[Federal Register Volume 65, Number 235 (Wednesday, December 6, 2000)]
[Notices]
[Pages 76244-76249]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-31057]


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ENVIRONMENTAL PROTECTION AGENCY

[PF-985; FRL-6755-5]


Notice of Filing a Pesticide Petition to Establish a Tolerance 
for a Certain Pesticide Chemical in or on Food

AGENCY:  Environmental Protection Agency (EPA).

ACTION:  Notice.

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SUMMARY:  This notice announces the initial filing of a pesticide 
petition proposing the establishment of regulations for residues of a 
certain pesticide chemical in or on various food commodities.

DATES:  Comments, identified by docket control number PF-985, must be 
received on or before January 5, 2001.

ADDRESSES:  Comments may be submitted by mail, electronically, or in 
person. Please follow the detailed instructions for each method as 
provided in Unit I.C. of the SUPPLEMENTARY INFORMATION. To ensure 
proper receipt by EPA, it is imperative that you identify docket 
control number PF-985 in the subject line on the first page of your 
response.

FOR FURTHER INFORMATION CONTACT:  By mail: James Tompkins, Registration 
Support Branch, Registration Division (7505C), Office of Pesticide 
Programs, Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460; telephone number: (703) 305-5697; e-mail address: 
[email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be affected by this action if you are an agricultural 
producer, food manufacturer or pesticide manufacturer. Potentially 
affected categories and entities may include, but are not limited to:

------------------------------------------------------------------------
                                                          Examples of
           Categories                 NAICS codes         potentially
                                                      affected  entities
------------------------------------------------------------------------
Industry                          111                 Crop production
                                  112                 Animal production
                                  311                 Food manufacturing
                                  32532               Pesticide
                                                       manufacturing
------------------------------------------------------------------------

    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in the table could also be 
affected. The North American Industrial Classification System

[[Page 76245]]

(NAICS) codes have been provided to assist you and others in 
determining whether or not this action might apply to certain entities. 
If you have questions regarding the applicability of this action to a 
particular entity, consult the person listed under FOR FURTHER 
INFORMATION CONTACT.

B. How Can I Get Additional Information, Including Copies of this 
Document and Other Related Documents?

    1. Electronically. You may obtain electronic copies of this 
document, and certain other related documents that might be available 
electronically, from the EPA Internet Home Page at http://www.epa.gov/. 
To access this document, on the Home Page select ``Laws and 
Regulations'', and then look up the entry for this document under the 
``Federal Register--Environmental Documents.'' You can also go directly 
to the Federal Register listings at http://www.epa.gov/fedrgstr/.
    2. In person. The Agency has established an official record for 
this action under docket control number PF-985. The official record 
consists of the documents specifically referenced in this action, any 
public comments received during an applicable comment period, and other 
information related to this action, including any information claimed 
as confidential business information (CBI). This official record 
includes the documents that are physically located in the docket, as 
well as the documents that are referenced in those documents. The 
public version of the official record does not include any information 
claimed as CBI. The public version of the official record, which 
includes printed, paper versions of any electronic comments submitted 
during an applicable comment period, is available for inspection in the 
Public Information and Records Integrity Branch (PIRIB), Rm. 119, 
Crystal Mall #2, 1921 Jefferson Davis Highway, Arlington, VA, from 8:30 
a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
PIRIB telephone number is (703) 305-5805.

C. How and to Whom Do I Submit Comments?

    You may submit comments through the mail, in person, or 
electronically. To ensure proper receipt by EPA, it is imperative that 
you identify docket control number PF-985 in the subject line on the 
first page of your response.
    1. By mail. Submit your comments to: Public Information and Records 
Integrity Branch (PIRIB), Information Resources and Services Division 
(7502C), Office of Pesticide Programs (OPP), Environmental Protection 
Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460.
    2. In person or by courier. Deliver your comments to: Public 
Information and Records Integrity Branch (PIRIB), Information Resources 
and Services Division (7502C), Office of Pesticide Programs (OPP), 
Environmental Protection Agency, Rm. 119, Crystal Mall #2, 1921 
Jefferson Davis Highway, Arlington, VA. The PIRIB is open from 8:30 
a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
PIRIB telephone number is (703) 305-5805.
    3. Electronically. You may submit your comments electronically by 
e-mail to: [email protected], or you can submit a computer disk as 
described above. Do not submit any information electronically that you 
consider to be CBI. Avoid the use of special characters and any form of 
encryption. Electronic submissions will be accepted in Wordperfect 6.1/
8.0 or ASCII file format. All comments in electronic form must be 
identified by docket control number PF-985. Electronic comments may 
also be filed online at many Federal Depository Libraries.

D. How Should I Handle CBI That I Want to Submit to the Agency?

    Do not submit any information electronically that you consider to 
be CBI. You may claim information that you submit to EPA in response to 
this document as CBI 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. In addition to one complete 
version of the comment that includes any information claimed as CBI, a 
copy of the comment that does not contain the information claimed as 
CBI must be submitted for inclusion in the public version of the 
official record. Information not marked confidential will be included 
in the public version of the official record without prior notice. If 
you have any questions about CBI or the procedures for claiming CBI, 
please consult the person identified under FOR FURTHER INFORMATION 
CONTACT.

E. What Should I Consider as I Prepare My Comments for EPA?

    You may find the following suggestions helpful for preparing your 
comments:
    1. Explain your views as clearly as possible.
    2. Describe any assumptions that you used.
    3. Provide copies of any technical information and/or data you used 
that support your views.
    4. If you estimate potential burden or costs, explain how you 
arrived at the estimate that you provide.
    5. Provide specific examples to illustrate your concerns.
    6. Make sure to submit your comments by the deadline in this 
notice.
    7. To ensure proper receipt by EPA, be sure to identify the docket 
control number assigned to this action in the subject line on the first 
page of your response. You may also provide the name, date, and Federal 
Register citation.

II. What Action is the Agency Taking?

    EPA has received a pesticide petition as follows proposing the 
establishment and/or amendment of regulations for residues of a certain 
pesticide chemical 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 this 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 support granting of the petition. Additional data 
may be needed before EPA rules on the petition.

List of Subjects

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


    Dated: November 21, 2000.
James Jones,

Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

    The petitioner summary of the pesticide petition is printed below 
as required by section 408(d)(3) of the FFDCA. The summary of the 
petition was prepared by the petitioner and represents the view of the 
petitioners. EPA is publishing the petition summary verbatim without 
editing it 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.

[[Page 76246]]

Dow AgroSciences

 PP 4F4412

    EPA has received a pesticide petition (PP 4F4412) from Dow 
AgroSciences, 9330 Zionsville Road, Indianapolis, IN 46268-1054 
proposing, pursuant to section 408(d) of the Federal Food, Drug, and 
Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 by 
extending the time-limited tolerance for residues of picloram, 4-amino-
3,5,6-trichloropicolinic acid and its potassium salt in or on in or on 
the raw agricultural commodities (RACs) sorghum grain at 0.3 parts per 
million (ppm), sorghum grain forage at 0.2 ppm, and sorghum stover at 
0.5 ppm; and for residues of picloram in or on the RAC aspirated grain 
fractions at 4 ppm until December 31, 2002. EPA issued a final rule, 
published in the Federal Register of January 5, 1999 (64 FR 418) (FRL-
6039-4), which announced that it established a time-limited tolerance 
for the indirect or inadvertent residues of the herbicide picloram, 4-
amino-3,5,6- trichloropicolinic acid and its potassium salt in or on 
sorghum grain at 0.3 ppm, sorghum grain forage at 0.2 ppm, and sorghum 
stover at 0.5 ppm; and for residues of picloram in or on the RAC 
aspirated grain fractions at 4 ppm, with an expiration date of December 
31, 2000. A condition of this rule required Dow AgroSciences to submit 
an aspirated grain residue study before December 31, 1999, which they 
did on December 9, 1999. The extension of the time-limited tolerances 
to December 31, 2002 will allow time for review of this additional data 
and establishment of final tolerances. 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.

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 Dow AgroSciences 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 1.-Summary of residues of Picloram (ppm) found in Grain Sorghum
------------------------------------------------------------------------
                  Matrix                                Range
------------------------------------------------------------------------
Grain                                       ND \a\-0.23
Forage                                      ND-0.17
Fodder                                      ND-0.44
Aspirated grain fractions                   ND
------------------------------------------------------------------------
\a\ ND = less than one-half of the validated lower limit of quantitation
  of 0.05 g/g in grain, 0.1 g/g in forage and fodder,
  and 0.25 g/g in aspirated grain fractions.

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 milligram/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 milligram/liter (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. Genotoxicty. Picloram acid was evaluated in the Ames test using 
Salmonella typhimurium. Doses ranged up to 5,000  g/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 (1,750 gram/milliliter 
(g/mL) without metabolic activation; 4,500 g/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 intra gastric 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 g/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 g/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 gavage at dosage levels of 0, 40, 200, and 400 mg/kg/day (picloram 
acid equivalents) during days 6 to 18 of gestation. The maternal no 
observed adverse effect level (NOAEL) is 40 (34) mg/kg/day, where the 
lowest observed adverse effect level (LOAEL) is 200 (172) mg/kg/day 
based on reduced maternal weight gain during gestation. The 
developmental NOAEL is 400 (340) mg/kg/day and the LOAEL 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 LOAEL is 347 (298) mg/kg/day based upon excessive salivation 
in the dams of the high dose group. Hence, the developmental toxicity 
NOAEL is

[[Page 76247]]

greater than or equal to 347 (298) mg/kg/day. The maternal toxicity 
LOAEL is 347 (298) mg/kg/day and NOAEL 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 LOAEL 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 LOAEL is 
1,000 mg/kg/day and the NOAEL is 200 mg/kg/day. The reproductive LOAEL 
was not identified and the NOAEL 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 LOAEL is 150 mg/kg/day. The NOAEL 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 NOAEL is 35 
mg/kg/day and the LOAEL is 175 mg/kg/day based on decreases in body 
weight gain and food consumption and increases in liver weights 
(relative), alkaline phosphatase and alanine transaminase. Increased 
liver to body weight ratios and absolute liver 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 (vehicle control) 0, 75.3, 251, or 753 mg/kg/
day (0, 65, 217, or 650 mg/kg/day picloram acid equivalents) for a 
total of 15 applications over the 21-day period. The NOAEL is greater 
than or equal to 753 mg/kg/day for both sexes; hence, a LOAEL 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 LOAEL is 175 mg/kg/day based 
on increased liver weight (absolute and relative). The NOAEL 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 two years. The chronic toxicity LOAEL 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 NOAEL 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, 
picloram acid was evaluated at doses of 0, 100, 500, or 1,000 mg/kg/
day. The systemic NOAEL 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 (May 26, 1988).
    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 May 26, 1988). Thus, a cancer 
risk assessment would not be appropriate.
    Hexachlorobenzene (HCB), a recognized impurity in picloram 
compounds, is considered to be an animal carcinogen and probable human 
carcinogen as discussed in the 1988 Registration Standard for picloram. 
The Q* is 1.02 (mg/kg/day)-1. The maximum level of HCB in 
picloram is considered to be 0.005%.
    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.
    7. Endocrine disruption. 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.

 C. Aggregate Exposure

    1. Dietary exposure.-i. Food. For purposes of assessing the 
potential

[[Page 76248]]

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 the 
HED exposure assessment: 100% of the crops were treated, the RAC 
residues would be at the level of the tolerance, and some refinements 
were made based on marketing information previously supplied to HED by 
BEAD. This screening level analysis results in an overestimate of human 
exposure and a conservative assessment of risk.
    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 0.0011 mg/kg bw/day, 
< 1 of the reference dose (RfD). The subgroup with the greatest routine 
chronic exposure is Non-nursing Infants (Less Than 1-Year Old), which 
has a TMRC of 0.0042 mg/kg bw/day (2% of the RfD).
    There is currently no form of sorghum observed in human consumption 
surveys utilized by EPA in their dietary risk evaluation model (DRES) 
assessments. Furthermore, residues of picloram in sorghum do not 
increase the dietary burden of picloram in animal feeds. 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.
    The estimated carcinogenic dietary risk for HCB as an impurity in 
picloram only for the U.S. population is 1.5 X10-7 which is 
less than the 1.0 X10-6 point below which risk is generally 
considered to be negligible.
    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.
    The Agency has published screening methods for estimating chemical 
residues in both ground water (SCI-GROW2) and surface water (GENEEC). 
Employing these methods yields the following 56-day Expected 
Environmental Concentrations (EEC) for a range of application rates:

             Table 2.-Expected Environmental Concentrations
------------------------------------------------------------------------
   Application rate (lb. acid        SCI-GROW2 EEC    GENEEC EEC (g/L)          m>g/L)
------------------------------------------------------------------------
0.023 (wheat, barley,and oats     4.4                 1.2
 use rate)
1 (maximum broadcastrate in       189                 51.3
 label)
2(maximum spottreatment rate in   379                 103.1
 label)
------------------------------------------------------------------------

    The 56-day value is an appropriate endpoint to employ for the 
chronic exposure scenario. Default, conservative inputs were used for 
the models, as described in July 27, 1998 memorandum from EPA to Dow 
AgroSciences. Employing these values, a worst-case drinking water risk 
assessment can be performed as summarized below:

                                                         Table 3.-Drinking Water Risk Assessment
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                            Maximum water
      Population subgroup1         RfD (mg/kg/day)   Food exposure (mg/   exposure (mg/kg/   DWLOC(g/L)3     SCI-GROW2 EEC        GENEEC EEC
                                                           kg/day)              day)2                                (g/L)      (g/L)
--------------------------------------------------------------------------------------------------------------------------------------------------------
U.S population                   0.2                 0.0011              0.2                 7,000                 379                 103.1
Females(13-19, not nursing       0.2                 0.00090             0.2                 6,000                 379                 103.1
 orpregnant)
Non-Nursing infants( 1 yr. old)  0.2                 0.0043              0.2                 2,000                 379                 103.1
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Population subgroups chosen in EPA memorandum of July/27/98.
\2\=RfD - ARC from DRES (cited above)
\3\ Drinking water level of concern, based on default water body weights and water consumption of: 70 kg/2L (adult males), 60 kg/2L (adult female), 10
  kg/1L (infant).

    This tables shows that for even the most highly exposed population, 
exposure from water is below HED's DWLOC for chronic dietary exposure. 
Further refinement is also possible based on monitoring data. 
Monitoring data available from the Pesticides in Ground Water Data base 
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 detections are known to be 
related to point source contamination including spills at mixing/
loading sites, near wells and back siphoning events. Of the detections 
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 detections 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 data base maintained by the USEPA Office of Drinking Water 
indicates that picloram has been reported in surface water

[[Page 76249]]

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. Comparing these 
values to the DWLOC shows an even greater degree of protection for all 
of the population subgroups.
    HCB contamination of ground water resources is relatively unlikely 
due to its high binding potential. Based on monitoring data and fate 
properties it is unlikely that long term HCB concentrations in surface 
water would exceed 10 ppt. Therefore, exposure from water is below 
EPA's drinking water level of concern of 34 ppt for chronic dietary 
exposure to HCB for the U.S. population.
    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 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 NOAEL 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  1% 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% of the RfD for the U.S. population. Generally, 
exposures below 100% 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 
(i) information relating to effects from exposure to the pesticide on 
the reproductive capability of mating animals and (ii) data on systemic 
toxicity.
    Developmental toxicity was studied using rats and rabbits. The 
developmental study in rats resulted in a developmental NOAEL of > 298 
mg/kg/day and a maternal toxicity NOAEL of 280 mg/kg/day. A study in 
rabbits resulted in a maternal NOAEL of 34 mg/kg/day and a 
developmental NOAEL 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 NOAEL 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 NOAEL 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-natal and post-natal toxicity and the completeness of 
the data base. Based on the current toxicological data requirements, 
the data base relative to pre-natal and post-natal effects for children 
is complete. Therefore, it is concluded that an additional UF 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% 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.

 F. International Tolerances

    There are no Codex maximum residue levels established for residues 
of picloram.
[FR Doc. 00-31057 Filed 12-5-00; 8:45 am]
BILLING CODE 6560-50-S