabolized in a well 
understood pathway in the systems of the various animal test systems. 
The new moiety formed in this acidic medium is the sulfite ion which 
also is well understood and is quickly oxidized to sulfate. The FDA 
instituted studies in 1975 and 1985 on the GRAS status of sulfite and, 
as a result of these studies, has substantiated the GRAS status except 
for a few individuals that might be allergic to sulfite. In this 
proposed usage however, the sulfite will not reach the possibly 
allergic people, since the sulfite will be metabolized to sulfate in 
the plant system before reaching any sensitive people who may consume 
the treated tissue. The data waivers requested are as follows:
    i. Teratology in rats.
    ii. Teratology in rabbits.
    iii. 2-Generation reproduction in rats.
    4. Subchronic Toxicity. The data requirements listed below are 
requested to be waived on the basis illustrated above at paragraph 3.
    i. 28-Day dermal in rats.
    ii. 13-Week oral feeding in rats.
    iii. 90-Day oral feeding in dogs.
    5. Chronic toxicity. The data requirements listed below are 
requested to be waived for reasons listed above at paragraph 3.
    i. 1-Year chronic toxicity in dogs.
    ii. 18-Month chronic toxicity & carcinogenicity in mice.
    iii. 24-Month chronic toxicity & carcinogenicity in rats.
    6. Animal metabolism. The metabolism of ammonium thiosulfate is 
well understood in animals. As listed above, this substance rapidly 
ionizes in the acidic portion of the animal gut, giving rise to 
ammonium ion and sulfate ion. Both of these substances are required and 
occur in the metabolism of animals.
    7. Metabolite toxicology. No toxicologically significant 
metabolites will be detected in plant or animal metabolism studies 
using ammonium thiosulfate. Therefore, no metabolites are required to 
be regulated.
    8. Endocrine effects. There is no information available that 
suggest that ammonium thiosulfate would be associated with endocrine 
effects.

C. Aggregate Exposure

    1. Dietary exposure--i. Food. There will be no residues of ammonium 
thiosulfate that will reach any portion of the US population as a 
result of using ammonium thiosulfate as a blossom thinner on apples. 
The ammonium and sulfate ions that will arise will not be different 
from the naturally occurring forms of the ions, which exceed by far the 
amount that will be applied as a result of the use of the ammonium 
thiosulfate.
    ii. Drinking water. Ammonium and sulfate ions that arise from 
ammonium thiosulfate use will add no additional burden to the drinking 
water. The end points of the two ions formed as a result of ammonium 
thiosulfate use will both be used in plant nutrition. The ammonium form 
of nitrogen resists leaching by binding to the colloid fraction in the 
soil to resist ground water contamination. The amount of sulfate added 
as a result of the described use will add an imperceptible amount to 
the sulfate level already in existence in the soil.
    There is a reasonable certainty that no harm will result from 
dietary exposure to ammonium thiosulfate, because dietary exposures to 
residues on food cannot be differentiated from those that

[[Page 26313]]

will occur naturally in food, and exposure through drinking water is 
expected to be insignificant.
    2. Non-dietary exposure. There is no non-dietary exposure expected, 
since any ammonium thiosulfate finding its way onto the plants or 
around any plants will be absorbed and metabolized into naturally 
occurring plant constituents.

D. Cumulative Effects

    There are no cumulative effects expected since the ammonium 
thiosulfate metabolites are all incorporated into naturally occurring 
constituents found in all plant systems.

E. Safety Determination

    1. U.S. population. The natural occurrence of the metabolites of 
the ammonium and sulfate ions in all plants and in humans is the basis 
for the Generally Recognized As Safe characterization of the 
thiosulfate ion and the use of the ammonium ion as a component in 
nearly all fertilizers, supports the conclusion that there is a 
``reasonable certainty of no harm'' from aggregate exposure to ammonium 
thiosulfate.
    2. Infants and children. No developmental, reproductive or 
fetotoxic effects have been associated with ammonium thiosulfate and 
its use as a fertilizer. The calculation of safety margins with respect 
to ammonium thiosulfate is unnecessary since the ammonium and sulfate 
ions that will arise from the use of ammonium thiosulfate will add only 
slightly to the already naturally occurring nitrogen and sulfur pools 
in existence in various plants. Since there will be no residues of 
toxicological significance resulting from ammonium thiosulfate, 
calculations of safety margins are not necessary based on the lack of 
any unnatural residues.

F. International Tolerances

    There is no Codex maximum residue level established for ammonium 
thiosulfate on apple. However, ammonium thiosulfate is widely used as a 
nutrient in many parts of the world.

[FR Doc. 97-12472 Filed 5-12-97; 8:45 am]
BILLING CODE 6560-50-F