[Federal Register Volume 69, Number 166 (Friday, August 27, 2004)]
[Notices]
[Pages 52679-52684]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-19620]


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ENVIRONMENTAL PROTECTION AGENCY

[OPP-2004-0271; FRL-7676-7]


Iodine-potassium iodide; 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 identification (ID) number OPP-
2004-0271, must be received on or before September 27, 2004.

ADDRESSES:  Comments may be submitted electronically, by mail, or 
through hand delivery/courier. Follow the detailed instructions as 
provided in Unit I. of the SUPPLEMENTARY INFORMATION.

FOR FURTHER INFORMATION CONTACT: Mary Waller, Registration Division 
(7505C), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 308-9354; e-mail address: [email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
Potentially affected entities may include, but are not limited to:
     Crop production (NAICS 111)
     Animal production (NAICS 112)
     Food manufacturing (NAICS 311)
     Pesticide manufacturing (NAICS 32532)
    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in this unit could also be 
affected. The North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether this action might apply to certain entities. If you have any 
questions regarding the applicability of this action to a particular 
entity, consult the person listed under FOR FURTHER INFORMATION 
CONTACT.

B. How Can I Get Copies of this Document and Other Related Information?

    1. Docket. EPA has established an official public docket for this 
action under docket identification (ID) number OPP-2004-0271. The 
official public docket consists of the documents specifically 
referenced in this action, any public comments received, and other 
information related to this action. Although a part of the official 
docket, the public docket does not include Confidential Business 
Information (CBI) or other information whose disclosure is restricted 
by statute. The official public docket is the collection of materials 
that is available for public viewing at the Public Information and 
Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall 2, 
1801 S. Bell St., Arlington, VA. This docket facility is open from 8:30 
a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
docket telephone number is (703) 305-5805.
    2. Electronic access. You may access this Federal Register document 
electronically through the EPA Internet under the ``Federal Register'' 
listings at http://www.epa.gov/fedrgstr/.
    An electronic version of the public docket is available through 
EPA's

[[Page 52680]]

electronic public docket and comment system, EPA Dockets. You may use 
EPA Dockets at http://www.epa.gov/edocket/ to submit or view public 
comments, access the index listing of the contents of the official 
public docket, and to access those documents in the public docket that 
are available electronically. Although not all docket materials may be 
available electronically, you may still access any of the publicly 
available docket materials through the docket facility identified in 
Unit I.B.1. Once in the system, select ``search,'' then key in the 
appropriate docket ID number.
    Certain types of information will not be placed in the EPA Dockets. 
Information claimed as CBI and other information whose disclosure is 
restricted by statute, which is not included in the official public 
docket, will not be available for public viewing in EPA's electronic 
public docket. EPA's policy is that copyrighted material will not be 
placed in EPA's electronic public docket but will be available only in 
printed, paper form in the official public docket. To the extent 
feasible, publicly available docket materials will be made available in 
EPA's electronic public docket. When a document is selected from the 
index list in EPA Dockets, the system will identify whether the 
document is available for viewing in EPA's electronic public docket. 
Although not all docket materials may be available electronically, you 
may still access any of the publicly available docket materials through 
the docket facility identified in Unit I.B. EPA intends to work towards 
providing electronic access to all of the publicly available docket 
materials through EPA's electronic public docket.
    For public commenters, it is important to note that EPA's policy is 
that public comments, whether submitted electronically or in paper, 
will be made available for public viewing in EPA's electronic public 
docket as EPA receives them and without change, unless the comment 
contains copyrighted material, CBI, or other information whose 
disclosure is restricted by statute. When EPA identifies a comment 
containing copyrighted material, EPA will provide a reference to that 
material in the version of the comment that is placed in EPA's 
electronic public docket. The entire printed comment, including the 
copyrighted material, will be available in the public docket.
    Public comments submitted on computer disks that are mailed or 
delivered to the docket will be transferred to EPA's electronic public 
docket. Public comments that are mailed or delivered to the docket will 
be scanned and placed in EPA's electronic public docket. Where 
practical, physical objects will be photographed, and the photograph 
will be placed in EPA's electronic public docket along with a brief 
description written by the docket staff.

C. How and to Whom Do I Submit Comments?

    You may submit comments electronically, by mail, or through hand 
delivery/courier. To ensure proper receipt by EPA, identify the 
appropriate docket ID number in the subject line on the first page of 
your comment. Please ensure that your comments are submitted within the 
specified comment period. Comments received after the close of the 
comment period will be marked ``late.'' EPA is not required to consider 
these late comments. If you wish to submit CBI or information that is 
otherwise protected by statute, please follow the instructions in Unit 
I.D. Do not use EPA Dockets or e-mail to submit CBI or information 
protected by statute.
    1. Electronically. If you submit an electronic comment as 
prescribed in this unit, EPA recommends that you include your name, 
mailing address, and an e-mail address or other contact information in 
the body of your comment. Also include this contact information on the 
outside of any disk or CD ROM you submit, and in any cover letter 
accompanying the disk or CD ROM. This ensures that you can be 
identified as the submitter of the comment and allows EPA to contact 
you in case EPA cannot read your comment due to technical difficulties 
or needs further information on the substance of your comment. EPA's 
policy is that EPA will not edit your comment, and any identifying or 
contact information provided in the body of a comment will be included 
as part of the comment that is placed in the official public docket, 
and made available in EPA's electronic public docket. If EPA cannot 
read your comment due to technical difficulties and cannot contact you 
for clarification, EPA may not be able to consider your comment.
    i. EPA Dockets. Your use of EPA's electronic public docket to 
submit comments to EPA electronically is EPA's preferred method for 
receiving comments. Go directly to EPA Dockets at http://www.epa.gov/edocket/, and follow the online instructions for submitting comments. 
Once in the system, select ``search,'' and then key in docket ID number 
OPP-2004-0271. The system is an ``anonymous access'' system, which 
means EPA will not know your identity, e-mail address, or other contact 
information unless you provide it in the body of your comment.
    ii. E-mail. Comments may be sent by e-mail to [email protected], 
Attention: Docket ID number OPP-2004-0271. In contrast to EPA's 
electronic public docket, EPA's e-mail system is not an ``anonymous 
access'' system. If you send an e-mail comment directly to the docket 
without going through EPA's electronic public docket, EPA's e-mail 
system automatically captures your e-mail address. E-mail addresses 
that are automatically captured by EPA's e-mail system are included as 
part of the comment that is placed in the official public docket, and 
made available in EPA's electronic public docket.
    iii. Disk or CD ROM. You may submit comments on a disk or CD ROM 
that you mail to the mailing address identified in Unit I.C.2. These 
electronic submissions will be accepted in WordPerfect or ASCII file 
format. Avoid the use of special characters and any form of encryption.
    2. By mail. Send your comments to: Public Information and Records 
Integrity Branch (PIRIB) (7502C), Office of Pesticide Programs (OPP), 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460-0001, Attention: Docket ID number OPP-2004-0271.
    3. By hand delivery or courier. Deliver your comments to: Public 
Information and Records Integrity Branch (PIRIB), Office of Pesticide 
Programs (OPP), Environmental Protection Agency, Rm. 119, Crystal Mall 
2, 1801 S. Bell St., Arlington, VA, Attention: Docket ID 
number OPP-2004-0271. Such deliveries are only accepted during the 
docket's normal hours of operation as identified in Unit I.B.1.

D. How Should I Submit CBI to the Agency?

    Do not submit information that you consider to be CBI 
electronically through EPA's electronic public docket or by e-mail. You 
may claim information that you submit to EPA as CBI by marking any part 
or all of that information as CBI (if you submit CBI on disk or CD ROM, 
mark the outside of the disk or CD ROM as CBI and then identify 
electronically within the disk or CD ROM the specific information that 
is 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

[[Page 52681]]

docket and EPA's electronic public docket. If you submit the copy that 
does not contain CBI on disk or CD ROM, mark the outside of the disk or 
CD ROM clearly that it does not contain CBI. Information not marked as 
CBI will be included in the public docket and EPA's electronic public 
docket without prior notice. If you have any questions about CBI or the 
procedures for claiming CBI, please consult the person listed 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 
ID 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 Cosmetic Act (FFDCA), 21 U.S.C. 346a. 
EPA has determined that this petition contains data or information 
regarding the elements set forth in FFDCA 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: August 20, 2004.
Betty Shackleford,
Acting Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

    The petitioner summary of the pesticide petition is printed below 
as required by FFDCA section 408(d)(3). The summary of the petition was 
prepared by the petitioner and represents the view of the petitioner. 
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.

Ajay North America L.L.C.

PP 3E6572

    EPA has received a pesticide petition (3E6572) from Ajay North 
America L.L.C., 1400 Industry Road, Powder Springs, Georgia 30127 
proposing, pursuant to section 408(d) of the FFDCA, 21 U.S.C. 346a(d), 
to amend 40 CFR part 180 to establish an exemption from the requirement 
of a tolerance for iodine-potassium iodide in or on the raw 
agricultural commodities bananas, grapes, and melons. 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 primary residue of iodine-potassium iodide 
(AJ1629) is the inorganic halide, iodide (I). In the presence of 
organic matrices such as food items, the iodine in the iodine-potassium 
iodide complex is very rapidly reduced to iodide (I), with a reaction 
rate on the order of seconds. Due to the natural occurrence in all 
fruits and vegetables of anti-oxidants, which are the likely agents in 
this reduction, there is little likelihood of iodine remaining intact 
in any crop matrix.
    2. Analytical method. A residue method was developed which converts 
all iodine species present to the iodide ion, which is then quantitated 
(This methodology measures total iodine in the crop, similar to the 
method used in the Food and Drug Administration (FDA) Total Diet 
Study). Since iodine is naturally present in most foods, there is a 
natural background level of iodine that varies by crop and location. 
(Natural levels of iodine in the environment are higher in coastal 
areas due to the proximity to oceanic sources of the element).
     3. Magnitude of residues. The results of the Chilean and Costa 
Rican non-GLP residue studies demonstrate that the average residues 
found in the soil-treated grapes and melons and foliar applied banana 
crops are virtually identical to the residues found in the control 
samples. In the Chilean grape trials AJ1629 34EC was applied to the 
soil at a variety of rates. The average residue for treated Thompson 
grapes was 0.39 parts per million (ppm) compared to 0.40 ppm for 
untreated Thompson grapes. The average residue for treated Red Globe 
grapes was 0.21 ppm, compared to 0.22 ppm for untreated Red Globe 
grapes. AJ1629 EC was also used in a foliar application to bananas in 
Costa Rica. Iodine residues in the whole treated bananas ranged from 
non-detectable to 0.11 ppm, in comparison to the untreated bananas with 
a range of residues from non-detectable to 0.13 ppm. Residues were 
below the limit of quantitation (0.05 ppm) in both treated and control 
banana pulp samples. In Costa Rican melon samples, iodide was not 
detected in either control or AJ1629 treated samples.

B. Toxicological Profile

    Iodine is an essential element necessary to maintain human health 
and normal function of the thyroid gland. The effects of both iodine 
deficiency and excessive iodine intake in humans are well known and 
have been documented in a robust body of scientific literature. The 
levels of iodine intake considered optimal for various populations are 
based on Recommended Daily Allowances (RDAs) established by various 
Agencies. The proposed uses of iodine for disease and nematode control 
on grapes and melons, and for disease control on banana plants would 
not result in significant changes in iodine intake for any populations 
or subpopulations. Thus, the proposed use will not have any impact on 
individuals or subpopulations that are currently at risk for either 
deficiencies or excesses in iodine intake.
    There is universal agreement on the dangers of iodine deficiency. 
Iodine deficiency is well known to result in a range of disorders 
including hypothyroidism, goiter, reproductive impairment and 
developmental abnormalities. While it is clear that excess iodine 
intake can cause adverse health effects, there are differences of 
opinion in the scientific community

[[Page 52682]]

with regard to the dangers of iodine excess. Health professionals 
consider the risk of iodine deficiency to be a more serious concern 
than the risk of excess dietary iodine.
    A number of organizations, including Agency for Toxic Substances 
and Disease Registry (ATSDR), International Programme on Chemical 
Safety (IPCS), National Academy of Sciences, and the Joint Food and 
Agriculture Organization/World Health Organization (FAO/WHO) Expert 
Committee on Food Additives, have reviewed the literature regarding 
iodine and detailed its effects on human health. The toxicology 
information provided below has been assembled primarily from these 
sources.
    Iodine has been approved by FDA for use in drugs and has been 
deemed GRAS as a food additive. There are also a number of 
antimicrobial uses already approved by the EPA for iodine and iodophors 
including sanitization of food handling equipment. A cleared review 
dated February 26, 1993 (Case No.3080, Toxicology Branch, Phase 4 
Review, Pat McLaughlin) indicated that iodine and potassium iodide are 
well known in the literature, and while iodine is very irritating, it 
is not very toxic internally. EPA accepted the interchangeability of 
iodine and potassium iodide (EPA Cleared review dated July 5, 1996, 
Iodine Greybeard submission No. S496959, Toxicology Branch, Sanjivani 
Diwan). Potassium iodide is not toxic and has been deemed GRAS by the 
FDA as a food additive.
    In an FDA Assessment entitled ``Potassium Iodide and Potassium and 
Calcium Iodates: Proposed Affirmation of GRAS Status as Direct Human 
Food Ingredients with Specific Limitations'' (42 FR 29925, June 10, 
1977), the opinion of the Select Committee was that ingested potassium 
iodine and other iodides are readily absorbed and utilized to the 
extent required for nutritional needs, the excess being excreted 
primarily in the urine. There was no evidence in the studies on 
experimental animals and man available to the Committee that indicated 
acute or chronic toxic effects, including mutagenic, teratogenic, and 
carcinogenic effects, resulting from the consumption of potassium 
iodide by euthyroid individuals in amounts that are several orders of 
magnitude greater than those now being consumed in the daily diet.
    In the 2002 National Academy of Sciences Report, the RDA of iodine 
for adult men and women is 0.15 mg/day (150 [mu]g/day) and the 
Tolerable Upper Intake Level for adults is 1.1 mg/day. Intake varies 
considerably from day to day and the RDAs are based on average intakes. 
The RDA for children 1-8 years old is 0.09 milligram/day (mg/day) (90 
[mu]g/day). The Tolerable Upper Intake Level is 0.2 mg/day for children 
1-3 years old, 0.3 mg/day for children 4-8 years old and 0.6 mg/day for 
children 9-13. The Tolerable Upper Intake Level is 0.9 mg/day for 
adolescents 14-18 years of age.
    The Joint FAO/WHO Expert Committee on Food Additives assessed the 
human data on iodine for the purpose of establishing a maximum 
tolerated daily intake [661. Iodine (WHO Food Additives Series 24)]. 
The assessment concluded that iodine is an essential dietary element 
which is required for synthesis of thyroid hormones. The Committee 
concluded that the human response to excess iodine is variable and that 
the maximum tolerable level of iodine appears to be in the range from 
somewhat above recommended dietary allowances to one (1.0) mg/day. As 
indicated by Pennington (Pennington, J.A.T. (1990): A review of iodine 
toxicity reports. J. Am. Diet Assoc. 90: 1571-1581.), most people are 
very tolerant of excess iodine intake from food. Subpopulations with 
autoimmune thyroid disease and iodine deficiency respond adversely to 
intake of iodine, which would be considered safe for the general 
population.
    The principal sources of iodine in the diet include, milk and dairy 
products, seafood, iodized salt and infant formula. The mean intake of 
iodine from food in the United States is 0.29 to 0.41 mg/day for 
females and males age 19 and above. For children 1-3 years old the mean 
intake is 0.3 mg/day, for children 4-8 years old the mean intake is 
0.38 mg/day and for children 9-13 years old the mean intake is 0.38 to 
0.49 mg/day. For adolescents 14-18 years of age, the mean intake is 
0.33 to 0.53 mg/day. While this level of intake is considered adequate 
for the general population, the results of the National Health and 
Nutrition Examination Surveys I and III (NHANES I and III), conducted 
during the periods 1971-1974 and 1988-1994, respectively, show that the 
median iodine concentration in the population decreased more than 50% 
between the two surveys.
    Residue trials of AJ1629 using maximum application rates on soil-
treated grapes and melons and foliar applied bananas show that iodine 
residue levels in the food commodities are comparable for control and 
treated crops. Therefore, the proposed uses of iodine for disease and 
nematode control on grapes and melons, and for disease control on 
banana plants would not result in significant changes in iodine intake 
for any populations or subpopulations.
    The toxicology data described below has been developed from human 
studies rather than animal studies. Therefore, an uncertainty factor is 
not needed to account for interspecies variability. The acute Minimal 
Risk Level (MRL) for iodine has been set at 0.01 milligram/kilogram/day 
(mg/kg/day) based on a NOAEL of 0.024 mg/kg/day for healthy adult 
humans. The chronic MRL is 0.01 mg/kg/day based on a no observed 
adverse effect level (NOAEL) of 0.01 mg/kg/day total iodide intake and 
a lowest observed effect level (NOAEL) of 0.029 mg/kg/day for 
subclinical hypothyroidism in healthy human children. An uncertainty 
factor is not needed to account for variability in sensitivity within 
species because the NOAEL is based on children, a sensitive 
subpopulation.
    1. Acute toxicity. Acute oral: 315 mg/kg (Category II); acute 
dermal: >3,000 mg/kg Category III); acute inhalation: 0.363 mg/L 
(Category II); dermal irritation: corrosive (Category I); eye 
irritation: waived based on dermal irritation; dermal sensitization: 
not a sensitizer.
    2. Genotoxicty. Iodine has been examined in a number of studies and 
it has not been found to be mutagenic in a variety of eukaryotic cell 
systems. The ATSDR draft report indicates that, ``potassium iodide, I2, 
and povidone iodine (0.1-10 mg/mL) did not show mutagenic effects in 
L5178Y mouse lymphoma cells or in transforming activity in Balb/c 3T3 
cells grown in culture.'' Additionally, potassium iodide and I2 were 
negative for mutagenicity in drosophila melanogaster and I2 was 
negative in His+ revertant assay in saccharomyces cerevisiae. Iodide is 
a free-radical scavenger and has been shown to decrease hydrogen 
peroxide-induced reversion in strain TA104 of Salmonella typhimurium.
    3. Reproductive and developmental toxicity--i. Reproductive. 
According to the ATSDR draft report on iodine toxicology, excessive 
iodine intake may result in hypothyroidism or hyperthyroidism. The 
effects of excess iodine on reproductive function are secondary to 
thyroid gland dysfunction.
    To counteract the negative effects of iodine deficiency during 
pregnancy, the RDA for iodine in pregnant women is higher than that for 
the general population. In addition, the authors of the comparative 
iodine nutrition surveys, NHANES I (1971-1974) and III (1988-1994), 
voiced concern about the increased proportion of women of child-bearing 
age and pregnant women who

[[Page 52683]]

are in the iodine deficiency range. This trend is particularly 
important because iodine deficiency disorders include goiter, 
hypothyroidism, mental retardation, reproductive impairment, cretinism, 
decreased child survival and varying degrees of other growth and 
developmental abnormalities. The most damaging effect of iodine 
deficiency is on the developing brain. If severe enough to affect 
thyroid hormone synthesis during fetal and postnatal life, iodine 
deficiency will result in hypothyroidism and brain damage. Such iodine 
deficiency, therefore, can lead to irreversible intellectual deficits 
with great impact on populations. Correction of iodine deficiency 
dramatically decreases the prevalence of these disorders. In the U.S., 
it is an FDA requirement that infant formula must contain supplemental 
iodine.
    ii. Developmental. While there are developmental effects related to 
excessive iodine consumption, ATSDR indicated in their draft 
toxicological profile for iodine, that ``iodine deficiency is far more 
likely to cause prenatal and postnatal hypothyroidism and be associated 
with neurologic injury leading to cretinism, a developmental effect.'' 
Other effects that might be caused by iodine deficiency during 
development include severe mental retardation, neurologic 
abnormalities, growth retardation, or abnormal pubertal development. 
Iodine deficiency during pregnancy, infancy, or early childhood also 
may cause endemic cretinism. The symptoms of cretinism are mental and 
physical retardation, deaf-mutism, and various neurological 
abnormalities. Hypothyroidism due to iodine deficiency may be cured 
with iodine administration, but the effects of cretinism are not 
reversible. The effects of iodine deficiency on development far 
outweigh the effects of excess iodine intake.
    4. Subchronic toxicity. Dietary iodine deficiency stimulates TSH 
secretion which results in thyroid hypertrophy. The enlargement of the 
thyroid gland due to iodine deficiency is called endemic goiter. Iodine 
intakes consistently lower than 0.050 mg/day usually result in goiter. 
Women and adolescent girls seem especially at risk. Most goiterous 
individuals are clinically euthyroid. Large goiters may cause 
obstructive complications of the trachea, esophagus, and blood vessels 
of the neck. Goiters also are associated with an increased risk of 
other thyroid diseases and malignant growth.
    Hypothyroidism is the primary effect of subchronic exposures to 
excess iodine. Below are summaries of several human studies conducted 
with iodine over 14 to 28 day periods. The ATSDR draft report has set 
the MRL for acute-duration oral exposure (1-14 days) at 0.01 mg/kg/day.
    Several subchronic studies on humans were reviewed by ATSDR 
including one conducted on 18 healthy male and female adults over 14 
days at daily oral doses of 1.5 mg I/day as sodium iodide with a 
background intake of 0.2 mg/day. The total iodide intake was 
approximately 1.7 mg I/day (approximately 0.024 mg/kg/day). There were 
significantly depressed serum concentrations of TT4, FT4 and TT3 and 
significantly elevated serum TSH concentrations compared with 
pretreatment levels. Hormone levels were within the normal range and, 
therefore, the subjects were not clinically hypothyroid.
    Another study was conducted on ten healthy male adults over a 14-
day period using oral doses of 0, 0.5, 1.5 and 4.5 mg I/day as sodium 
iodide. Including a background iodide intake of between 0.25-0.32 mg/
day, total intake was 0.3, 0.8, 1.8 and 4.8 mg/day. These levels are 
approximately equivalent to 0.004, 0.011, 0.026 and 0.069 mg/kg/day. 
Small but significant, transient decreases in serum TT4 and FT4 
concentrations and an increase in serum TSH concentrations were seen at 
the 1.8 and 4.8 mg/day dose level relative to the pretreatment values. 
The magnitude of the changes at the higher iodide dosages yielded 
hormone concentrations that were within the normal range and, thus, 
would not represent clinically significant thyroid suppression.
    A 14 to 28 day study was conducted on 30 elderly adult females 
given daily doses of 0.5 mg I/day, with a background exposure of about 
0.072-0.1 mg/day, for a total iodide intake of 0.6 mg/day or 0.0086 mg/
kg/day. There were significantly decreased serum concentrations of FT4 
but, on average, the magnitude of the changes did not produce 
clinically significant depression in thyroid hormone levels. Five 
subjects had serum TSH concentrations typically considered at the high 
end of the normal range.
    5. Chronic toxicity. Severe and prolonged iodine deficiency results 
in deficient supply of thyroid hormones. This condition, which is 
referred to as hypothyroidism or myxedema, is characterized by reduced 
metabolic rate, cold intolerance, weight gain, puffy facial features, 
edema, a hoarse voice, and mental sluggishness.
    Chronic exposure to an excess of iodine primarily results in 
conditions such as hypothyroidism, hyperthyroidism, and/or thyroid 
autoimmunity. A NOAEL of 0.01 mg/kg/day and a LOAEL of 0.029 mg/kg/day 
were established for subclinical hypothyroidism in healthy human 
children. This NOAEL was used to set the MRL of 0.01 mg/kg/day for 
humans. The NOAEL was not adjusted for sensitivity, because it was 
based upon a sensitive subpopulation, children. The LOAEL based upon 
slight thyroid enlargement is not indicative of functional impairment.
    Studies have shown that the chronic MRL for children, adults and 
the elderly is the same.
    6. Animal metabolism. The above proposed iodine potassium- iodide 
uses do not include any animal feed items; therefore, animal metabolism 
data are not necessary.
    7. Metabolite toxicology. There are no metabolites of toxicological 
concern.
    8. Endocrine disruption. The thyroid effects normally associated 
with iodine result from either a deficiency or from excessive iodine 
intake as noted in the toxicology discussion above. The principal 
direct effects of excessive iodine ingestion on the thyroid gland are 
hypothyroidism, hyperthyroidism and thyroiditis. Most iodine-induced 
hypothyroidism is transient. Epidemiological and clinical literature 
suggests that hyperthyroidism occurs most often in people who have a 
previous history of iodine deficiency, goiter or thyroid disease. 
Thyroiditis is an inflammation of the thyroid gland which is often 
secondary to thyroid gland autoimmunity. The proposed use of iodine 
will not add to overall intake or exposure, and therefore will not 
increase risk of endocrine disruption.
    9. Additional information.. Iodine deficiency disorders include 
goiter, hypothyroidism, mental retardation, reproductive impairment, 
cretinism, decreased child survival and varying degrees of other growth 
and developmental abnormalities. The most damaging effect of iodine 
deficiency is on the developing brain. If severe enough to affect 
thyroid hormone synthesis during fetal and postnatal life, iodine 
deficiency will result in hypothyroidism and brain damage. Correction 
of iodine deficiency dramatically decreases the prevalence of these 
disorders. Thus, in the United States, infant formula must contain 
0.005 to 0.075 mg (5 to 75 [mu]g) of iodine per 100 kilocalories.
    As indicated by Pennington (1990), most people are very tolerant of 
excess iodine intake from food. Subpopulations with autoimmune thyroid 
disease and iodine deficiency respond adversely to intake of iodine, 
which would be considered safe for the general population. The 
principal effects of

[[Page 52684]]

excess iodine intake for the general population are thyroiditis, 
goiter, hypothyroidism, hyperthyroidism, sensitivity reactions, thyroid 
papillary cancer, and acute responses in some individuals. There may be 
other unrecognized sources (i.e., in addition to food, water, and 
supplements) of iodine that increase the risk of adverse effects. 
Available evidence clearly corroborates that the adverse effects of 
iodine deficiency far outweigh the risks associated with the ingestion 
of excess iodine.

C. Aggregate Exposure

    1. Dietary exposure. An exemption from the requirement of tolerance 
is proposed for iodine-potassium iodide on bananas, grapes, and melons. 
For purposes of assessing the potential dietary exposure to iodine, a 
review of the open literature has been conducted.
    i. Food. Nearly every food (raw agricultural commodity or 
processed/prepared food item) contains measurable amounts of iodine. As 
discussed in the Residue Chemistry, Magnitude of the Residues section 
(A.3.), residue studies conducted to date for AJ1629 demonstrated that 
residues from AJ1629 in the soil-treated grapes and melons and foliar 
applied banana crops are virtually identical to the residues found in 
the control samples. Therefore, exposure to iodine through dietary 
intake is not expected to increase due to the use of AJ1629.
    ii. Drinking water. An exposure assessment for drinking water is 
not necessary due to the proposed use pattern of iodine-potassium 
iodide.
    2. Non-dietary exposure. Iodine is widely used in disinfectants, 
germicides, and related products. These products are readily available 
and have been widely used for many years. A non-dietary exposure 
assessment is not necessary due to the proposed use pattern of iodine-
potassium iodide.

D. Cumulative Effects

    To our knowledge there are currently no available data or other 
reliable information indicating that any toxic effects produced by 
iodine would be cumulative with those of other chemical compounds; thus 
only the potential risks of iodine have been considered in this 
assessment of its aggregate exposure.

E. Safety Determination

    1. U.S. population. Iodine is a naturally occurring element, 
present in air, soil, water and food at levels that vary, depending on 
geographic location. It is ubiquitous and is found in all non-treated 
crops in varying amounts. Residue studies with crops from AJ1629 trials 
have shown that the average residues of iodine (as iodide) in treated 
crops are indistinguishable from residues in untreated crops. Since the 
dietary intake of iodine is not expected to increase because of the 
proposed uses of AJ1629, there is a reasonable certainty that no harm 
will result from its use.
    2. Infants and children. As noted above, iodine is a naturally 
occurring element that infants and children will be exposed to through 
a variety of sources including water and food. In the U.S. iodine is a 
mandated nutrient in baby formula, required to be present at levels of 
5 to 75 micrograms/100 kilocalories of formula. Residues from the use 
of AJ1629 are virtually indistinguishable from residues in untreated 
crops, therefore, exposure from pesticidal use will be very minimal.

F. International Tolerances

    There are no known international tolerances for residues of iodine- 
potassium iodide in food or animal feed.
[FR Doc. 04-19620 Filed 8-26-04; 8:45 am]
BILLING CODE 6560-50-S