[Federal Register Volume 70, Number 153 (Wednesday, August 10, 2005)]
[Rules and Regulations]
[Pages 46706-46740]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-15840]



[[Page 46705]]

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Part IV





Environmental Protection Agency





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40 CFR Part 180



Order Denying Objections to Issuance of Tolerances; Final Rule

  Federal Register / Vol. 70, No. 153 / Wednesday, August 10, 2005 / 
Rules and Regulations  

[[Page 46706]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-2005-0190; FRL-7727-4]


Order Denying Objections to Issuance of Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final Order.

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SUMMARY: On four occasions in the first half of 2002, the Natural 
Resources Defense Council (NRDC) and various other parties filed 
objections with EPA to final rules under section 408 of the Federal 
Food, Drug, and Cosmetic Act (FFDCA), (21 U.S.C. 346a), establishing 
pesticide tolerances for various pesticides. The objections apply to 14 
pesticides and 112 separate pesticide tolerances. Although the 
objections raise numerous pesticide-specific issues, they all focus on 
the potential risks that the pesticides pose to farm children. This 
Order responds to NRDC's objections as to all of the challenged 
tolerances with the exception of the objections pertaining to the 
imidacloprid tolerance on blueberries which were previously denied. The 
objections to the other tolerances are denied for the reasons stated 
herein.

FOR FURTHER INFORMATION CONTACT: Nicole Williams, Registration 
Division, (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001; telephone number: (703) 308-5551; fax number: (703) 308-6920; e-
mail address: [email protected].

SUPPLEMENTARY INFORMATION: This order is outlined as follows:

I. General Information
 A. Does This Action Apply to Me?
 B. How Can I Get Additional Information, Including Copies of this 
Document and Other Related Documents?
 1. Docket
 2. Electronic access
II. Introduction
 A. What Action Is the Agency Taking?
 B. What Is the Agency's Authority for Taking This Action?
III. Statutory and Regulatory Background
 A. Statutory Background
 B. Assessing Risk Under the FFDCA
 C. Science Policies
 1. Children's Safety Factor Policy
 2. Aggregate Exposure Policies
 D. NRDC Farmworker Children Petition
IV. The Challenged Tolerance Decisions
 1. Halosulfuron-methyl
 2. Pymetrozine
 3. Mepiquat
 4. Bifenazate
 5. Zeta-cypermethrin
 6. Diflubenzuron
 7. 2,4-D
 8. Isoxadifen-ethyl
 9. Acetamiprid
 10. Propiconazole
 11. Furilazole
 12. Fenhexamid
 13. Fluazinam
V. NRDC Objections
 A. In General
 B. Generic Issues
 1. Children's safety factor issue
 2. Aggregate exposure issues.
 3. Reliance on LOAELs and NOAELs
 C. Pesticide-specific Issues
VI. Public Comment
 A. In General
 B. Individual Comments
 1. The FQPA Implementation Working Group
 2. Inter-Regional Research Project Number 4 (IR-4)
 3. ISK Biosciences - Fluazinam
 4. Bayer CropScience - Isoxadifen-ethyl
 5. Aventis CropScience - Acetamiprid
 6. FMC Corporation - Zeta-cypermethrin
 7. Crompton Corporation - Diflubenzuron and Bifenazate
 a. Diflubenzuron
 b. Bifenazate
 8. Syngenta Crop Protection - Propiconazole and Pymetrozine
 a. Propiconazole
 b. Pymetrozine
 9. BASF Corporation - Mepiquat
 10. Industry Task Force II on 2,4-D Research Data
VII. Response to Objections
 A Expired Tolerances
 B. Children's Exposure to Pesticides in Agricultural Areas
 1. Studies Focusing on Exposure to Children in Agricultural Areas
 2. Information Bearing on Exposure Levels as a Result of Spray 
Drift and Post-Application Drift of Volatilized Residues
 a. Pesticide Spray Drift During Application
 (1) Comparison of AgDrift Model estimates with exposurefrom 
residential lawn use generally.
 (2)Evaluation of MOE's based on AgDrift Model for the pesticides in 
the Objections
 b. Volatilization of Applied Pesticides
 (1) Analysis of CFPR Report and Ranking Study
 (2) Vapor Pressure
 c. Conclusion
 C. Failed to Retain Children's 10X Safety Factor
 1. Introduction
 2. Lack of DNT Study Generally
 a. Pesticides may cause neurological developmental effects
 b. 1998 Retrospective Study on Submitted DNT Studies
 c. 10X Task Force Report
 d. EPA's 10X Policy
 e. Conclusion
 3. Other Pesticide-specific Missing Toxicity Data
 a. Diflubenzuron
 b. Fluazinam
 c. Furilazole
 d. 2,4-D
 4. Missing Exposure Data - General
 a. Farm Children Exposure
 b. Lack of comprehensive drinking water (DW) monitoring data
 5. Missing Exposure Data - Specific
 a. Mepiquat
 b. Bifenazate
 c. Zeta-cypermethrin
 d. Diflubenzuron
 e. Acetamiprid
 6. Missing Risk Assessments
 a. Halosulfuron-methyl
 b. Bifenazate
 c. Isoxadifen-ethyl
 d. Propiconazole
 e. Fenhexamid
 f. Fluazinam
 g. 2,4-D
 7. Conclusion on Children's Safety Factor Objections
 C. LOAEL/NOAEL
 1. Generic Legal Argument
 2. Objections Pertaining to Specific Pesticides
 a. Pymetrozine
 b. Mepiquat
 c. Zeta-cypermethrin
 d. Fluazinam
 e. Isoxadifen-ethyl, Acetamiprid, Propiconazole, Furilazole, and 
Fenhexamid
 D. Aggregate Exposure
 1. Worker Exposure
 2. Classification of Farm Children as a Major Identifiable 
Population Subgroup
 3. Adequacy of EPA's Assessment of the Aggregate Exposure of 
Children, Including Children in Agricultural Areas
 4. Residential Exposure as a Result of Use Requiring a Tolerance
 5. Anticipated Residues/Exposures Due to Purchase of Food at 
Farmstands
 6. Population Percentile Used in Aggregate Exposure Estimates
 a. In General
 b. Choice of Population Percentile
 7. Alleged Inadequacies Pertaining to Specific Pesticides
 a. Pymetrozine
 b. Bifenazate
 c. Zeta-cypermethrin
 d. Diflubenzuron
 e. 2,4-D
 f. Isoxadifen-ethyl, acetamiprid, fluazinam
E. Human Testing
F. Conclusion on Objections
VIII. Response to Comments on NRDC's Objections
IX. Regulatory Assessment Requirements
X. Submission to Congress and the Comptroller General
XI. Time and Date of Issuance of This Order
XII. References

I. General Information

A. Does This Action Apply to Me?

    In this document EPA denies objections to a tolerance actions filed 
by the Natural Resources Defense Council (NRDC) and the following 
additional parties: Boston Women's Health Book Collective, Breast 
Cancer Action, Californians for Pesticide Reform, Commonweal, Lymphoma 
Foundation of America, Natural Resources Defense

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Council, Northwest Coalition for Alternatives to Pesticides, Pesticide 
Action Network, North America, Pineros y Campesinos Unidos del 
Noroeste, SF-Bay Area Chapter of Physicians for Social Responsibility, 
and Women's Cancer Resource Center. This action may also be of interest 
to agricultural producers, food manufacturers, or other pesticide 
manufacturers. Potentially affected categories and entities may 
include, but are not limited to:
     Industry, e.g., NAICS 111, 112, 311, 32532, Crop 
production, Animal production, Food manufacturing, Pesticide 
manufacturing.
    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities who may be interested in today's 
action.

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

    1. Docket. EPA has established an official public docket for this 
action under docket identification (ID) number OPP-2005-0190. 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 electronic public docket and comment system, EPA Dockets. You may 
use EPA Dockets at http://www.epa.gov/edocket/ to 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.

II. Introduction

A. What Action Is the Agency Taking?

    On four occasions in the first half of 2002, the NRDC and various 
other parties filed objections with EPA to final rules under section 
408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), (21 U.S.C. 
346a), establishing pesticide tolerances for various pesticides. [The 
objectors are hereinafter collectively referred to as ``NRDC.'']. The 
objections apply to 14 pesticides and 112 separate pesticide 
tolerances. This Order responds to objections as to all of the 
tolerances other than the objections as to the imidacloprid tolerance 
on blueberries. Those objections were denied previously. (69 FR 30042, 
May 26, 2004).
    Although the objections raise numerous pesticide-specific issues, 
they all primarily focus on the potential risks that the pesticides 
pose to farm children. Further, each of the objections makes two main 
assertions with regard to the pesticide tolerances in question: (1) 
That EPA has not properly applied the additional 10X safety factor for 
the protection of infants and children in section 408(b)(2)(C); and (2) 
that EPA has not accurately assessed the aggregate exposure of farm 
children to pesticide residues. NRDC did not exercise the option 
provided in section 408(g)(2) to request a hearing on its objections, 
but instead asked that the Agency rule on its objections on the basis 
of its written objections and attached submissions.
    Because the objections raised questions of broad interest, EPA 
published a representative copy of the objections in the Federal 
Register for comment, (67 FR 41628, June 19, 2002), and made all of the 
objections available for public review on its website. On May 26, 2004, 
EPA denied the objections as to one of the challenged tolerances 
(imidacloprid on blueberries) because that tolerance had expired. (69 
FR 30042, May 26, 2004). At the same time EPA denied the objections to 
the imidacloprid tolerance on mootness grounds, EPA also established a 
new imidacloprid blueberry tolerance and as part of that action 
addressed the issues raised by the NRDC objections. (69 FR 30076, May 
26, 2004). In the course of addressing these issues, EPA responded to a 
petition concerning farm children filed in 1998 by NRDC and various 
other parties. (69 FR at 30069-70, May 26, 2004). This Order relies 
heavily on much of the reasoning set forth in connection with the 
establishment of the new imidacloprid blueberry tolerance.
    The body of this document contains the following sections. First, 
there is a background section which explains the applicable statutory 
and regulatory provisions, the relevant EPA science policy documents, 
and prior NRDC actions with regard to farm children. Second, EPA 
describes the objected-to tolerance actions. Third, there is a section 
setting forth in greater detail the substance of the objections. 
Fourth, a summary of the public comment is presented. Finally, EPA 
announces its response to the objections and responds to public 
comments.

B. What Is the Agency's Authority for Taking This Action?

    The procedure for filing objections to tolerance actions and EPA's 
authority for acting on such objections is contained in section 408(g) 
of the FFDCA and regulations at 40 CFR part 178. (21 U.S.C. 346a(g)).

III. Statutory and Regulatory Background

A. Statutory Background

    EPA establishes maximum residue limits, or ``tolerances,'' for 
pesticide residues in food under section 408 of the FFDCA. (21 U.S.C. 
346a). Without such a tolerance or an exemption from the requirement of 
a tolerance, a food containing a pesticide residue is ``adulterated'' 
under section 402 of the FFDCA and may not be legally moved in 
interstate commerce. (21 U.S.C. 331, 342). Monitoring and enforcement 
of pesticide tolerances are carried out by the U.S. Food and Drug 
Administration (FDA) and the U. S. Department of Agriculture (USDA).
    A pesticide tolerance may only be promulgated by EPA if the 
tolerance is ``safe.'' (21 U.S.C. 346a(b)(2)(A)(i)). ``Safe'' is 
defined by the statute to mean that ``there is a reasonable certainty 
that no harm will result from aggregate exposure to the pesticide 
chemical residue, including all anticipated dietary exposures and all 
other exposures for which there is reliable information.'' (21 U.S.C. 
346a(b)(2)(A)(ii)). Section 408 directs EPA, in making a safety 
determination, to ``consider, among other relevant factors- . . . 
.available information concerning the aggregate exposure levels of 
consumers (and major identifiable subgroups of consumers) to the 
pesticide chemical residue and to other related substances, including 
dietary exposure under the tolerance and all other tolerances in effect 
for the pesticide chemical residue, and

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exposure from other non-occupational sources.'' (21 U.S.C. 
346a(b)(2)(D)(vi)). Other provisions address in greater detail exposure 
considerations involving ``anticipated and actual residue levels'' and 
``percent of crop actually treated.'' (See 21 U.S.C. 346a(b)(2)(E) and 
(F)). Section 408(b)(2)(C) requires EPA to give special consideration 
to risks posed to infants and children. This provision directs that 
``an additional tenfold margin of safety for the pesticide chemical 
residue and other sources of exposure shall be applied for infants and 
children to take into account potential pre- and post-natal toxicity 
and completeness of the data with respect to exposure and toxicity to 
infants and children.'' (21 U.S.C. 346a(b)(2)(C)). EPA is permitted to 
``use a different margin of safety for the pesticide chemical residue 
only if, on the basis of reliable data, such margin will be safe for 
infants and children.'' (Id.). [The additional safety margin for 
infants and children is referred to throughout this notice as the 
``children's safety factor.''] These provisions establishing the 
detailed safety standard for pesticides were added to section 408 by 
the Food Quality Protection Act of 1996 (FQPA), an act that 
substantially rewrote this section of the statute.
    Tolerances are established by rulemaking under the unique 
procedural framework set forth in the FFDCA. Generally, the rulemaking 
is initiated by the party seeking the tolerance by means of filing a 
petition with EPA. (See 21 U.S.C. 346a(d)(1)). EPA publishes in the 
Federal Register a notice of the petition filing along with a summary 
of the petition, prepared by the petitioner. (21 U.S.C. 346a(d)(3)). 
After reviewing the petition, and any comments received on it, EPA may 
issue a final rule establishing the tolerance, issue a proposed rule, 
or deny the petition. (21 U.S.C. 346a(d)(4)). Once EPA takes final 
action on the petition by either establishing the tolerance or denying 
the petition, any affected party has 60 days to file objections with 
EPA and seek an evidentiary hearing on those objections. (21 U.S.C. 
346a(g)(2)). EPA's final order on the objections is subject to judicial 
review. (21 U.S.C. 346a(h)(1)).
    EPA also regulates pesticides under the Federal Insecticide, 
Fungicide, and Rodenticide Act (FIFRA), (7 U.S.C. 136 et seq). While 
the FFDCA authorizes the establishment of legal limits for pesticide 
residues in food, FIFRA requires the approval of pesticides prior to 
their sale and distribution, (7 U.S.C. 136a(a)), and establishes a 
registration regime for regulating the use of pesticides. FIFRA 
regulates pesticide use in conjunction with its registration scheme by 
requiring EPA review and approval of pesticide labels and specifying 
that use of a pesticide inconsistent with its label is a violation of 
Federal law. (7 U.S.C. 136j(a)(2)(G)). In the FQPA, Congress integrated 
action under the two statutes by requiring that the safety standard 
under the FFDCA be used as a criterion in FIFRA registration actions as 
to pesticide uses which result in dietary risk from residues in or on 
food, (7 U.S.C. 136(bb)), and directing that EPA coordinate, to the 
extent practicable, revocations of tolerances with pesticide 
cancellations under FIFRA. (21 U.S.C. 346a(l)(1)).

B. Assessing Risk Under the FFDCA

    In assessing and quantifying non-cancer risks posed by pesticides 
under the FFDCA as amended by the FQPA, EPA first determines the 
toxicological level of concern and then compares estimated human 
exposure to this level of concern. This comparison is done through 
either calculating a safe dose in humans (incorporating all appropriate 
safety factors) and expressing exposure as a percentage of this safe 
dose (the reference dose (RfD) approach) or dividing estimated human 
exposure into the lowest dose at which no adverse effects from the 
pesticide are seen in relevant studies (the margin of exposure (MOE) 
approach). How EPA determines the level of concern, chooses safety 
factors, and assesses risk under these two approaches is explained in 
more detail below. EPA's general approach to estimating exposure is 
also briefly discussed.
    For dietary risk assessment (for risks other than cancer), the dose 
at which no adverse effects are observed (the ``NOAEL'') from the 
toxicology study identified as appropriate for use in risk assessment 
is used to estimate the toxicological level of concern. However, the 
lowest dose at which adverse effects of concern are identified (the 
``LOAEL'') is sometimes used for risk assessment if no NOAEL was 
achieved in the toxicology study selected. A safety or uncertainty 
factor is then applied to this toxicological level of concern to 
calculate a safe dose for humans, usually referred to by EPA as an 
acute or chronic reference dose (RfD). The RfD is equal to the NOAEL 
divided by all applicable safety or uncertainty factors. Typically, a 
safety or uncertainty factor of 100X is used, 10X to account for 
uncertainties inherent in the extrapolation from laboratory animal data 
to humans and 10X for variations in sensitivity among members of the 
human population as well as other unknowns. Further, under the FQPA, an 
additional safety factor of 10X is presumptively applied to protect 
infants and children, unless reliable data support selection of a 
different factor. To quantitatively describe risk using the RfD 
approach, estimated exposure is expressed as a percentage of the RfD. 
Dietary exposures lower than 100 percent of the RfD are generally not 
of concern.
    For non-dietary, and combined dietary and non-dietary, risk 
assessments (other than cancer risk assessments) the same safety 
factors are used to determine the toxicological level of concern. For 
example, when 1,000X is the appropriate safety factor (10X to account 
for interspecies differences, 10X for intraspecies differences, and 10X 
for FQPA), the level of concern is that there be a 1,000-fold margin 
between the NOAEL from the toxicology study identified as appropriate 
for use in risk assessment and human exposure. To estimate risk, a 
ratio of the NOAEL to aggregate exposures (margin of exposure (MOE) = 
NOAEL/exposure) is calculated and compared to the level of concern. In 
contrast to the RfD approach, the higher the MOE, the safer the 
pesticide. Accordingly, if the level of concern for a pesticide is 
1,000, MOE's exceeding 1,000 would generally not be of concern.
    For cancer risk assessments, EPA generally assumes that any amount 
of exposure will lead to some degree of cancer risk. Using a model 
based on the slope of the cancer dose-response curve in relevant 
studies, EPA estimates risk in terms of the probability of occurrence 
of additional cancer cases as a result of exposure to the pesticide. An 
example of how such a probability risk is expressed would be to 
describe the risk as one in one hundred thousand (1 X 10-5), 
one in a million (1 X 10-6), or one in ten million (1 X 
10-7). Under certain specific circumstances, MOE 
calculations will be used for the carcinogenic risk assessment. No 
further discussion of cancer risk assessment is included here because 
NRDC's objections do not relate to cancer risks.
    Equally important to the risk assessment process as determining the 
toxicological level of concern is estimating human exposure. As 
explained in more detail in Unit VII.D.5. of this document, EPA uses a 
tiering system to estimate exposure which attempts to minimize 
resources expended in exposure estimates. The first tier is generally a 
worst case assessment that is relatively easy to conduct because it 
relies on conservative (health-protective) assumptions. Only if that 
tier suggests

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that the pesticide may pose a risk of concern are more resource-
intensive tiers triggered where the focus is on obtaining more 
realistic exposure values. (Ref. 1).

C. Science Policies

    As part of implementation of the major changes to FFDCA section 408 
included in the FQPA, EPA has issued a number of policy guidance 
documents addressing critical science issues. Of particular interest to 
the NRDC objections are the science policies covering the children's 
safety factor, aggregate pesticide exposure, and the population 
percentile of exposure used in estimating aggregate exposure.
    1. Children's safety factor policy. On January 31, 2002, EPA 
released its science policy guidance on the children's safety factor. 
(Ref. 2) [This policy is hereinafter referred to as the ``Children's 
Safety Factor Policy'']. That policy had undergone an intensive and 
extended process of public comment as well as internal and external 
science peer review. An EPA-wide task force was established to consider 
the children's safety factor in March 1998. Taking into account reports 
issued by the task force on both toxicity and exposure issues, EPA's 
Office of Pesticide Programs (OPP) released a draft children's safety 
policy document in May 1999. That document was subject to an extended 
public comment period as well as review by the FIFRA Scientific 
Advisory Panel. (Id. at 5). Although the January 31, 2002 policy 
differed in some respects from prior Agency practice, for the most part 
the policy statement reflected EPA's experience in implementing the 
children's safety factor provision since the passage of the FQPA.
    The Children's Safety Factor Policy emphasizes throughout that EPA 
interprets the children's safety factor provision as establishing a 
presumption in favor of application of an additional 10X safety factor 
for the protection of infants and children. (Id. at 4, 11, 47, A-6). 
Further, EPA notes that the children's safety factor provision permits 
a different safety factor to be substituted for this default 10X factor 
only if reliable data are available to show that the different factor 
will protect the safety of infants and children. (Id.). Given the 
wealth of data available on pesticides, however, EPA indicates a 
preference for making an individualized determination of a protective 
safety factor if possible. (Id. at 11). EPA states that use of the 
default factor could under- or over-protect infants and children due to 
the wide variety of issues addressed by the children's safety factor. 
(Id.). EPA notes that ``[i]ndividual assessments may result in the use 
of additional factors greater or less than, or equal to 10X, or no 
additional factor at all.'' (Id.). Concluding that individualized 
assessments would be able to be made in most cases, EPA indicates that 
``this guidance document focuses primarily on the considerations 
relevant to determining a safety factor `different' from the default 
10X that protects infants and children. Discussions in this document of 
the appropriateness, adequacy, need for, or size of an additional 
safety factor are premised on the fact that reliable data exist for 
choosing a `different' factor than the 10X default value.'' (Id. at 
12).
    In making such individual assessments regarding the magnitude of 
the safety factor, EPA stresses the importance of focusing on the 
statutory language that ties the children's safety factor to concerns 
regarding potential pre- and post-natal toxicity and the completeness 
of the toxicity and exposure databases. (Id. at 11-12). As to the 
completeness of the toxicity database, EPA recommends use of a weight-
of-the-evidence approach which considers not only the presence or 
absence of data generally required under EPA regulations and guidelines 
but also the availability of ``any other data needed to evaluate 
potential risks to children.'' (Id. at 20). EPA indicates that the 
principal inquiry concerning missing data would center on whether the 
missing data would significantly affect calculation of a safe exposure 
level (commonly referred to as the RfD). (Id. at 22; accord 67 FR 
60950, 60955, September 27, 2002) (finding no additional safety factor 
necessary for triticonazole despite lack of developmental neurotoxicity 
(DNT) study because the ``DNT [study] is unlikely to affect the manner 
in which triticonazole is regulated.'')). When the missing data are 
data above and beyond general regulatory requirements, EPA indicates 
that the weight of evidence would generally only support the need for 
an additional safety factor where the data ``is being required for 
`cause,' that is, if a significant concern is raised based upon a 
review of existing information, not simply because a data requirement 
has been levied to expand OPP's general knowledge.'' (Ref. 2 at 23). 
Finally, with regard to the DNT study, EPA lists several important 
factors addressing the weight of evidence bearing on the degree of 
concern when such a study has been required but has not yet been 
completed. (Id. at 24). Moreover, EPA reiterates that, like any other 
missing study, the absence of the DNT study does not trigger a 
mandatory requirement to retain the default 10X value, but rather 
requires an individualized assessment centering on the question of 
whether ``a DNT study is likely to identify a new hazard or effects at 
lower dose levels of the pesticide that could significantly change the 
outcome of its risk assessment . . . .'' (Id.). The extent to which the 
policy stresses the need for EPA's evaluation of the completeness of 
the database to focus directly on whether missing data might possibly 
lower an existing RfD was a change in emphasis from past actions.
    As to potential pre- and post-natal toxicity, the Children's Safety 
Factor Policy lists a variety of factors that should be considered in 
evaluating the degree of concern regarding any identified pre- or post-
natal toxicity. (Id. at 27-31). As with the completeness of the 
toxicity database, EPA emphasizes that the analysis should focus on 
whether any identified pre- or post-natal toxicity raises uncertainty 
as to whether the RfD is protective of infants and children. (Id. at 
31). Once again, the presence of pre- or post-natal toxicity, by 
itself, is not regarded as determinative as to the children's safety 
factor. Rather, EPA stresses the importance of evaluating all of the 
data under a weight-of-evidence approach focusing on the safety of 
infants and children. (Id.). This attention on the overall database 
also indicated a shift in emphasis for EPA's implementation of the 
children's safety factor provision as previous decisions had often 
treated a finding of increased sensitivity in the young as almost 
necessitating some additional safety factor.
    In evaluating the completeness of the exposure database, EPA 
explains that a weight-of-the-evidence approach should be used to 
determine the confidence level EPA has as to whether the exposure 
assessment ``is either highly accurate or based upon sufficiently 
conservative input that it does not underestimate those exposures that 
are critical for assessing the risks to infants and children.'' (Id. at 
32). EPA describes why its methods for calculating exposure through 
various routes and aggregating exposure over those routes generally 
produce conservative exposure estimates - i.e. health-protective 
estimates due to overestimation of exposure. (Id. at 40-43). 
Nonetheless, EPA emphasizes the importance of verifying that the 
tendency for its methods to overestimate exposure in fact were 
adequately

[[Page 46710]]

protective in each individual assessment. (Id. at 44).
    Given that this policy was released at roughly the same time the 
challenged tolerance actions were issued and that the toxicological, 
exposure, and risk assessments leading up to such actions can take 
several months or even years, the challenged tolerance actions were not 
evaluated prior to being finalized under this new restatement of EPA's 
policy on the children's safety factor. EPA's experience in making 
decisions under the 2002 policy is that while for many pesticides the 
safety factor determination remains unchanged, for others the safety 
factors may go up or down. To generalize, in situations where the 
database is incomplete, EPA's heightened emphasis on whether the 
missing data may affect the assessment of risk has tended to make it 
more likely that EPA will retain the full 10X children's safety factor. 
(See, e.g., 70 FR 7876, 7882, February 16, 2005) (avermectin - 10X 
factor retained due to lack of DNT study and acute and subchronic 
neuorotoxicity studies and residual toxicological concerns as to safety 
of young); 70 FR 7886, 7891, February 16, 2005) (clothianidim - 10X 
factor retained due to lack of developmental immunotoxicity study); 69 
FR 58058, 58062-58063, September 29, 2004) (fenamidone - 10X factor 
retained due to lack of DNT study); but see 69 FR 52182, 52187, August 
25, 2004) (folpet - 10X removed despite lack of DNT study because the 
DNT study is unlikely to change RfD)). On the other hand, in instances 
where a study shows increased sensitivity in the young, the focus on 
whether in the context of the overall database such sensitivity 
indicates that EPA's risk assessment is not protective of infants and 
children, has frequently resulted in the removal of the factor. (See, 
e.g., 69 FR 63083, 63092-63093, October 29, 2004) (pyraclostrobin - 10X 
factor removed because additional sensitivity well-characterized); 69 
FR 58290, 58295, September 30, 2004) (cyazofamid - 10X factor removed 
because additional sensitivity well-characterized); but see 69 FR 
62602, 62610, October 27, 2004) (deltamethrin - 10X factor lowered but 
not removed taking into consideration level at which additional 
sensitivity was observed)). As these decisions evidence, the 
determination on the children's safety factor is heavily dependent on 
the results from the studies specific to the pesticide in question. 
(See, e.g., 70 FR 14535, 14541-14542, March 23, 2005) (dinotefuran - 
10X factor retained as to some risk assessments due to the lack of a 
developmental immunotoxicity study; no additional factor on any risk 
assessment found necessary to address lack of a DNT study)).
    2. Aggregate exposure policies. As mentioned above, the FQPA-added 
safety standard directs that the safety of pesticide residues in food 
be based on ``aggregate exposure'' to the pesticide. (21 U.S.C. 
346a(b)(2)(A)(ii)). Aggregate exposure to a pesticide includes all 
``anticipated dietary exposure and all other exposures for which there 
is reliable information.'' (Id.). The statute makes clear that in 
assessing aggregate exposure pertaining to a pesticide EPA must 
consider not only exposure to the pesticide in the food covered by the 
tolerance in question but exposure to the pesticide as a result of 
other tolerances and from ``other non-occupational sources.'' (Id. 
346a(b)(2)(D)(vi)). Further, the statute directs EPA to consider 
aggregate exposure to other substances related to the pesticide so long 
as that exposure results from a non-occupational source. (Id. 
346a(b)(2)(D)(vi)). In November 2001, EPA released a science guidance 
document entitled ``General Principles for Performing Aggregate 
Exposure and Risk Assessments.'' This document deals primarily with the 
complex subject of integrating distributional and probabilistic 
techniques into aggregate exposure analyses. (Ref. 3).
    More relevant to the current objections is the science guidance 
document issued in March 2000 addressing the population percentile of 
exposure used in making acute exposure estimates for applying the 
safety standard under section 408. (Ref. 4) [hereinafter referred to as 
``Percentile Policy'']. Traditionally, EPA had used the 95th percentile 
of human exposure in acute dietary exposure assessments as representing 
a reasonable worst case scenario. (Id. at 15). Due to the very 
conservative (health-protective) assumptions used for acute exposure 
assessments, the 95th percentile was viewed as a reasonable 
approximation of an exposure level not likely to be exceeded by any 
individuals. (Id. at 15-17). For these assessments EPA generally 
assumed that all crops for which there is a tolerance are treated with 
the pesticide and all treated crops have residues at the highest level 
legally permitted.
    More recently, because of the availability of better data on 
residue values and new risk assessment techniques, EPA has restructured 
its approach to the use of population exposure percentiles in making 
safety determinations for acute risks under section 408. EPA has 
retained the 95th percentile as the starting point of analysis for 
worst case (tolerance level) assessments. EPA, however, generally uses 
higher percentiles of exposure when less conservative assumptions are 
made concerning residue values. (Id.). For example, beginning in the 
late 1990's, EPA has increasingly relied upon probabilistic assessment 
techniques for assessing acute dietary exposure and risk. Because EPA 
generally uses much more realistic exposure values (e.g., monitoring 
data on pesticide levels in food) in conducting probabilistic 
assessments, a higher population exposure percentile was generally 
found to be necessary to ensure that exposure for the overall 
population was not understated. The Percentile Policy explains and 
defends EPA's choice of the 99.9th percentile as a starting point for 
evaluating exposure and acute risk with probabilistic assessments.
    EPA confirms in the Percentile Policy document that it will 
generally continue to use the 95th percentile of exposure for non-
probabilistic, or what has been referred to as ``deterministic'' acute 
risk assessments that use worst case exposure assumptions.'' (Id. at 
17, 29). The conservative (health-protective) nature of this approach 
is confirmed by data EPA cites showing that deterministic assessments 
of exposure at the 95th percentile assuming residues at tolerance 
levels regularly result in exposure predictions significantly higher 
than probabilistic exposure estimates of the 99.9th percentile using 
monitoring data. (Id. at 16-17).
    Importantly, EPA's Percentile Policy makes clear that in choosing a 
population percentile to estimate exposure, EPA is not intending to 
define the portion of the population that is to be protected. The 
policy explicitly states that: ``OPP's goal is to regulate pesticides 
in such a manner that everyone is reasonably certain to experience no 
harm as a result of dietary and other non-occupational exposures to 
pesticides.'' (Id. at 28).

D. NRDC Farmworker Children Petition

    On October 22, 1998, NRDC and 58 other public interest 
organizations and individuals submitted a petition to EPA asking that 
EPA ``find that farm children are a major identifiable subgroup and 
must be protected under FQPA when setting allowable levels of pesticide 
residue in food.'' (Ref. 5) [hereinafter referred to as the ``Farm 
Children Petition'']. The Farm Children Petition claims that ``[a]n 
increasing body of scientific evidence, including biomonitoring data 
and residential exposure studies, indicates that farm children face 
particularly significant

[[Page 46711]]

exposures and health risks from pesticides.'' (Id. at 3). In addition 
to requesting the ``major identifiable subgroup'' designation, the 
Petition also asked that EPA use the children's safety factor to 
protect farm children, require additional exposure data on farm 
children exposure and not issue any new tolerances until such data are 
available, deny registration for any pesticide without a validated 
method for detecting residues in food, increase research into issues 
concerning farm children exposure to pesticides, and honor the 
President's Executive Order on Environmental Justice.
    EPA responded to the Farm Children Petition in the Imidacloprid 
Order. EPA declined to name farm children as a separate major, 
identifiable subgroup pointing out that any pesticide exposures to 
children as a result of proximity to agricultural fields can be fully 
taken into account as part of the consideration of EPA's already 
existing major identifiable subgroups of children. (69 FR 30069, May 
26, 2004). EPA agreed with most of the other aspects of NRDC's 
petition. (69 FR 30076-30077, May 26, 2004).

IV. The Challenged Tolerance Decisions

    Table 1 lists the tolerance actions challenged by NRDC. The 
tolerance actions are grouped as they were by NRDC in NRDC's four sets 
of objections.

                 Table 1.--Challenged Tolerance Actions
------------------------------------------------------------------------
         Pesticides Involved              FR Citations (respectively)
------------------------------------------------------------------------
halosulfuron-methyl, pymetrozine      66 FR 66333, December 26, 2001; 66
                                       FR 66778, December 27, 2002; 66
                                       FR 66786, December 27, 2001
-------------------------------------
imidacloprid, mepiquat, bifenazate,   67 FR 2580, January 18, 2002; 67
 zeta-cypermethrin, diflubenzuron      FR 3113, January, 23, 2002; 67 FR
                                       4913, February 1, 2002; 67 FR
                                       6422, February 12, 2002; 67 FR
                                       7085, February 15, 2002
-------------------------------------
2,4-D                                 67 FR 10622, March 8, 2002
-------------------------------------
isoxadifen-ethyl, acetamiprid,        67 FR 12875, March 20, 2002; 67 FR
 propiconazole, furilazole,            14649, March 27, 2002; 67 FR
 fenhexamid, fluazinam                 14866, March 28, 2002; 67 FR
                                       15727, April 3, 2002; 67 FR
                                       19114, April 18, 2002; 67 FR
                                       19120, April 18, 2002
------------------------------------------------------------------------

    Each of these tolerance actions, except imidacloprid, is summarized 
briefly below.
    1. Halosulfuron-methyl. NRDC challenged two separate tolerance 
actions on halosulfuron-methyl: (1) A December 26, 2001 action 
establishing tolerances on the melon subgroup; (66 FR 66333, December 
26, 2001), and (2) a December 27, 2001 action establishing time-limited 
tolerances in connection with an emergency exemption under FIFRA on 
asparagus, (66 FR 66778, December 27, 2002). The risk assessments for 
both actions yielded similar results. Given halosulfuron-methyl's 
exposure pattern and toxicological characteristics, EPA determined that 
halosulfuron-methyl potentially presented acute, chronic, short-term, 
and intermediate-term risks and EPA quantitatively assessed these risks 
in making its safety determination. (66 FR 66336-66339; 66 FR 66783-
66784). All of these risks were found to be below the Agency's level of 
concern. (Id.). Although a DNT study was outstanding, EPA determined 
that the additional 10X children's safety factor was not needed to 
protect infants and children because the toxicological data showed no 
evidence of greater sensitivity to the young and indicated that the DNT 
study was unlikely to affect the risk assessment. EPA explained the 
latter conclusion by noting that:
    (a) The alterations in the fetal nervous system occurred in only 
one species (in rats and not in rabbits); (b) the fetal effects 
which will be investigated in the required developmental 
neurotoxicity study were seen only at a dose of 750 mg/kg/day which 
is close to the Limit-Dose (1,000 mg/kg/day); (c) there was no 
evidence of clinical signs of neurotoxicity, brain weight changes, 
or neuropathology in the subchronic or chronic studies in rats; (d) 
the developmental neurotoxicity study is required only as 
confirmatory data to understand what the effect is at a high 
exposure (dose) level.
(66 FR at 66782).
    2. Pymetrozine. NRDC challenged a December 27, 2001 action 
establishing tolerances for pymetrozine on cotton seed, cotton gin 
byproducts, the fruiting vegetables crop group, the cucurbit vegetables 
crop group, the leafy vegetables crop group (except Brassica), head and 
stem Brassica, leafy Brassica, turnip greens, dried hops, and pecans. 
(66 FR 66786, December 27, 2001). Given pymetrozine's exposure pattern 
and toxicological characteristics, EPA determined that pymetrozine 
potentially presented acute, chronic, short-term, and cancer risks and 
EPA quantitatively assessed these risks in making its safety 
determination. (66 FR at 66791-66792). All of these risks were found to 
be below the Agency's level of concern. (Id.). Although a DNT study was 
outstanding, EPA determined that the additional 10X children's safety 
factor could generally be reduced to 3X because the toxicological data 
showed no evidence of greater sensitivity to the young and there was no 
evidence of abnormalities in the development of the fetal nervous 
system. (64 FR 52438, 52444, September 29, 1999). Because the endpoint 
used for assessing acute dietary and short-term risk for the general 
population, including infants and children, was based on a LOAEL a 
second 3X safety factor was used for these risk assessments. (Id.).
    3. Mepiquat. NRDC challenged a January 23, 2002 action establishing 
tolerances for mepiquat on cotton gin byproducts and meat byproducts of 
cattle, goats, hogs, horses and sheep. (67 FR 3113, January, 23, 2002). 
Given mepiquat's exposure pattern and toxicological characteristics, 
EPA determined that mepiquat potentially presented acute and chronic 
risks and EPA quantitatively assessed these risks in making its safety 
determination. (67 FR at 3116). All of these risks were found to be 
below the Agency's level of concern. (Id.). Although a DNT study was 
outstanding, EPA determined that the additional 10X children's safety 
factor was not needed to protect infants and children because the 
toxicological data showed no evidence of greater sensitivity to the 
young and the evidence signaling a need for a DNT study did not show 
``some special concern for the developing fetuses or young'' such as 
``neuropathy in adult animals; [central nervous system] malformations 
following prenatal exposure; brain weight or sexual maturation changes 
in offspring; and/or functional changes in offspring.`` (65 FR 1790, 
1794, January 12, 2000)).

[[Page 46712]]

    4. Bifenazate. NRDC challenged a February 1, 2002 action 
establishing tolerances for bifenazate on wet apple pomace, undelinted 
cotton seed, cotton gin byproducts, the pome fruit crop group, grapes, 
raisins, dried hops, nectarines, peaches, plums, strawberries and the 
fat of cattle, goats, hogs, horses, and sheep. (67 FR 4913, February 1, 
2002). Given bifenazate's exposure pattern and toxicological 
characteristics, EPA determined that bifenazate potentially presented a 
chronic risk and EPA quantitatively assessed this risk in making its 
safety determination. (67 FR at 4919). As assessed, chronic risk was 
below the Agency's level of concern. (Id.). Because there was no 
outstanding toxicity data, the existing toxicity data showed no 
evidence of increased sensitivity of the young, and exposure data were 
deemed unlikely to understate exposure, EPA determined that it was safe 
for infants and children to remove the children's safety factor. (67 FR 
at 4918-4919).
    5. Zeta-cypermethrin. NRDC challenged a February 12, 2002 action 
establishing tolerances for zeta-cypermethrin on the podded legume 
vegetable crop group; the succulent, shelled peas and beans crop group; 
dried shelled peas and beans crop group; soybeans; the fruiting 
vegetables crop group; grain sorghum; sorghum stover; sorghum forage; 
wheat grain; wheat forage; wheat hay; wheat straw; aspirated grain 
fractions; and meat of cattle, goats, hogs, horses and sheep. (67 FR 
6422, February 12, 2002). Given zeta-cypermethrin's exposure pattern 
(including the exposure pattern of a toxicologically similar pesticide, 
cypermethrin) and toxicological characteristics, EPA determined that 
zeta-cypermethrin potentially presented acute, chronic, short-term, 
intermediate-term, and cancer risks and EPA quantitatively assessed 
these risks in making its safety determination. (67 FR at 6426-6429). 
All of these risks were found to be below the Agency's level of 
concern. (Id.). Although a DNT study was outstanding, EPA determined 
that the additional 10X children's safety factor was not needed to 
protect infants and children because the toxicological data showed no 
evidence of greater sensitivity to the young and the evidence signaling 
a need for a DNT study did not show ``some special concern for the 
developing fetuses or young'' such as ``neuropathy in adult animals; 
[central nervous system] malformations following prenatal exposure; 
brain weight or sexual maturation changes in offspring; and/or 
functional changes in offspring.'' (Id. at 6426).
    6. Diflubenzuron. NRDC challenged a February 15, 2002 action 
establishing a tolerance for diflubenzuron on pears. (67 FR 7085, 
February 15, 2002). Given diflubenzuron's exposure pattern and 
toxicological characteristics, EPA determined that diflubenzuron 
potentially presented a chronic risk and EPA quantitatively assessed 
this risk in making its safety determination. (Id. at 7089-7090). As 
assessed, chronic risk was below the Agency's level of concern. (Id.). 
EPA determined that the additional 10X children's safety factor was not 
needed to protect infants and children because the toxicological data 
showed no evidence of greater sensitivity to the young, there was no 
missing toxicological data, and the exposure assessments were unlikely 
to understate exposure. (Id. at 7089).
    7. 2,4-D. NRDC challenged a March 8, 2002, action establishing a 
time-limited tolerance for 2,4-D on soybeans. (67 FR 10622, March 8, 
2002). Given 2,4-D's exposure pattern and toxicological 
characteristics, EPA determined that 2,4-D potentially presented acute, 
chronic, and short-term risks and EPA quantitatively assessed these 
risks in making its safety determination. (Id. at 10628-10629). All of 
these risks were found to be below the Agency's level of concern. 
(Id.). Although a DNT study was outstanding, EPA determined that the 
additional 10X children's safety factor could be reduced because the 
toxicological data showed no evidence of greater sensitivity to the 
young and all other required toxicological data was complete. (Id. at 
10627-10628). A factor of 3X was retained because the DNT study was 
triggered based on a finding of neuropathology (retinal degeneration) 
and was applied to all population subgroups for all durations of 
exposure.
    8. Isoxadifen-ethyl. NRDC challenged a March 20, 2002, action 
establishing tolerances for isoxadifen-ethyl on corn commodities. (67 
FR 12875, March 20, 2002). Given isoxadifen-ethyl's exposure pattern 
and toxicological characteristics, EPA determined that isoxadifen-ethyl 
potentially presented acute and chronic risks and EPA quantitatively 
assessed these risks in making its safety determination. (Id. at 12876-
12877; 66 FR 33179, 33184-33185, June 21, 2001). All of these risks 
were found to be below the Agency's level of concern. (Id.). Although 
the data showed evidence of increased pre-natal sensitivity, EPA 
determined that the additional 10X children's safety factor could be 
reduced to 3X because the toxicological data were complete (i.e., there 
were no outstanding studies such as a DNT study). (Id. at 33184). This 
additional factor was applied to the acute dietary risk assessment for 
females aged 13-50 because the increased sensitivity resulted from in 
utero exposure. (Id.).
    9. Acetamiprid. NRDC challenged a March 27, 2002, action 
establishing tolerances for acetamiprid on dried citrus pulp, the 
citrus fruit crop group, cotton gin byproducts, cotton undelinted seed, 
grapes, the fruiting vegetable crop group, the leafy brassica vegetable 
crop group, the leafy vegetable crop group, the pome fruit group, 
tomato paste, as well as various animal products. (67 FR 14649, March 
27, 2002). Given acetamiprid 's exposure pattern and toxicological 
characteristics, EPA determined that acetamiprid potentially presented 
acute, chronic, short-term, and intermediate-term risks and EPA 
quantitatively assessed these risks in making its safety determination. 
(Id. at 14656-14657). All of these risks were found to be below the 
Agency's level of concern. (Id.). Although the data showed qualitative 
evidence of increased pre-natal sensitivity and a DNT study was 
outstanding, EPA determined that the additional 10X children's safety 
factor could be reduced to 3X because two of the three toxicological 
studies bearing on effects on the young showed no increased sensitivity 
in the young, the evidence of increased sensitivity was only 
qualitative and not quantitative, and the DNT study was not requested 
based on evidence indicating a special concern for developing fetuses 
or the young. (Id. at 14656). This additional factor was applied for 
all population subgroups for all exposures other than acute dietary 
exposure because the increased sensitivity resulted from chronic 
exposure. (Id.).
    10. Propiconazole. NRDC challenged a March 28, 2002, action re-
establishing a time-limited tolerance for propiconazole on blueberries 
in connection with an emergency exemption under FIFRA. (67 FR 14866, 
March 28, 2002). Given propiconazole's exposure pattern and 
toxicological characteristics, EPA determined that propiconazole 
potentially presented acute, chronic, short-term, intermediate-term, 
and cancer risks and EPA quantitatively assessed these risks in making 
its safety determination. (64 FR 2995, 2999-3001, January 20, 1999). 
All of these risks were found to be below the Agency's level of 
concern. (Id.). Based on the completeness of the toxicity database and 
the lack of any evidence showing increased pre- or post-natal 
sensitivity, EPA determined that removing the additional 10X children's 
safety factor

[[Page 46713]]

would be protective of infants and children. (Id. at 3000).
    11. Furilazole. NRDC challenged an April 3, 2002, action 
establishing tolerances for furilazole on corn commodities. (67 FR 
15727, April 3, 2002). Given furilazole's exposure pattern and 
toxicological characteristics, EPA determined that furilazole 
potentially presented acute, chronic, and cancer risks and EPA 
quantitatively assessed these risks in making its safety determination. 
(Id. at 15732-15733). All of these risks were found to be below the 
Agency's level of concern. (Id.). Although EPA was lacking a chronic 
toxicity study in dogs for furilazole, EPA determined that the 
additional 10X children's safety factor could be removed and that a 3X 
additional factor would be protective of infants and children because 
otherwise the database was complete, there was no evidence of pre- or 
post-natal sensitivity, and the subchronic toxicity studies in rats and 
dogs show that the toxicity of furilazole is similar, both 
qualitatively and quantitatively, in both species. The 3X factor was 
applied to the chronic risk assessment because the missing study was a 
chronic study. (Id. at 15730).
    12. Fenhexamid. NRDC challenged an April 18, 2002, action 
establishing tolerances for fenhexamid on the caneberry crop subgroup, 
the bushberry crop subgroup, juneberry, lingonberry, salal, and 
pistachio. (67 FR 19114, April 18, 2002). Given fenhexamid's exposure 
pattern and toxicological characteristics, EPA determined that 
fenhexamid potentially presented a chronic risk and EPA quantitatively 
assessed this risk in making its safety determination. (Id. at 19118). 
As assessed, chronic risk was found to be below the Agency's level of 
concern. (Id.). Although the data showed qualitative evidence of 
increased pre-natal sensitivity, EPA determined that the additional 10X 
children's safety factor could be reduced to 3X because the 
toxicological data were complete, two of the three toxicological 
studies bearing on effects on the young showed no increased sensitivity 
in the young, and the evidence of increased sensitivity was only 
qualitative and not quantitative. (Id. at 19117).
    13. Fluazinam. NRDC challenged an April 18, 2002, action 
establishing a tolerance for fluazinam on the wine grapes. (67 FR 
19120, April 18, 2002). Given fluazinam's exposure pattern and 
toxicological characteristics, EPA determined that fluazinam 
potentially presented acute and chronic risks and EPA quantitatively 
assessed these risks in making its safety determination. (Id. at 19127-
19128). All of these risks were found to be below the Agency's level of 
concern. (Id.). Because the data showed qualitative evidence of 
increased pre-natal sensitivity and a DNT study had been required (but 
not yet submitted) based on evidence of neurotoxic lesions, EPA 
retained the additional 10X safety factor for acute dietary exposure to 
the population subgroup females aged 13-50. For other populations and 
exposures the additional 10X factor was reduced to 3X because the 
increased sensitivity had only been seen with in utero exposure. (Id. 
at 19126-19127).

V. NRDC Objections

A. In General

    As mentioned above, NRDC submitted four separate sets of objections 
on various pesticide tolerances during the first half of 2002. The 
objections were received on February 25, 2002; March 19, 2002; May 7, 
2002; and May 20, 2002. (Refs. 6, 7, 8, and 9). NRDC was joined in the 
objections concerning 2,4-D by the following public interest and/or 
advocacy organizations: Boston Women's Health Book Collective, Breast 
Cancer Action, Californians for Pesticide Reform, Commonweal, Lymphoma 
Foundation of America, Northwest Coalition for Alternatives to 
Pesticides, Pesticide Action Network North America, Pineros y 
Campesinos Unidos del Noroeste, SF-Bay Area Chapter of Physicians for 
Social Responsibility, and Women's Cancer Resource Center.

B. Generic Issues

    NRDC raises a myriad of claims in its objections. Most of the 
claims fall fairly neatly into three categories: (1) Children's safety 
factor issues; (2) aggregate exposure issues; and (3) issues regarding 
use of findings from hazard studies in calculating safe exposure levels 
- the``no observed effect level'' (NOEL) versus ``no observed adverse 
effect level'' (NOAEL) and the ``lowest observed adverse effect level'' 
(LOAEL) questions.
    1. Children's safety factor issues. For each of the pesticides 
included in the objections, NRDC asserts that EPA used an additional 
safety factor for the protection of infants and children that is 
different from the default 10x value. NRDC claims that EPA erred in 
doing so due to the ``significant toxicity and exposure data gaps'' 
corresponding to the tolerances established. (See, e.g., Ref. 7 at 3). 
Three types of data gaps are cited by NRDC. First, NRDC notes that as 
to certain of the pesticides EPA has required a developmental 
neurotoxicity study but such study has not yet been submitted. Pointing 
to various EPA documents recommending that this study be widely 
required and EPA's specific finding that this study is required as to 
the pesticides in question, NRDC argues that use of a factor different 
than the default 10X is precluded. Second, NRDC claims EPA lacks 
``pesticide-specific data on water-based exposure'' to the pesticides. 
(Id. at 6). NRDC argues that exposure estimates EPA calculated through 
the use of models cannot qualify as the ``reliable data'' needed to 
vary from the default 10X value. (Id.). Third, NRDC claims that ``EPA 
failed to consider important exposure routes for millions of infants 
and children, including exposure to children living on farms and who 
accompany their parents into farm fields [], and exposure from spray 
drift.'' (Ref. 9 at 5).
    2. Aggregate exposure issues. NRDC raises several issues relating 
to whether EPA properly estimated ``aggregate exposure'' for the 
pesticides in question. First, NRDC argues that farm children are a 
``major identifiable subgroup'' and that EPA has failed to consider 
information concerning the sensitivities and exposures of farm children 
as a major identifiable subgroup'' in conducting its aggregate exposure 
assessment. According to NRDC, farm children have unique exposures to 
pesticides ``from their parents' clothing, dust tracked into their 
homes, contaminated soil in areas where they play, food eaten directly 
from the fields, drift from aerial spraying, contaminated well water, 
and breast milk.'' (Ref. 7 at 12). Further, NRDC asserts farm 
children's exposure is increased because they ``often accompany their 
parents to work in the fields . . . .'' (Id.). NRDC cites various 
studies collected in its ``Farm Children Petition'' as well as more 
recent studies in support of these claims. (Ref. 7 at 12-13). Second, 
NRDC argues that EPA's aggregate exposure assessment is flawed for 
these pesticides because EPA did not consider the added exposure to 
pesticides that farmworkers receive as a result of their occupation. 
(Id. at 14). NRDC states that EPA's interpretation of the statute as 
excluding occupational exposure is incorrect. (Id.). Third, NRDC claims 
that EPA has underestimated aggregate exposure for several of the 
pesticides because EPA used ``anticipated residues'' for estimating 
exposure rather than assuming residues would be at the tolerance level. 
NRDC argues that ``EPA must ensure that the legal level of pesticide 
chemical residue - the established tolerance levels - are themselves 
safe.'' (Ref. 9 at 20). Additionally, NRDC asserts that using

[[Page 46714]]

``anticipated residues'' does not take into account the ``significant 
number of consumers who purchase produce at farmers markets, farm 
stands, and `pick-your-own' farming operations.'' (Id. at 19). These 
``potentially millions of consumers,'' NRDC contends, are exposed ``to 
residues of these pesticides at the tolerance level.'' (Id. at 20). 
Fourth, NRDC argues that for several of the pesticides EPA has, in 
effect, underestimated aggregate exposure by using the 95th population 
percentile of exposure instead of the 99.9th percentile in determining 
whether exposure to the pesticide meets the safety standard. (Ref. 7 at 
19). NRDC claims that this is inconsistent with existing Agency policy. 
(Id.).
    3. Reliance on LOAELs and NOAELs. NRDC asserts that, in the absence 
of identifying a NOEL in relevant animal studies, EPA cannot make a 
safety finding under section 408(b)(2). In support of this argument, 
NRDC cites to legislative history using the term NOEL. NRDC calls 
particular attention to the instances where EPA determined safety 
relying on a LOAEL: Use of acute neurotoxicity LOAEL to evaluate oral 
exposure for pymetrozine; (Ref. 6 at 9), use of reproductive toxicity 
LOAEL for mepiquat; (Id.), use of developmental toxicity LOAEL for 
zeta-cypermethrin; (Ref. 7 at 19), use of LOAEL for dermal toxicity for 
fluazinam; (Ref. 9 at 18), and reliance on rat and mouse dietary 
studies for fluazinam that identified only a LOAEL. (Id.). NRDC, 
however, also objects to several pesticide tolerances for use of a 
NOAEL in making the safety determination. (Ref. 9 at 17-18).

C. Pesticide-specific Issues

    NRDC's pesticide-specific objections to some extent build upon the 
more general objections described immediately above. As to each of the 
pesticides, NRDC identifies allegedly missing toxicity or exposure data 
and argues that these missing data necessitate retention of the default 
10X children's safety factor. Additionally, for several of the 
pesticides, NRDC raises specific issues regarding the aggregate 
exposure estimate. One aggregate exposure issue raised repeatedly is 
EPA's reliance on allegedly arbitrary processing factors for estimating 
residues in processed food. These objections are addressed in detail in 
Unit VIID.7.b. and f. below, respectively.
    Finally, NRDC objects to the 2,4-D tolerance on soybeans arguing 
that EPA relied upon a human exposure study ``in an arbitrary departure 
from the Agency's stated policy on considering human tests and a 
violation of international and federal law.'' (Ref. 8 at 22). Also with 
regard to 2,4-D, NRDC discusses various toxicological studies that 
according to NRDC show that 2,4-D is a carcinogen, an endocrine 
disruptor, and a neurotoxicant. (Id. at 4-7). NRDC did not link these 
toxicological claims to its specific objections.

VI. Public Comment

A. In General

    On June 19, 2002, EPA published a notice in the Federal Register 
calling attention to and requesting comments on the NRDC Objections. 
(67 FR 41628, June 19, 2002). As part of that notice, EPA published the 
full text of one set of objections in the Federal Register. A period of 
60 days was initially allowed for comment but that period was extended 
twice and was closed on October 16, 2002. (See 67 FR 58536, September 
17, 2003; 67 FR 53505, August 16, 2002). In addition to a large number 
of form letters (principally supporting the objections) and the NRDC's 
comments mentioned above, EPA received roughly 20 sets of substantive 
comments. These comments were for the most part from pesticide 
manufacturers and each requested denial of the objections. The most 
significant of these comments are summarized below. EPA has not 
repeated comments in instances where they were made by more than one 
commenter.

B. Individual Comments

    1. The FQPA Implementation Working Group. Extensive comments were 
filed by the FQPA Implementation Working Group (IWG), an organization 
comprised of associations representing pesticide manufacturers, 
growers, and food processors. (Ref. 10) [hereinafter cited as ``IWG 
comments'']. The IWG comments provided two alternative approaches as to 
why the NRDC's objections should be denied. First, the IWG asserted 
that EPA has misinterpreted the concept of ``aggregate exposure'' ever 
since passage of the FQPA, and once this interpretation is corrected, 
it becomes clear that the objections, for the most part, are flawed. 
These comments by IWG were thoroughly described and responded to in the 
Imidacloprid Order. (69 FR at 30072-30073, May 26, 2004).
    Second, in the alternative, the IWG, assuming the EPA's aggregate 
exposure interpretation is retained, explained that the NRDC objections 
are factually flawed. IWG's comments concerning pesticide exposure to 
farm children and exposure to pesticides in drinking water were 
discussed in the Imidacloprid Order. (69 FR at 30049, 30069). One issue 
not addressed was IWG's comments on pesticide exposure from food 
purchased at farm stands. The IWG challenges the NRDC's assertion that 
levels of pesticide residues in foods purchased at farm stands are 
higher than residue levels in food purchased at other retail outlets. 
The IWG notes that ``NRDC does not provide information to support its 
allegations, and we are not aware of any credible data to suggest that 
this is the case.'' (Ref. 10 at 16). The IWG cites two demonstrable 
reasons undermining NRDC's claim: first, label directions and 
restrictions on pesticide use apply equally to food grown for sale at 
farmstands and food grown for distribution through broader channels of 
trade; and second, ``[t]he various circumstances (weather, pest 
pressure, etc.) that affect residue levels resulting from a given 
treatment regimen are the same for those who grow crops to market 
through wholesale channels and for those who grow crops to sell at 
retail.'' (Id.). Finally, the IWG notes that assuming residue levels 
are at the tolerance value would vastly overstate exposure amounts 
given that FDA data has shown ``no pesticide residues in 41 percent and 
73.5 percent of fruit and vegetable samples and either no residues or 
below tolerance residues in 99.5 percent and 98.9 percent of fruit and 
vegetable samples.'' (Id. at 17).
    2. Inter-Regional Research Project Number 4 (IR-4). The IR-4 is a 
program sponsored by the US Department of Agriculture and land grant 
universities and directed toward obtaining regulatory approval for 
pesticide uses on minor and speciality food crops that are not likely 
to be supported by private sector companies. In its comments, the IR-4 
notes that several of the pesticides covered in the objections - 
diflubenzuron, halosulfuron-methyl, and fenhexamid - are both 
``critical to minor crop growers'' and safer, reduced risk pesticides. 
(Ref. 11). The IR-4 asserts that diflubenzuron provides an alternative 
to the organophosphate pesticides and that halosulfuron-methyl is a 
methyl bromide alternative. (Id.).
    3. ISK Biosciences - Fluazinam. ISK Biosciences is the owner of the 
data used to support the fluazinam tolerance on wine grapes. (Ref. 12). 
ISK Biosciences notes that this is an import tolerance for wine grapes 
meaning that as to this use there will be no exposure in the United 
States other than through the consumption of wine. (Id. at 4). ISK 
Biosciences also points out that children do not usually consume wine. 
(Id.). ISK Biosciences notes several factors that contributed to the 
conservativeness of EPA's risk assessment, including (1) use

[[Page 46715]]

of tolerance level residues; (2) assumption of 100 percent crop treated 
even though fluazinam can be at most used on wine imported to the 
United States (22 percent of the wine); and (3) use of a default 
processing factor for wine of 1.0 even though wine processing studies 
show significant reductions in residue levels. (Id. at 5-7). As regards 
reliance on a LOAEL, ISK Biosciences states that EPA did indicate the 
21-day dermal toxicity study did not identify a NOAEL for dermal 
irritation but that EPA did find a systemic NOAEL from that study which 
was used for aggregate risk assessment. According to ISK Biosciences, 
NOAELs were used for dietary risk. (Id. at 7).
    4. Bayer CropScience - Isoxadifen-ethyl. Bayer CropScience claims 
that EPA assigned a 3X children's safety factor to isoxadifen-ethyl due 
to concerns regarding a rat teratology study and EPA requested 
historical control information pertaining to the study. (Ref. 13). 
Bayer states that that information has been submitted and should 
alleviate any concerns EPA has with regard to the study regarding 
potential increased sensitivity of the young. With respect to the 
conservativeness of EPA drinking water exposure estimates Bayer 
CropScience cites a study which it asserts demonstrates that EPA models 
typically overstate exposures by 100- to 10,000-fold. (Id. at 2 (citing 
Ref. 14)). Finally, as to EPA's use of default processing factors, 
Bayer CropScience argues they are not arbitrary because they assume a 
worst case concentration of residues in the processed food based on the 
ratio of the weights of the raw and processed foods. (Ref. 13 at 6).
    5. Aventis CropScience - Acetamiprid. Aventis CropScience asserts 
``there was no specific concern on the part of [EPA with regard to 
acetamiprid] that would give concern for the developing fetuses or 
young. The developmental neurotoxicity study was required by EPA to 
expand knowledge, not for reasons of specific concerns.'' (Ref. 15). 
Further, Aventis CropScience claims that ``[t]here is no reason to 
expect that a lower NOEL than previously determined will be found for 
acetamiprid in a developmental neurotoxicity study.'' (Id.).
    6. FMC Corporation - Zeta-cypermethrin. FMC Corporation argues that 
no DNT study has been required for zeta-cypermethrin because no data 
call-in has been issued. (Ref. 16). If a DNT study has not been 
required, FMC Corporation reasons, then the absence of a DNT study 
cannot make the database incomplete. Further, FMC asserts that even if 
such a study was requested any decision on the children's safety factor 
would have to be based on whether the data ``give rise to concerns for 
potential developmental effects.'' (Id.). Challenging claims by NRDC, 
FMC contends that the DCVA degradates of zeta-cypermethrin were 
considered by EPA, (Id. at 3-4), and the residential exposure due to 
cypermethrin was taken into account in the aggregate risk assessment 
for zeta-cypermethrin. (Id. at 6). As to the DCVA metabolites, FMC 
asserts that EPA considered them and decided not to include them in an 
aggregate assessment due to their lack of toxicological significance. 
(Id. at 3).
    7. Crompton Corporation - Diflubenzuron and Bifenazate--a. 
Diflubenzuron. Crompton Corporation argues that NRDC's criticisms of 
the adequacy of the residential exposure assessment for diflubenzuron 
are misplaced given that an exposure assessment for agricultural 
workers showed minimal exposure under conditions much more likely to 
result in exposure than the sole registered residential use for 
diflubenzuron on trees and shrubs limited to professional application 
only. (Ref. 17).
    b. Bifenazate. Crompton Corporation asserts that NRDC has 
misconstrued a statement in Federal Register notice establishing the 
bifenazate tolerances in question. (Id. at 4). In a table summarizing 
toxicological studies, EPA at one point states that ``a clear 
assessment of developmental toxicity was not possible.'' (67 FR at 
4915,). Crompton Corporation contends that this statement only applied 
to a range-finding study and that once the main study was completed 
developmental toxicity could be clearly assessed. Crompton Corporation 
acknowledges that the database does not include, as NRDC has noted, 
several inhalation studies; however, Crompton argues this does not 
render the database incomplete because ``significant toxicity by this 
exposure route would not be expected'' given data from short-term 
inhalation studies and information pertaining to the particle size of 
bifenazate formulations. (Ref. 17 at 4). In response to NRDC's claim 
that arbitrary processing factors were used for estimating bifenazate 
residues on processed apples and grapes, Crompton points out that, at 
least in part, actual processing data from bifenazate-treated grapes 
and apples were used to derive processing factors. (Id. at 7-8).
    8. Syngenta Crop Protection - Propiconazole and Pymetrozine--a. 
Propiconazole. Syngenta Crop Protection responds to NRDC's claim that 
drinking water models cannot be relied upon to provide reliable data on 
exposure by citing to a study done to evaluate the residue levels of 
propiconazole in drinking water reservoirs. (Ref. 18). According to 
Syngenta,``[i]n 312 samples of raw water, propiconazole was detected in 
only one, and that at the limit of detection. Propiconazole was not 
detected in ANY finished water samples analyzed. (Id.). As to exposure 
to farm children, Syngenta notes that:
    [m]any of the exposure scenarios depicted in the NRDC objections 
are the result of poor hygiene (contaminated work clothing being 
worn inside the home instead of being washed after use, . . .) 
substandard living conditions due to poverty, and lack of 
information on safe pesticide handling. These kinds of issues cannot 
be managed within the constraints of a risk assessment based on 
labeled use of a pesticide, but rather must be addressed through 
appropriate stewardship, education, and outreach. Recognizing this 
as an issue, particularly in the growing Latino community of North 
Carolina, Syngenta has sponsored and actively participated in 
projects with the Department of Family and Community Medicine at 
Wake Forest University to develop safety videos in Spanish for 
pesticide handlers. These modules include a discussion of proper 
hygiene for pesticide handlers/field workers once inside the home.
(Id. at 3-4).
    b. Pymetrozine. Syngenta defends the use of a LOAEL reduced by a 
factor of 3X for assessing the acute dietary risk of pymetrozine by 
noting that the effects observed at the LOAEL ``were reversible and not 
of severe magnitude (for example, body temperature was decreased at the 
LOEL, but only by about 2 percent compared to controls).'' (Id. at 5). 
Syngenta cites to reports indicating that a very high percentage of 
toxicity studies have a ratio between LOAELs and NOAELs of 5X to 6X or 
less. (Id.). Syngenta notes that ``Dourson et al. (1996) conclude that 
when faced with a LOEL and not a NOEL, the choice of uncertainty factor 
should generally depend on the severity of the effect at the LOEL.'' 
(Ref. 18 at 5).
    9. BASF Corporation - Mepiquat. BASF Corporation disputes NRDC's 
claim that a NOEL was not identified by EPA for the mepiquat 
reproductive toxicity study in rats. Citing to EPA's Reregistration 
Eligibility Document for mepiquat chloride, BASF Corporation concludes 
that ``this study established a NOEL for all parameters investigated, 
both for parents and pups.'' (Ref. 19).
    10. Industry Task Force II on 2,4-D Research Data. A good portion 
of the 2,4-D Industry Task Force II's comments pertain to NRDC 
statements regarding the toxicity of 2,4-D. (Ref. 20). Because NRDC did 
not directly relate these statements to its objections, neither its 
allegations nor the Industry Task Force's

[[Page 46716]]

rebuttal is repeated in any detail here. In sum, the Industry Task 
Force disagreed with NRDC's conclusions asserting that NRDC had focused 
on a few studies of questionable reliability without considering the 
extensive database on 2,4-D. The Task Force noted that ``[i]t is 
difficult to understand the toxicological arguments put forth by NRDC 
as many are simply threads of ideas that have been only loosely woven 
into a fabric.'' (Id. at 2). To the extent necessary, toxicological 
issues concerning 2,4-D are discussed below in EPA's response to the 
objections.
    On the children's safety factor for 2,4-D, the Industry Task Force 
defends EPA's selection of a 3X factor based on the assertion that it 
would be ```double counting''' to ``require both a database uncertainty 
factor for the lack of a DNT study and an FQPA safety factor for 
neurological sensitivity.'' (Id. at 15). The Industry Task Force also 
notes that the neurological sensitivity was only found at a high dose. 
(Id. at 14). As to regulation of farm children as a major identifiable 
subgroup, the Industry Task Force protests that ``NRDC did not define 
farm children as a subgroup by their type of living situation, food 
consumption, and other population characteristics that would 
discriminate them from children generally.'' (Id. at 16). The Industry 
Task Force also challenges NRDC's claims regarding high exposures for 
farm children noting that in three recent biomonitoring studies of farm 
applicators, spouses, and their children ``only a small fraction of the 
spouses and children have levels of 2,4-D detectable at 1 part per 
billion.'' (Id.). Studies cited by NRDC in support of its claims 
regarding high exposure to farm children, the Industry Task Force 
asserts, ``fail to concurrently demonstrate a measurable internal dose 
of 2,4-D to the home residents.'' (Id. at 20). Finally, as to the human 
testing data relied upon by EPA in evaluating the safety of 2,4-D, the 
Industry Task Force points out that they were biomonitoring studies 
conducted by a provincial Canadian government agency and not ``third-
party clinical trials [conducted by the pesticide industry] to 
determine effects in humans.'' (Id. at 25).

VII. Response to Objections

    As summarized above, NRDC's Objections can be grouped into a few 
main categories and EPA has organized its response to the objections 
around these categories instead of by pesticide. Further, even among 
these categories, one consistent theme emphasized by NRDC is the 
potential heightened exposure of ``farm children'' to pesticides. For 
that reason, EPA begins its substantive response in Unit VII.B. below 
with an analysis of the data bearing on children's exposure to 
pesticides in agricultural areas. Then EPA turns to NRDC's specific 
objections. Unit VII. C. below addresses the objections raising issues 
regarding the children's safety factor. Unit VII.D. below covers 
aggregate exposure questions. Unit VII.E. below responds to claims 
regarding use of LOAELs and NOAELs. Finally, Unit VII.F. below 
addresses the human study issue.
    Prior to addressing these substantive issues, EPA responds in Unit 
VII.A. below to the objections as to several tolerances which have now 
expired.

A. Expired Tolerances

    The following time-limited tolerances that were objected to by NRDC 
have now expired and are, therefore, no longer in effect: halosulfuron-
methyl on asparagus, (66 FR 66778, December 27, 2001) (expired on 
December 31, 2003); 2,4-D on soybeans, (67 FR 10622, March 8, 2002) 
(expired on December 31, 2004); and propiconazole on blueberries, (67 
FR 14866, March 28, 2002) (expired December 31, 2003). Because these 
tolerance actions are without legal force, NRDC's objections are denied 
as moot. Other halosulfuron tolerances objected to by NRDC have not 
expired and are included in the response below. Additionally, because 
EPA has already, or may in the future, undertake tolerance actions as 
to propiconazole and 2,4-D, EPA's analysis to the specific issues 
raised by propiconazole and 2,4-D are included in this notice.

B. Children's Exposure to Pesticides in Agricultural Areas

    Children can be exposed to pesticides through multiple sources and 
pathways. The Agency currently considers children's exposure to 
pesticides by three broad pathways: food, drinking water, and 
residential use. NRDC, however, has asserted that children residing in 
agricultural communities also are significantly exposed to agricultural 
pesticides through additional exposure pathways.
    Children in agricultural areas may be exposed to agricultural 
pesticides through pathways such as contact with treated fields, 
roadsides and other areas; contact with residues on clothing of parents 
who work in agriculture; contact with moving spray drift while near 
application areas; contact with spray drift residues left by any spray 
drift that may reach their homes, yards or other areas they frequent, 
such as schools and schoolyards; and contact with pesticide residues 
that have volatilized after application. In addition, some of these 
children may also be exposed to agricultural pesticides in their homes 
via other pathways.
    In analyzing the potential exposure of children in agricultural 
areas, EPA first focused on data from studies relied upon by NRDC or 
otherwise known to EPA that attempted: To measure levels of pesticides 
in the homes of children in agricultural areas; to measure levels of 
pesticide metabolites in body fluids of children in agricultural areas; 
and/or to compare levels of pesticide exposure of farm children to 
those experienced by non-farm children, based on similar types of 
measurements. In addition, EPA examined data NRDC submitted relating to 
airborne levels of pesticides (stemming from spray drift or post-
application volatilization drift) in farm communities. Finally, EPA 
reviewed data it has concerning the potential for pesticides to drift 
offsite during application.
    1. Studies focusing on exposure to children in agricultural areas. 
In response to objections filed by NRDC with regard to the imidacloprid 
tolerance on blueberries, EPA discussed various studies focusing on 
exposure to children in agricultural areas (other than the data cited 
by NRDC regarding airborne residues). In brief, EPA found that the data 
concerning levels of pesticides in homes or children's bodily fluids 
are limited and inconclusive, and do not demonstrate that children in 
agricultural areas as a group receive more pesticide exposure than 
children in non-agricultural areas. (In fact, some data suggest that 
pesticide residues in houses in urban or non-agricultural areas may be 
higher than those in houses in agricultural areas.) EPA incorporates 
that discussion into this response. (69 FR at 30050-30054, May 26, 
2004).
    Since issuing its response to the imidacloprid objections, EPA has 
received several additional studies bearing on exposure of farm 
children. First, EPA has received a study it funded investigating, 
among other things, aggregate exposure of children to persistent 
pollutants, including pesticides. (Ref. 21 ). Pesticides in the study 
included chlorpyrifos, diazinon, permethrin, and 2,4-D. The Pilot Study 
of Children's Total Exposure to Persistent Pesticides and Other 
Persistent Organic Pollutants (CTEPP) was designed to investigate the 
relative contribution of various routes of exposure (dietary, indirect 
oral exposure, and inhalation) and to determine if there are 
differences in exposure due to such factors as income

[[Page 46717]]

level, child care location, and regional location. CTEPP was conducted 
in two states, Ohio and North Carolina, and involved 257 children in 
both urban and rural (farmland) areas of these states. What the results 
of CTEPP show are that (1) the dietary route is the dominant route of 
exposure for the pesticides and other pollutants in the study (ranging 
from 55 to 95 percent for the six pesticides studied); (Id. at 9-75), 
and (2) although there were some differences in exposure for some 
pesticides for some routes of exposure, where differences were present 
it was the urban children that received higher exposures than rural 
children (e.g. exposure of urban children in North Carolina to 2,4-D 
through indirect ingestion exceeded exposure of rural children to 2,4-D 
by the same route by a factor of 3), (Id. at 9-66, 9-67).
    A second source of information bearing on farm children exposure is 
a partial report from the Agricultural Health Study (AHS), which is a 
prospective epidemiologic study of pesticide applicators and their 
spouses in Iowa and North Carolina. (Ref. 22). Exposure to 2,4-D was 
measured in conjunction with agricultural applications for a subset of 
applicators in the AHS Pesticide Exposure Study. Urinary Biomarker 
levels were measured in pre-and post-application samples collected from 
applicators and their spouses and children using 2,4-D in broadcast and 
hand spray applications. The results indicated applicator exposure 
increased approximately 3-fold between the pre- and post-application 
periods. For spouses and children exposure increased but in smaller 
increments, approximately 50 percent and 25 percent, respectively. The 
values, however, are questionable due to the fact that one of the 
spouses admitted using a 2,4-D product, there were a low number (9) of 
children participating, and it is not clear whether any of the children 
assisted in farm work.
    The final study, the Farm Family Exposure Study (FEES), which was 
funded by a group of pesticide manufacturers, was designed to quantify 
real world pesticide exposures in farmers and family members around the 
time of a single pesticide application. (Ref.23). Pesticides involved 
in the study included 2,4-D, chlorpyrifos, and glyphosate. The farm 
families were randomly selected from a public list of licensed private 
pesticide applicators from Minnesota and South Carolina. Exposures were 
measured in applicators, spouses and children by collection of 24 hour 
urine samples on the day of and for three days following a pesticide 
application. Urine samples were also collected prior to application. 
With regard to children, the study concluded that exposure levels of 
chlorpyrifos and glyphosate increased marginally on post-application 
days and that these marginal increases were caused by children who 
directly assisted in pesticide application or who were around the 
application process. Greater increases were seen between pre-
application and post-application exposure levels of children in 
connection with use of 2,4-D. The study found that the highest levels 
of exposure were seen in children who assisted with application 
although increases were seen in some children not directly involved in 
the application process. Specifically, the study concluded:

    Exposure related to chemical application was also higher in 
children when compared to spouses. Unlike the spouses, the children 
were more often present during the application process and some 
assisted their parent with the application. These opportunities for 
direct exposure accounted for the higher concentrations of the 
chemicals in the urine. While the children did exhibit an overall 
positive change from baseline, the geometric mean differences in 
urine concentration were very small (2 [mu]gL for 2,4-D). Not all 
children who had measurable changes in urine concentration were 
directly involved with the application process, yet identifying a 
potential route of exposure will be difficult as the exposures are 
subtle.

(Ref. 23 at 28). Comparisons of the exposure levels in this study with 
other population-based exposure data showed mixed results. To evaluate 
the significance of the exposures measured in the study, EPA compared 
the exposure levels for children aged 4-15 to the dose level of 
concern. Children in that range were chosen because fewer children of 
this age would be expected to directly assist or otherwise participate 
in agricultural activities. All exposure levels for this group were 
found to be well below safe levels with margins of exposure ranging 
from 4,000 to 2.6 million and averaging 42,000. (Ref. 24). Thus, 
although there were increases in exposure for some children, these 
increases were not meaningful in terms of risk.
    The CTEPP study further confirms EPA's conclusions in the 
Imidacloprid Order regarding differential exposures of urban and rural 
(farm) children. The other two studies suggest that some farm children 
may be exposed to pesticides as a result of living in proximity to 
fields treated with pesticides; however, these exposures for farm 
children are generally a result of occupational-type exposures from the 
children participating in the application of pesticides or otherwise 
assisting in or being present in the field during agricultural 
operations. Occupational source exposure to pesticides is not 
appropriately considered under FFDCA section 408. 21 U.S.C. 
346a(b)(2)(D)(vi). Importantly, even as to the increases in 2,4-D 
exposure in the FFES, the only pesticide as to which increased exposure 
could not be definitively tied to occupational-type exposures, the data 
did not indicate that children were receiving any exposures that were 
even close to levels of concern. Moreover, these studies did not 
indicate EPA's risk assessment process was under-protective. For 
example, EPA's risk assessment for 2,4-D, both as presented in the 
tolerance document and as described in Unit VII.B.2.a., predicts 
significantly higher risks (i.e., lower margins of exposure) for 
children from exposure to 2,4-D. Thus, EPA reaffirms its earlier 
finding that data concerning levels of pesticides in homes or 
children's bodily fluids are limited and inconclusive, and do not 
demonstrate that children in agricultural areas as a group receive 
significantly more non-occupational pesticide exposure than children in 
non-agricultural areas.
    2. Information bearing on exposure levels as a result of spray 
drift and post-application drift of volatilized residues. Although the 
epidemiology data mentioned above and discussed in the Imidacloprid 
Order generally do not indicate that pesticide exposures to children in 
agricultural areas differ significantly from such exposures to children 
in urban or suburban areas, EPA has examined whether data on the drift 
of pesticide during applications (spray drift) and the transport of 
volatized pesticide residues following application (post-application 
drift) suggest that these sources of exposure should be included in EPA 
calculations of aggregate exposure.
    a. Pesticide spray drift during application. EPA defines spray 
drift as the movement of droplets off-target during or shortly after 
application, which is independent of the chemical properties of the 
pesticide being sprayed. EPA has gathered substantial data on the 
potential of pesticides, as applied, to drift offsite through the work 
of the Spray Drift Task Force (SDTF). The SDTF is a group of pesticide 
registrants who have worked collaboratively to develop a database to 
meet the majority of their collective spray drift data requirements 
under 40 CFR 158.440. The group was chartered on April 17, 1990. (Ref. 
25). Since its formation, the SDTF has generated standardized data on 
spray drift levels resulting from different application

[[Page 46718]]

methods under varying meteorological conditions. The data developed by 
the SDTF was reviewed by EPA internally, through external peer review 
workshops, and through FIFRA Scientific Advisory Panel meetings. The 
reviews generally identified the data set associated with aerial 
applications to be the most robust, followed by the data sets from 
ground boom applications, orchard/vineyard airblasting, and 
chemigation, respectively. After the spray drift data were available, 
the SDTF worked with EPA's Office of Research and Development, as well 
as the USDA's Agricultural Research Service and Forest Service to use 
the data in the development/evaluation of the AgDRIFT model. (See 
generally Refs. 26, 27, and 28).
    The AgDRIFT model has been incorporated to a limited extent in EPA 
exposure assessments. It is used most prominently in environmental 
assessments in estimating potential exposure of offsite animals and 
plant life to pesticide residues. The AgDRIFT model has also been used 
in the context of FFDCA risk assessment through use of model estimates 
as an input to the various models used to estimate potential exposure 
in drinking water. Importantly, EPA has regarded its drinking water 
models as screening models and not as realistic predictors of actual 
exposure. For that reason, until recently EPA has not directly summed 
exposure estimates from its drinking water models with estimates of 
exposure from food in calculating aggregate exposure. Rather, EPA has 
used water model estimates more indirectly by comparing them to 
Drinking Water Levels of Comparison which are estimates of the amount 
of safe exposure that can occur taking exposure through residues in 
food into account. This indirect approach to the use of water model 
estimates of pesticide exposure keeps distinct the screening nature of 
water model estimates.
    In estimating pesticide exposure from various pathways EPA is 
careful to avoid relying on maximum values from every input because 
such an approach can grossly overestimate exposure. As EPA's exposure 
guidelines note: ``When constructing this [exposure] estimate from a 
series of factors [environmental concentrations, intake rates, 
individual activities, etc.], not all factors should be set to values 
that maximize exposure or dose, since this will almost always lead to 
an estimate that is much too conservative.'' (Ref. 29). Given that 
EPA's approach to estimating pesticide exposure from food, water, and 
residential uses already tends to be very conservative (health-
protective), EPA has been cautious about simply adding in yet another 
screening level value in calculating aggregate exposure. Certainly, the 
epidemiology data discussed above and in the Imidacloprid Order does 
not strongly suggest that EPA exposure estimates have been ignoring a 
major pathway of exposure.
    That does not mean that the AgDRIFT model does not have a role to 
play in considering aggregate exposure to pesticides. It may prove 
useful in designing buffer zones for pesticides that otherwise have 
potentially high exposures. Alternatively, as data on exposure expands 
and modeling improves, some aspect of AgDRIFT modeling may be 
meaningfully incorporated into probabilistic modeling of exposure. 
However, as the analysis below shows, exposure as a result of spray 
drift is unlikely to be a significant contributor to any substantial 
number of individuals.
    To evaluate potential exposures from spray drift, EPA: (1) Compared 
potential spray drift exposures to exposures from residential lawn 
uses; and (2) computed MOE's for each of the 13 pesticides assuming 
spray drift exposure is a component of residential exposure. Both 
exercises confirm EPA's view that spray drift is unlikely to be a 
significant contributor to risk.
    1. Comparison of AgDrift model estimates of exposure with exposure 
from residential lawn use generally. AgDRIFT version 2.01 is a computer 
model that can be used to estimate downwind deposition of spray drift 
from aerial, ground boom, and orchard and vineyard airblast 
applications. The model contains ``Toolbox'' screens that can be used 
to estimate deposition levels in terrestrial and aquatic environments 
and estimate concentrations in water bodies. The model contains three 
tiers of increasing complexity for aerial application. In Tier 1, the 
user can estimate downwind deposition resulting from each of the 
application methods under several predefined scenarios. In higher tiers 
more options are available. AgDRIFT only allows Tier 1 level analyses 
for ground boom and airblast application methods. The aerial portion of 
the model is based on a mechanistic U.S. Forest Service model, (Ref. 
30). The SDTF field trial data were used to validate the aerial portion 
of AgDRIFT, (Refs. 31 and 32). The ground boom and orchard airblast 
portions use data collected by the Spray Drift Task Force (SDTF) to 
empirically calculate spray drift deposition. AgDRIFT was developed 
under a cooperative research and development agreement between EPA, 
USDA, and the SDTF.
    The AgDRIFT model can provide a picture for each of the three 
application techniques (aerial, groundboom, and airblast) of what 
amount of an agriculturally-applied pesticide may drift onto areas 
ranging from 10 feet to 210 feet from the treated field. In the 
following Table 2, high-end spray drift deposition as modeled by 
AgDrift is presented in terms of deposition rate offsite as a 
percentage of the pesticide application rate. (Ref. 33).

                 Table 2.--High-end Downwind Spray Drift Deposition Levels by Application Method
----------------------------------------------------------------------------------------------------------------
                                                           Spray drift deposition (percent of application rate)
                                                         -------------------------------------------------------
                                                                                     airblast
       Lawn placement relative to application area                           ------------------------
                                                           aerial    ground                dense or    granular
                                                                      boom      dormant      tall
                                                                               orchards    canopies
----------------------------------------------------------------------------------------------------------------
10 to 60 ft downwind                                          34.1       9.3        25.0         8.4           0
---------------------------------------------------------
20 to 80 ft downwind                                          31.6       6.4        16.1         6.0           0
---------------------------------------------------------
40 to 90 ft downwind                                          27.9       4.1         8.0         3.7           0
---------------------------------------------------------
80 to 130 ft downwind                                         22.0       2.4         3.0         1.9           0
---------------------------------------------------------
160 to 210 ft downwind                                        14.9       1.3         0.8         0.9           0
----------------------------------------------------------------------------------------------------------------


[[Page 46719]]

    As Table 2 shows, the highest off-target deposition levels from 
agricultural applications occur adjacent to the treated area and those 
levels decrease with increasing distance from the treatment area. 
Importantly, in EPA's experience, application rates for residential 
uses are generally equal to or greater than the levels allowed for 
agricultural applications. Thus, deposition on residential lawns from 
spray drift is generally a small fraction of deposition from direct 
residential treatment and, unless the residential lawn is relatively 
close to the treated agricultural field, the ratio of spray drift 
deposition to deposition from direct treatment is exceedingly low.
    2. Evaluation of MOE's based on AgDrift Model for the pesticides in 
the objections. Another way of evaluating the potential significance of 
application drift exposure is by calculating potential high-end 
application drift for each pesticide for areas adjacent to treated 
fields and combining these values with other exposure values for the 
pesticide. Due to the high-end nature of the estimates from the AgDrift 
model and the limited number of persons that would be exposed at the 
field boundary, EPA does not believe it is reasonable to simply add 
these values to other high-end exposure values in determining pesticide 
safety. Nonetheless, in the context of these objections, EPA has 
performed this calculation to show how even making such low probability 
exposure assumptions does not result in any safety concerns.
    The exposure/risk scenario deemed most appropriate for evaluating 
application drift exposures is the short-term exposure scenario. Short-
term exposures are those likely to occur over a 1- to 7-day window. 
This is the exposure window most commonly used with assessing exposure 
from residential turf use of a pesticide and the turf use is the 
residential use that most closely approximates the exposure that may 
result from application drift. To estimate potential exposure to 
application drift, EPA first calculated the amount of deposition that 
may drift to an area 10-60 feet downwind of the application site using 
the combination of permitted application technique and rate that 
yielded the highest deposition. Then EPA used the predicted deposition 
amount as an input in its model for estimating post-application 
exposure to toddlers on turf. EPA focused on toddlers because toddlers 
have the greatest post-application turf exposure to pesticides of any 
population subgroup due to their behavior patterns (i.e., crawling, 
rolling on turf; hand-to-mouth activity; soil ingestion). As is done 
with evaluating aggregate short-term post-application exposures to turf 
uses, predicted post-application exposure from drift was then summed 
with background exposures to the pesticide from residue-containing food 
and water. If the pesticide has residential exposures, those predicted 
exposures were summed as well. After combining all of these exposures, 
the overall exposure value was divided into the safety endpoint used to 
evaluate short-term exposure to quantify the Margin of Exposure (MOE). 
To ensure that this assessment was conservative, EPA combined oral and 
dermal exposure where appropriate. Where combining oral and dermal 
exposures was not supported by the data, EPA calculated separate MOEs 
for dermal and oral exposures and then combined the MOEs. (Ref. 33 at 
3-5).
    The following Table 3 presents estimated MOEs for the 13 pesticides 
for background food and water exposure, residential exposure (where 
applicable), application drift exposure, and combined exposure. Table 3 
also lists the Level of Concern (LOC) for each pesticide. The LOC is 
the minimum level that a MOE must obtain to ensure that the MOE 
includes adequate safety factors, including the children's safety 
factor. As can be seen, even when assessing risk using this unrealistic 
exposure approach, the MOEs for these pesticides remain above their 
respective LOC.

                               Table 3.--Combining Application Drift Short-term Exposures with Other Exposures of Toddlers
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                       Food and Water            Residential MOE           Appl. Drift MOE
                                                       Background MOE      ----------------------------------------------------   Combined
                    Pesticide                    --------------------------                                                         MOE          LOC
                                                      food        water         oral        dermal        oral        dermal
--------------------------------------------------------------------------------------------------------------------------------------------------------
halosulfuron-methyl                                   140,000      300,000       60,000        3,100    2,500,000      110,000        2,800          100
-------------------------------------------------
pymetrozine                                           220,000       63,000        2,200           na       15,000           na        1,800        1,000
-------------------------------------------------
mepiquat                                               29,000      550,000           na           na      180,000       27,000       13,000          100
-------------------------------------------------
bifenazate                                              2,500      880,000           na           na        3,700        1,100          650          100
-------------------------------------------------
zeta-cypermethrin                                         710       22,000        4,400           na       40,000           na          570          100
-------------------------------------------------
diflubenzuron                                          13,000      220,000           na           na        1,600       15,000        1,300          100
-------------------------------------------------
2,4-D                                                  17,000       17,000          970        1,100        2,500        1,600          330          300
-------------------------------------------------
isoxadifen-ethyl                                        5,600        3,500           na           na       33,000        9,100        1,600          300
-------------------------------------------------
acetamiprid                                             1,000       38,000           na           na       12,000        1,800          610          300
-------------------------------------------------
propiconazole                                          18,000    3,300,000           na           na       19,000        1,800        1,500          100
-------------------------------------------------
furilazole                                            330,000      130,000           na           na      200,000       19,000       15,000          300
-------------------------------------------------
fenhexamid                                              3,500      300,000           na           na       13,000       14,000        1,300          300
-------------------------------------------------
fluazinam                                              93,000        4,300           na           na        3,800          370          310          300
--------------------------------------------------------------------------------------------------------------------------------------------------------


[[Page 46720]]

    Table 3 has been compiled based on analyses and data in existence 
at the time of the tolerance action. Since the tolerance actions, EPA 
has received new information or conducted new analyses as to these 
pesticides. That data and analyses has resulted in changes, or 
potential changes to the assessment of the risk posed by these 
pesticides. The changes come in the form of adjusted safety factors, 
more realistic exposure estimates, and new toxicity endpoints. EPA has 
not incorporated that information into this objection response because 
consideration of this new information was not needed to address NRDC's 
objections. EPA would have considered expanding its response to address 
new information if NRDC's objections had convinced EPA that its prior 
analysis was flawed or EPA had a completed risk assessment showing 
risks of concern.
    EPA cautions that it would be inappropriate to focus on any one 
aspect of the underlying risk assessment variables and conclude that 
based on a change in that one variable alone the risk of a particular 
pesticide is unacceptable. Not only must EPA assess all of the 
variables in combination, but EPA's risk assessment process is tiered 
such that more elaborate techniques to predict realistic exposure 
values are not used if use of worst case default exposure assumptions 
suggest there is not a risk of concern. (Refs. 29 at 22922; 1 at 11). 
For example, NRDC has argued that for some of the pesticides in the 
objections, use of a different safety factor would demonstrate that the 
objected-to tolerances are unsafe. Given, however, the very 
conservative exposure assumptions for many of these pesticides, such 
arguments are likely to be incorrect even if NRDC could support its 
argument for a greater safety factor.
    b. Volatilization of applied pesticides. On June 19, 2003, NRDC 
supplemented its submission to the Agency with several pieces of 
additional information. Included was a report by the Californians for 
Pesticide Reform generally addressing the issue of spray drift from 
pesticide applications in California. (Ref. 34) [hereinafter referred 
to as the ``CFPR Report'']. Although EPA defines spray drift as the 
movement of droplets off-target during or shortly after application, 
which is independent of the chemical properties of the pesticide being 
sprayed, the CFPR Report looked more broadly at atmospheric pesticide 
transport including pesticide volatilization as a potential mechanism 
by which pesticides travel beyond treated fields. Also included in 
NRDC's supplemental information was a research article containing an 
analysis and ranking of the degree of inhalation risk posed by certain 
migrating pesticides in California, based on ambient air monitoring 
data gathered, in part, by the California Air Resources Board and the 
California Department of Pesticide Regulation. (Ref. 35) [hereinafter 
referred to as the ``Ranking Study''].
    The Ranking Study conducted screening level assessments for many of 
the pesticides regarded as having the highest potential as toxic air 
contaminants by the California Department of Pesticide Regulation as 
well as several pesticides categorized as hazardous air pollutants by 
EPA. This screening level assessment, using conservative (health-
protective) assumptions, only identified three soil fumigants (MITC, 
methyl bromide, telone) and one heavily-used non-fumigant pesticide 
(chlorpyrifos) as potentially presenting non-cancer acute or chronic 
risks of concern. (Id. at 1179). The study concluded that ``vapor 
pressure is a significant predictor of [] ranking of inhalation risks. 
(Id. at 1182). The CFPR Report examined the potential health risks from 
air levels of three pesticides characterized as moderate to highly 
volatile (chlorpyrifos, diazinon, and molinate) measured at the field 
boundary and at more distant locations. The Report concluded that in 
many instances the measured air levels of these pesticides posed risks 
of concern. The Report also concluded that drift due to volatilization 
was not a concern for pesticides that are not highly volatile. (Ref. 34 
at 40).
    (1) Analysis of CFPR report and ranking study. In terms of 
volatility, pesticides can be broadly grouped into three categories: 
(1) Those of high volatility (vapor pressure of 10-1 to 
10-3 millimeter of mercury (mmHg)); (2) those of moderate 
volatility (vapor pressure of 10-4 to 10-5 mmHg); 
and (3) those of low volatility (vapor pressure of 10-6 mmHg 
and below). EPA and NRDC seem to be in general agreement regarding the 
exposure potential from the first and third groups. Both EPA and NRDC 
believe that significant airborne exposures may occur as a result of 
the application of pesticides of high volatility and that exposure 
through volatilization is unlikely for pesticides of low volatility. 
Where EPA and NRDC differ is regarding the middle group. NRDC argues, 
based on the CFPR Report, that pesticides in this group can result in 
exposures that raise levels of concern. EPA believes the evidence NRDC 
has presented on this point is open to question. Although there is a 
greater possibility for volatilization of residues of pesticides of 
moderate volatility than those of low volatility, EPA is not convinced 
that volatilization exposure from the former group is likely to be 
meaningful. In any event, as discussed below, there is no reason to 
expect any meaningful exposure due to volatilization from any of the 13 
pesticides involved in these objections.
    In the CFPR Report, CARB data is presented and analyzed for two 
pesticides that fall in the middle group: Diazinon and chlorpyrifos. 
The CFPR Report concludes that exposure to volatilized residues alone 
from these two pesticides raise risks of concern. The risks of concern 
were due to acute, not chronic exposures, and occurred primarily as a 
result of exposure in areas immediately adjacent to treated fields 
within a day or two of treatment. EPA questions the validity of this 
determination due to various assumptions made in the Report that tend 
to exaggerate exposure and risk. First, the CFPR Report estimates 
exposure based on the amount of air breathed in a 24-hour period. The 
field studies analyzed in the report, however, show that volatilization 
exposures peak in a relatively narrow time window that is significantly 
shorter than 24 hours.
    Second, the measured residues in the field studies were sampled in 
an outdoor location just a few feet from the field. Yet, it is unlikely 
that any individual would remain stationary outdoors in such a location 
for a 24-hour period. Moreover, even if an individual did stay in that 
same location for a 24-hour period, it is unlikely that he or she would 
be outdoors the entire time. Thus, the Report's exposure estimate rests 
on the assumption that indoor air concentrations are the same as 
concentrations measured in outdoor air. This assumption is reportedly 
based on a pilot study supporting the prospective Agricultural Health 
Study of American farmers and their families. (Ref. 36). These data 
suggested higher air concentrations were found inside the residences of 
farmers than were measured outdoors. The outdoor measurements were 
collected either on the farmer's lawn or porch. However, it is not 
clear either when the actual pesticide applications were made with 
respect to the timing of the air concentration data collection or their 
location with respect to the distance from the treated field. 
Meteorological details were not provided. In one example from this 
study (lindane), indoor concentrations were traced to work clothing 
while the application of lindane was made to hogs situated inside a 
separate production facility.

[[Page 46721]]

    In EPA's view, it is more likely that indoor levels of pesticides 
would be lower in homes situated near agricultural sites or other sites 
of pesticide application than levels that might be measured outdoors. 
This is particularly the case in situations involving acute exposures 
where airborne levels rapidly peak and dissipate. For example, Segawa 
et al. reported in 1991 that, when malathion was sprayed in Southern 
California for Mediterranean fruit fly control, indoor levels of 
malathion were 4 to 5 times lower than outdoor air concentrations. 
(Ref. 37). In a study evaluating the impact of track-in following 
applications of 2,4-D to lawns (Ref. 38), it was suggested that spray 
drift and particle intrusion had little effect on indoor carpet dust 
concentrations. Likewise, Solomon et al. (Ref. 39) have reported 
minimal impact on indoor air measurements of bystander homes adjacent 
to treatment areas (2,4-D applications to lawns). Therefore, the 
assumption that indoor air concentrations are equivalent to outdoor air 
concentrations appears to exaggerate risk. Consistent with this view, 
California DPR measurements of indoor air versus outdoor air following 
methyl bromide structural fumigations indicated that, within the first 
hour, outdoor air concentrations of methyl bromide (first 50 feet from 
treatment site) are approximately 5 to 8 times higher than those in 
indoor air, and up to 13 times higher than indoor air at distances 
equal to or greater than 100 feet. Only after 24 hours, when the 
majority of the plume had passed by the house, were indoor air 
measurements roughly the same as outdoor measurements.
    Third, the CFPR compares these exposure estimates to reference 
doses from subchronic inhalation studies. With chlorpyrifos, the 
reference dose is based on lack of effects in two 90-day rat inhalation 
studies at the highest dose tested and incorporates a 1,000-fold safety 
factor. For diazinon, the reference dose is from a LOAEL in a 21-day 
inhalation study and incorporates a 300-fold safety factor. Use of 
reference doses from subchronic studies to assess what, in the case of 
the field trials, are at most short-term exposures (1 to 7 day 
duration) - and more likely acute exposures (single event) - is a very 
conservative approach. This factor should be taken into account in 
characterizing any risk estimation.
    Finally, an EPA report on pesticide exposure to children along the 
United States/Mexico border (discussed in the Imidacloprid Order, (69 
FR at 30052)) presents a vivid contrast to conclusions reached in the 
CFPR report. (Ref. 40). This report concluded that both indoor and 
outdoor air concentrations had a minimal impact on the exposed 
population. The pesticides diazinon and chlorpyrifos are two chemicals 
widely used in that region. Thus, this report casts doubt on the 
conclusions in the CFPR Report.
    (2) Vapor pressure. As noted, EPA is in general agreement that 
vapor pressure is a key factor in predicting whether a pesticide has 
the potential to volatilize and drift offsite in significant amounts. 
Because soil fumigants traditionally have very high vapor pressures, 
and thus are highly volatile, EPA is now accounting for potential 
exposure due to volatilization of these pesticides in calculating their 
aggregate exposure. The CFPR Report concludes that post-application 
volatilization exposures are not of concern for pesticides with a low 
vapor pressure - i.e., less than or equal to 10-6 mmHg - but 
can be for pesticides with a moderate vapor pressure - i.e. between 
10-4 and 10-6 mmHg. In Table 4 below, EPA has 
listed, according to vapor pressure, the five non-fumigant pesticides 
examined by the CFPR Report (including the CFPR's characterization of 
the vapor pressure) as well as the 13 pesticides in these objections. 
(Ref. 41).

            Table 4. --Vapor Pressure of Selected Pesticides
------------------------------------------------------------------------
                                                         Vapor Pressure
            Pesticide               Reason Included          (mmHg)
------------------------------------------------------------------------
molinate                          CFPR (high vapor            5.3 x 10-3
                                   pressure)
---------------------------------
diazinon                          CFPR (moderate              1.4 x 10-4
                                   vapor pressure)
---------------------------------
chlorpyrifos                      CFPR (moderate             1.87 x 10-5
                                   vapor pressure)
---------------------------------
fluazinam                         Subject of                    8 x 10-6
                                   objection
---------------------------------
mepiquat                          Subject of                  2.3 x 10-6
                                   objection
---------------------------------
propiconazole                     Subject of                  4.2 x 10-7
                                   objection
---------------------------------
2,4-D                             Subject of                  1.4 x 10-7
                                   objection
---------------------------------
paraquat                          CFPR (low vapor               1 x 10-7
                                   pressure)
---------------------------------
halosulfuron                      Subject of                    1 x 10-7
                                   objection
---------------------------------
bifenazate                        Subject of                    1 x 10-7
                                   objection
---------------------------------
pymetrozine                       Subject of                    3 x 10-8
                                   objection
---------------------------------
isoxadifen-ethyl                  Subject of                 1.65 x 10-8
                                   objection
---------------------------------
acetamiprid                       Subject of                  7.5 x 10-9
                                   objection
---------------------------------
fenhexamid                        Subject of                    7 x 10-9
                                   objection
---------------------------------
propargite                        CFPR (low vapor             4.4 x 10-9
                                   pressure)
---------------------------------
zeta-cypermethrin                 Subject of                 3.07 x 10-9
                                   objection
---------------------------------

[[Page 46722]]

 
diflubenzuron                     Subject of                   9 x 10-10
                                   objection
---------------------------------
furilazole                        Subject of                6.63 x 10-10
                                   objection
------------------------------------------------------------------------

    As Table 4 illustrates, all but two of the pesticides in these 
objections have a low vapor pressure and thus, on this basis alone, are 
unlikely to result in significant exposures due to post-application 
volatilization. Two pesticides, fluazinam and mepiquat, have vapor 
pressures in the 10-5 to 10-6 mmHg range, but 
nonetheless below the vapor pressure of chlorpyrifos, the pesticide 
with the lowest vapor pressure that the CFPR Report concluded had 
significant levels of post-application drift. (A form of 2,4-D (2,4-
D(BEE)) has a vapor pressure of 2.4 X 10-6 mmHg; however, 
whatever potential to volatize exists for this form of 2,4-D is 
significantly lowered by its method of application (agitation into the 
water profile at aquatic sites)). Traditionally, general scientific 
opinion has been that substances with a vapor pressure of between 
10-4 and 10-6 mmHg are relatively non-volatile 
and thus unlikely to result in significant exposures due to 
volatilization. (Ref. 42). NRDC contends otherwise based on the CFPR 
Report. Even assuming NRDC is correct, however, there are several 
characteristics of fluazinam and mepiquat in addition to their lower 
vapor pressure, that distinguish them from chlorpyrifos and make it 
unlikely that they have any significant post-application drift 
exposures either in the acute or chronic exposure time-frame.
    In terms of acute exposure, it is first worth re-emphasizing that 
EPA has substantial questions as to whether the CFPR Report overstates 
the exposure that can be expected with regard to chlorpyrifos. Second, 
the maximum single application rates for fluazinam (0.8 lbs/acre) and 
mepiquat (0.25 lbs/acre) are much lower than chlorpyrifos (6 lbs/acre - 
this rate was used in the CFPR study) - factors of 7.5 and 24, 
respectively. (Refs. 43, 44 and 45). Finally, the acute inhalation 
endpoints of concern, adjusted by safety factors, for fluazinam (0.0046 
mg/kg/day) and mepiquat (0.584 mg/kg/day) are much higher than for 
chlorpyrifos (0.0001 mg/kg/day) - factors of 46 and 5,840, 
respectively. (Refs. 46, 47 and 48).
    As to chronic exposure, although a high enough vapor pressure 
appears to be a necessary condition to significant ambient air 
concentrations, vapor pressure alone is not sufficient for such 
significant chronic exposures to occur. Equally necessary, is a 
substantial overall usage amount. In this regard, chlorpyrifos dwarfs 
fluazinam and mepiquat. Average annual usage for chlorpyrifos for the 
years 2001-2003, is estimated to have been in the range of 8 to 9 
million pounds. On the other hand over the same period, mepiquat usage 
is estimated to have been in the range of 250,000 to 500,000 pounds. 
Fluazinam had so little usage it did not even show up in standard 
pesticide usage survey reports. (Ref. 49).
    Finally, it is worth considering that occupational exposure 
assessments for the three pesticides as a means of comparing the 
relative inhalation risk posed by these pesticides. EPA's principal 
tool for assessing occupational exposure and risk is Pesticide Handlers 
Exposure Database (PHED). (Ref. 50). PHED is a software system 
consisting of two parts -- a database of measured exposure values for 
workers involved in the handling of pesticides under actual field 
conditions and a set of computer algorithms used to subset and 
statistically summarize the selected data. Currently, the database 
contains values for over 1,700 monitored individuals (i.e., 
replicates). One of the measured values is the level of pesticide 
residue in ambient air at the time of application. This value contains 
a mixture of volatized residue as well as airborne non-volatized 
residue and is likely to be substantially higher than any post-
application levels even for highly volatile pesticides.
    What PHED assessments for the three pesticides show is that for 
inhalation risks both fluazinam and mepiquat have high MOEs that are 
well above the level of concern (i.e., there is a large margin of 
safety) even without any protective equipment (e.g., respirators or 
enclosed cabs) but that chlorpyrifos had MOEs for some scenarios that 
are below the level of concern even assuming that applicators used 
enclosed cabs. (Refs. 46 at 7-8; 47 at 37 and Ref. 51).
    For all of these reasons, EPA concludes the information submitted 
by NRDC does not suggest that the use of fluazinam and mepiquat, which 
have vapor pressures slightly above the 10-6 mmHg level, 
would result in significant post-application exposures due to 
volatilization of residues. As the material relied upon by NRDC notes, 
post-application drift is unlikely for the other 11 pesticides in the 
objections.
    c. Conclusion. EPA concludes that NRDC's arguments concerning 
exposure from application and post-application drift do not undermine 
EPA's conclusion that it has reliable data on exposure for these 
pesticides. Not only does the scientific literature not support a 
finding that pesticide drift is a major source of exposure but (1) 
EPA's application drift model demonstrates that exposure from 
application drift is likely to be marginal everywhere other than areas 
immediately adjacent to fields; (2) even combining application drift 
exposures with other aggregate exposures in a manner likely to 
significantly overstate exposure does not show a risk of concern for 
any of the 13 pesticides; (3) the vapor pressures for 11 of the 13 
challenged pesticides are sufficiently low that even NRDC appears to 
concede that significant post-application drift would not be expected 
from any of them; and (4) for the two pesticides that have slightly 
higher vapor pressures, individual factors regarding them indicate that 
siginificant post-application drift is unlikely.

C. Failed to Retain Children's 10X Safety Factor

    1. Introduction. NRDC's objections concerning the children's safety 
factor principally focus on an alleged lack of data that NRDC contends 
does not allow EPA to conclude that the children's safety factor may be 
reduced or removed. First, NRDC argues that 7 of the 13 pesticides 
(halosulfuron-methyl, pymetrozine, mepiquat, zeta-cypermethrin, 2,4-D, 
acetamiprid, and fluazinam) lack a required DNT study, and that this 
``is a crucial data gap that by itself should prohibit EPA from 
overturning the default 10X safety factor.'' (Refs. 6 at 4; 7 at 6-7; 8 
at 10; and 9 at 6). In support of this argument NRDC relies on 
information showing that pesticides may cause developmental neurotoxic 
effects and that these effects may come at lower doses than doses 
causing other adverse effects. Second, NRDC cites, on a pesticide-by-
pesticide basis, various

[[Page 46723]]

toxicological studies that NRDC claims are missing, or were not 
considered. The absence or non-consideration of these data, NRDC 
contends, warrants retention of the children's safety factor. Following 
the same pattern with exposure data, NRDC claims that the children's 
safety factor is required because EPA is lacking both generic data on 
exposure and various specific pieces of exposure information with 
regard to some of the individual pesticides named in the objections. 
NRDC's generic exposure data objections pertain to data on the exposure 
of farm children to pesticides and exposure to pesticides through 
drinking water. Additionally, NRDC claims that data are missing because 
EPA has allegedly failed to undertake certain, specific risk 
assessments as to some of the pesticides.
    Each of these objections will be addressed individually.
    2. Lack of DNT study generally. NRDC contends that ``the absence of 
required developmental (DNT) tests for 2,4-D is a crucial data gap that 
by itself should prohibit EPA from overturning the default 10X safety 
factor.'' (See, e.g., Ref. 8 at 9). NRDC cites essentially three 
grounds in support of this contention. First, NRDC claims that there is 
extensive evidence showing that ``pesticide exposures may disrupt the 
normal development of a child's brain and nervous system.'' (Id. at 9 
and fn.16 (citing studies)). Second, NRDC references a paper by EPA 
staff scientist Susan Makris that NRDC asserts demonstrates that ``DNT 
testing is more sensitive than other studies in measuring the effects 
of exposure on proper development of the brain and nervous system . . . 
.'' (Id. at 9). Third, NRDC cites the EPA's 10X Task Force Report which 
recommends the DNT testing be part of the minimum toxicity data set for 
pesticides requiring a tolerance for residues in or on food. (Id. at 
10). NRDC further asserts that EPA's Children's Safety Factor Policy 
fails in its purported attempt to justify choosing a factor other than 
10X when a required DNT study has not been submitted. According to 
NRDC, the Children's Safety Factor Policy ``completely reverses'' the 
statutory presumption in favor of an additional 10X factor by allowing 
EPA to choose a different factor not on the basis of reliable data but 
on a risk assessor's ``intuition or professional judgment.'' (Id. at 
11).
    EPA disagrees that the mere absence of a required DNT study should, 
by itself, conclusively bar EPA from applying a different additional 
safety factor than the 10X default value. After all, the statute 
expressly authorizes EPA to use a different additional factor if the 
Agency can determine on the basis of reliable data that a different 
factor ``will be safe for infants and children.'' (21 U.S.C. 
346A(b)(2)(C)). In line with the statute, EPA's Children's Safety 
Factor Policy calls for a careful examination of the existing database 
on a case-by-case basis to determine if a reliable basis exists for 
assigning a different factor. NRDC's argument here can only be 
successful if it can show that reliable data to support a different 
safety finding could never be available. This NRDC has not done. NRDC's 
objections contain no factual contention demonstrating that a case-
specific approach cannot work or is inappropriate for the 13 pesticides 
in question.
    a. Pesticides may cause neurological developmental effects. NRDC 
cites the National Research Council's 1993 Report on pesticides' 
effects on children in support of the claim that ``pesticide exposures 
may disrupt the normal development of a child's brain and nervous 
system.'' (Ref. 8 at 9). EPA does not dispute that some pesticides have 
that potential; however, that some pesticides have that potential does 
not mean that defensible judgments about that potential cannot be made 
in the absence of a DNT study. Further, EPA would note that the 
National Research Council Report did not conclude that the evidence 
showed that exposure to pesticides was currently resulting in 
neurological developmental effects. According to the National Research 
Council, ``[a]lthough the vulnerability of the developing brain to 
neurotoxic exposure is of serious concern, it is entirely unclear from 
the data available whether exposures at levels consistent with usual 
dietary exposures would pose a substantial risk to the long-term 
neurologic development of children in general or to particular 
subgroups of children that are neurologically vulnerable.'' (Id. at 
65.)
    NRDC also cites a number of studies showing that a particular 
pesticide, chlorpyrifos, does have neurological effects on the 
developing brain. Again, however, EPA does not deny that pesticides can 
cause such effects. The question is, however, whether in the absence of 
a DNT study, EPA can make a reliable prediction concerning whether a 
particular safety factor will be protective of infants and children 
from potential neurological effects. Citing the general capacity of a 
specific pesticide to cause neurological effects does not answer this 
question. EPA has received and reviewed a DNT study for the pesticide 
in question, chlorpyrifos. Although the results of the DNT study for 
chlorpyrifos were confirmatory of results in other chlorpyrifos 
toxicology studies, the DNT results did not alter the regulatory 
endpoints chosen for that pesticide. (Ref. 52).
    b. 1998 retrospective study on submitted DNT studies. The 
conclusions presented in the Makris study are more relevant to the 
question at hand. (Ref. 53). After reviewing nine DNT studies that had 
been submitted on pesticides, Makris found that (1) for eight out of 
nine pesticides the fetal NOEL from the DNT study was lower than the 
fetal NOEL from the standard prenatal developmental toxicity study; (2) 
for six out of nine pesticides the offspring NOEL from the DNT study 
was lower than the offspring NOEL from the standard two-generation 
reproduction study; (3) for two out of nine pesticides, the acute 
endpoints and associated NOELs from the DNT study were selected for the 
acute dietary risk assessment; and (4) the DNT study did not provide an 
endpoint and associated NOEL for chronic risk assessment for any of the 
nine pesticides. The first two findings provide valuable scientific 
information with regard to understanding how pesticides may affect the 
developing human. More relevant to a decision regarding the children's 
safety factor, however, are the latter two findings because they 
highlight whether a DNT study may affect how the risk posed by a 
pesticide is characterized.
    Some background information may be helpful in understanding the 
significance of Makris' findings. In assessing the risk posed by a 
pesticide, EPA examines numerous toxicological studies and identifies 
from each study the LOAEL resulting from exposure to the pesticide and 
the NOAEL. These NOAEL/LOAELs are then grouped by exposure scenario 
taking into account both the duration of the exposure (e.g., acute, 
chronic) and the route of exposure (e.g., oral, dermal). For each 
exposure scenario EPA selects the lowest of the appropriate NOAELs for 
the purpose of assessing risk. For evaluating acute and chronic oral 
dietary exposure, EPA uses this NOAEL to derive a safe dose - this safe 
dose is commonly referred to as a Reference Dose (RfD). Generally, a 
RfD is calculated by dividing the selected NOAEL by one or more safety 
or uncertainty factors. When more data becomes available, it may change 
a RfD but only if the NOAEL from the new data is lower than all 
previous NOAELs identified for the relevant exposure scenario.
    What Makris found in looking at the 9 pesticides was that, out of 
the 18 potential exposure scenarios examined

[[Page 46724]]

(1 acute oral and 1 chronic oral for each pesticide), in only 2 
instances did the DNT study produce a NOAEL that was below all other 
NOAELs for that exposure scenario for that pesticide. In other words, 
in 16 out of 18 cases, the DNT study made no difference in the 
calculation of the safe human dose (i.e., RfD) for the pesticide. 
Although this information shows that the DNT study can be an important 
study is assessing the risk of pesticides because it has the potential 
to show adverse effects at levels below those previously identified, 
the potential for a DNT study to change an existing RfD is hardly so 
overwhelming to suggest that there is no room for exercise of the 
discretion to examine the individual facts involving the safety of each 
pesticide that is expressly provided by the statute.
    Today, EPA has considerably more experience with the DNT study than 
when the 1998 Retrospective Study was conducted. That experience has 
confirmed both that the DNT study has a role to play in assessing the 
hazard posed by pesticides, (Ref. 54), and that DNT studies only 
infrequently affect the projection of a safe endpoint for a pesticide. 
EPA is currently in the process of completing another retrospective 
study of the DNT study based on the roughly 50 DNT studies it has now 
received. The full retrospective study will not be completed until 
later this year; however, some preliminary information is now 
available. (Ref. 55). It shows that out of the 38 pesticides for which 
a DNT study has been submitted and EPA's analysis completed, the DNT 
study has resulted in a lowering of at least 1 endpoint for a pesticide 
in 8 instances. Again, these numbers do not suggest there is no room 
for judgment in evaluating the impact a DNT study may have on a risk 
assessment.
    c. 10X Task Force Report. NRDC also cites the recommendation in the 
report of EPA's 10X Task Force that the DNT study be included in the 
core toxicology database for pesticides. Although the Task Force did 
note the significance of the DNT study for assessing potential risks 
for children, the Task Force also concluded that any decision on the 
size of any safety factor (described by the Task Force as a database 
uncertainty factor) used when a DNT study had not been submitted called 
for the exercise of ``good scientific judgment.'' (Ref. 56). According 
to the Task Force, ``[t]he size of the database uncertainty factor 
applied will depend on other information available in the database and 
how much impact the missing data may have on determining the potential 
toxicity of the pesticide for children.'' (Id.). As described above, 
EPA's policy on evaluating the size of the safety factor when a 
required DNT study has not yet been submitted is fully consistent with 
this recommendation by the 10X Task Force. When a required DNT study is 
absent, EPA has focused on the other information available on the 
pesticide and the possible impact the DNT study may have on estimating 
the risk of the pesticide.
    d. EPA's 10X Policy. Finally, EPA disagrees that its Children's 
Safety Factor Policy completely reverses the statutory presumption to 
include an additional 10X safety factor for the protection of infants 
and children. In the opening paragraph of the policy the Agency states 
that ``[t]he Office of Pesticide Programs (OPP) interprets this 
statutory provision [Section 408(b)(2)(C)] as establishing a 
presumption in favor of applying an additional 10X safety factor.'' 
(Ref. 2 at 4). The presumptive aspect of the additional 10X safety 
factor (also described as the ``default position'') is referenced 
throughout the document. (See, e.g., Id. at 10, 11, 17, 26, 46, 47-48, 
and A-6).
    NRDC cites to language in the policy statement stating that in 
evaluating what safety factor decision should be made for pesticides 
for which a DNT study has been requested, risk assessors should 
consider ``if the available information indicates that a DNT study is 
likely to identify a new hazard or effects at lower dose levels of the 
pesticide that could significantly change the outcome of its overall 
risk assessment . . . .'' (Ref. 7 at 8-9). NRDC argues that this 
language reverses the statutory presumption because it allows the 
presumption to be removed not based on reliable data but upon the 
''risk assessor's expectation. (Id. at 9).
    NRDC, however, is mistaken in its interpretation of this language. 
In directing the risk assessor to consider the likely impact of a DNT 
study on a risk assessment, EPA was not asking the risk assessor to 
guess at the results of the DNT study. Rather, EPA was directing the 
risk assessor to consider what the reliable data available on the 
pesticide told the risk assessor about the likely outcome of the DNT 
study. To ensure that the policy was not misunderstood on this point, 
the policy explicitly states that ``[d]iscussions in this document of 
the appropriateness, adequacy, need for, or size of an additional 
safety factor are premised on the fact that reliable data exist for 
choosing a `different' factor than the 10X default value.'' (Ref. 2 at 
12). To the extent the policy statement injects any uncertainty with 
regard to this issue, EPA herein confirms that a decision to choose a 
factor different than the default 10X factor must be based on reliable 
data.
    e. Conclusion. EPA rejects NRDC's contention that an EPA finding 
that a DNT study is needed in evaluating the risks posed by the 
pesticide is outcome-determinative as regards to retaining the 
children's safety factor until such time as the DNT study is submitted 
and reviewed. The statute specifically grants EPA discretion to apply a 
different additional safety factor where EPA can conclude based on 
reliable data that the different factor is safe for infants and 
children. NRDC has made no argument that would justify an across-the-
board conclusion that in the absence of a DNT study an individual 
examination of the existing data pertaining to a pesticide cannot 
provide a reliable basis for concluding that a different safety factor 
would be safe for infants and children. NRDC's claim that a DNT study 
may lower EPA's RfD (which EPA does not disagree with) is not by itself 
sufficient to bar EPA from making a case-by-case inquiry into the 
safety of a different additional safety factor for the protection of 
infants and children in the absence of such a study. Further, NRDC has 
offered no pesticide-specific arguments as to the pesticides in this 
proceeding as to why the absence of a DNT study requires the retention 
of the default 10X additional factor.
    3. Other pesticide-specific missing toxicity data--a. 
Diflubenzuron. NRDC claims that EPA is missing toxicology data for two 
diflubenzuron metabolites, deemed necessary by EPA to justify an 
unconditional registration.
    As EPA has previously noted, the toxicology database for 
diflubenzuron is complete for assessment of increased susceptibility to 
infants and children. (67 FR 59006, 59013, September 19, 2002; 67 FR 
7085, 7089, February 15, 2002). EPA has received and reviewed all 
required studies bearing on the assessment of the effects of 
diflubenzuron following in utero and/or postnatal exposure. These 
studies demonstrated that diflubenzuron presented a low risk to the 
developing organism. For example, in the prenatal developmental 
toxicity studies in rats and rabbits, no developmental toxicity was 
seen at the Limit Dose (1,000 mg/kg/day) and in the two-generation 
reproduction study in rats toxicity in the offspring was manifested as 
decreased body weight at approximately 4,000 mg/kg/day (4 times the 
Limit Dose) The Limit Dose is generally regarded as the highest dose 
that could be tested in animal studies to maximize detection of 
potential adverse effects of a chemical (e.g, systemic toxicity,

[[Page 46725]]

carcinogenicity) without overloading the metabolic and/or physiological 
process of the animals. This upper limit dose (1,000 mg/kg/day) is 
equivalent to dietary concentrations of approximately 20,000 parts per 
million (ppm) in the diet of rats, 7,000 ppm in the diet of mice, and 
40,000 ppm in the diet of dogs
    With regard to the alleged need for additional data on the 
diflubenzuron metabolites, PCA and CPU, the Federal Register notice 
establishing the challenged tolerance specifically stated that ``there 
are no residue chemistry or toxicology data requirements that would 
preclude the establishment of a conditional registration and permanent 
tolerance for the combined residues of diflubenzuron, . . . and its 
metabolites 4-chloroaniline [PCA] and 4-chlorophenylurea [PCU] in/on 
pears at 0.05 ppm.'' (Id. at 7090, February 15, 2002). EPA's risk 
assessment for diflubenzuron noted no toxicology data needs and no 
other data needs other than validation of the analytical enforcement 
method (which has now been submitted, see Unit VII.C.5.d. of this 
document). (Ref. 57) The diflubenzuron registration on pears was 
conditional because validation of the analytical method was required. 
(Id.) Further, EPA considered and rejected NRDC's claims regarding the 
need for more toxicology data on the diflubenzuron metabolites in a 
tolerance rulemaking in September 2002. EPA noted that ``the rate of 
metabolism of diflubenzuron to PCA or CPU in plants, ruminants, and the 
environment is low and, thus, exposure to these metabolites will be 
minimal.'' (67 FR 59006, 59013, September 19, 2002). EPA relied upon 
the fact that when PCA and CPU were evaluated using a low dose linear 
model for cancer risk assessment - the most sensitive and conservative 
method for evaluating risk, whether from cancer or any other endpoint - 
these metabolites were found to pose a negligible risk. (Id.) EPA 
concluded that ``additional hazard testing for these metabolites will 
not lead to a more protective regulatory decision.'' (Id.) In these 
circumstances, EPA is confident that it has adequate reliable data to 
assign a factor different than the 10x default value to diflubenzuron, 
taking into account its PCA and CPU metabolites.
    b. Fluazinam. NRDC asserts that for fluazinam EPA is missing a 28-
day inhalation study, and a conditionally-required subchronic 
neurotoxicity battery. In response, EPA notes that a subchronic 
neurotoxicity study conducted with fluazinam has been received and 
reviewed. No treatment-related effects were observed in males or 
females at the highest dose tested in this study. (Ref. 58). EPA 
reserved the right to require this study to be redone because a toxic 
impurity of fluazinam was at a low level in the test material used in 
the study. EPA plans to reevaluate this issue once the DNT study is 
submitted and reviewed. (Id. at 39-40). Nonetheless, a clear NOAEL and 
LOAEL was identified for the impurity in other studies and EPA has 
``high confidence in the hazard endpoints and dose-response 
assessments'' for fluazinam. (Id. at 42-44). Regarding the data 
requirement for the 28-day inhalation study, this study is primarily 
required to assess worker risk and is not relevant to the exposure 
patterns for fluazinam examined in making the safety determination 
under FFDCA section 408. Accordingly, there is reliable data to assess 
the risks of fluazinam to infants and children despite the lack of a 
repeat subchronic neurotoxicity study and 28-day inhalation study.
    c. Furilazole. NRDC claims that EPA lacks a chronic dog study for 
furilazole. NRDC is correct that EPA does not have a chronic dog study 
for furilazole. EPA determined that because furilazole is an inert 
ingredient (safener) with a limited use that the chronic dog study was 
not needed given consideration of the rest of the toxicological data on 
furilazole. Nonetheless, to be protective, EPA applied an additional 
FQPA safety factor of 3X in deriving the chronic reference dose. The 
chronic reference dose was calculated by dividing the NOAEL of 0.26 mg/
kg/day in the 2-year rat study (based on increased absolute and 
relative liver and kidney weights in males at 5.05 mg/kg/day in rats) 
by both the standard safety/uncertainty factors (10X for inter-species 
variability and 10X for intra-species variability) and a 3X factor to 
account for the lack of the chronic dog study (i.e, 0.26 / 300X = 
0.0009 mg/kg/day). A factor of 3X was judged to be adequate because the 
results from the subchronic toxicity studies in rats and dogs show that 
the toxicity of furilazole is similar, both qualitatively and 
quantitatively, in both species. The liver was the target organ in both 
species. EPA found there to be no significant quantitative difference 
in the relative responses of dogs and rats to the hepatotoxic effects 
of furilazole in the subchronic studies. The NOAELs/LOAELs for both 
species were based on hepatotoxicity and are effectively the same value 
(5/15 and 7/34 mg/kg/day in dogs and rats, respectively). No target 
organs were identified in dogs that were not also identified in rats. 
(Ref. 59).
    d. 2,4-D. In an introductory section to its objections that was not 
linked to any specific objection, NRDC expressed concern that EPA has 
not adequately considered epidemiological studies linking 2,4-D with 
non-Hodgkin's lymphoma and canine malignant lymphoma which NRDC; (Ref. 
8 at 5), animal studies showing potential endocrine effects of 2,4-D; 
(Id. at 5-6), epidemiological data showing endocrine effects on adverse 
reproductive outcomes; (Id. at 6), and animal studies evidencing 2,4-
D's affect on the developing brain and nervous system. Reference to 
cancer studies does not appear relevant to objections concerning the 
children's safety factor. That safety factor is designed to provide 
additional protection for risks that have a safe threshold and not non-
threshold risks such as cancer. (21 U.S.C. 346a(b)(2)(C)). The 
epidemiological data cited by NRDC is either weak (few subjects, 
questionable controls, not performed by epidemiologists) or not 
specific to 2,4-D. (See Ref. 60). As to the animal studies on brain/
nervous system effects, NRDC cites a published article involving single 
dose studies (Ref. 8 at 7) that show nervous system effects at levels 
consistent with the levels at which the data before EPA evidenced 
effects. (Ref. 61). Accordingly, the cited data does not materially 
affect EPA's analysis.
    As part of the reregistration of 2,4-D, EPA is comprehensively 
reviewing these issues. This review has considered a considerable 
amount of new data that have become available since 2002. EPA's draft 
risk assessment for 2,4-D is available in EPA's electronic docket under 
the docket number OPP-2004-0167.
    4. Missing exposure data - general--a. Farm children exposure. NRDC 
argues that EPA is lacking data on exposure to farm children and thus 
may not remove the additional 10X safety factor. EPA disagrees. As 
discussed above and in the Imidacloprid Order, the epidemiological data 
cited by NRDC have not shown that there are significant exposures to 
farm children that occur as a result of living in close proximity to 
agricultural operations. EPA concluded that the evidence presented by 
NRDC is fragmentary, at best, as to whether pesticide exposure levels 
in homes of children living in agricultural areas are significantly 
different than levels in other homes and whether children living in 
agricultural areas have significantly different exposures than non-
agricultural children.
    NRDC also submitted two articles addressing pesticide spray drift 
and post-application volatilization drift of pesticides. EPA's analysis 
of exposure due to pesticide drift in Unit VII.B.2., however, showed 
that, as to the

[[Page 46726]]

pesticides involved here, there was little basis to find that drift 
could result in exposure posing a risk of concern. In fact, the recent 
data from the CTEPP study suggest that dietary exposure is generally 
the dominant exposure. What the CTEPP data show, therefore, is that 
NRDC, by asserting that the 10X safety factor should be retained to 
protect farm children from additional exposures they allegedly receive, 
is essentially asking that the dominant dietary exposure and other 
quantified non-dietary exposures be multiplied by 10 in estimating risk 
to protect against underestimating a potential non-dietary exposure 
that is likely to be, at most, a fraction of the dietary exposure 
alone. This is so because retaining an additional 10X safety factor 
decreases the estimated safe dose for humans by a factor of 10 making 
estimated exposure 10 times greater compared to the revised safe dose.
    After considering all of data bearing on exposure to the 13 
pesticides in NRDC's objections, including both pesticide-specific data 
and the more general data on children's exposure to pesticides, EPA 
concludes it has sufficient reliable exposure data on these pesticides 
to find that an additional 10X factor is not needed to protect the 
safety of infants and children. Specifically, the data reviewed in this 
Order, in the Imidacloprid Order, and in the individual tolerance 
actions give EPA confidence that it has not underestimated exposure as 
to these pesticides.
    In this regard, EPA would note that, for 8 of the 13 pesticides, it 
used its most conservative (health protective) method of estimating 
dietary exposure assuming that all food covered by the pesticide 
tolerances contained residues at the tolerance level. (66 FR at 66335, 
December 26, 2001 (halosulfuron); 67 FR at 3115, January, 23, 2002 
(mepiquat); 67 FR at 4917, February 1, 2002 (bifenazate); (67 FR at 
6424-6425, February 12, 2002 (zeta-cypermethrin); 66 FR at 33182-33183, 
June 21, 2001(isoxadifen-ethyl); 67 FR at 14653-54, March 27, 2002 
(acetamiprid); 67 FR at 15731, April 3, 2002 (furilazole); 67 FR at 
19116, April 18, 2002 (fenhexamid). (The reasons these assumptions 
produce such large overestimates is discussed in detail in Unit 
VII.D.5). Even for the other five pesticides, EPA's dietary exposure 
estimate was not highly refined. In none of these exposure estimates 
did EPA use a probabilistic risk assessment, the assessment technique 
that produces the most realistic picture of potential risk, or rely on 
food monitoring data to estimate residue levels. For all but one of the 
pesticides, EPA refined exposure estimates as to only some but not all 
food commodities. (See Unit VII.D.6; 66 FR at 66786, December 27, 2001 
(for pymetrozine, exposure assessment refined only as to chronic 
risks); 67 FR at 7087, February 15, 2002 (for diflubenzuron, exposure 
assessment refined only as to chronic risks and only as to some crops); 
67 FR at 10625, March 8, 2002 (for 2,4-D, exposure estimates refined 
for only citrus for acute risk and for only some crops for chronic 
risk); 64 FR at 2998, January 20, 1999 (for propiconazole, exposure 
estimates refined for only some crops for chronic risk; no refinement 
for acute risk); 67 FR at 19120, April 18, 2002, Ref. 46 at 6 (for 
fluazinam, exposure estimates refined for one of three crops for 
chronic risk; no refinement for acute risk)). Further, EPA's 
conservative method of modeling drinking water exposure was used, at 
least in part, for all of the pesticides. (See 69 FR at 30058-30065, 
May 26, 2004). For those pesticides that have residential uses, EPA 
relied upon its very conservative approach for estimating exposures 
that can occur around the home from such uses. (See 69 FR at 30055, May 
26, 2004). The conservativeness of EPA's exposure estimates is perhaps 
evidenced most dramatically by a comparison between exposure estimates 
for 2,4-D from a study relied upon by NRDC involving actual sampling of 
2,4-D residues in homes and the EPA's exposure estimates. The 2,4-D 
exposure estimate EPA prepared for this Order is almost two orders of 
magnitude greater than the estimates from the cited study and the 
exposure estimate for the challenged tolerance action is well over an 
order of magnitude greater. (See Unit VII.D.7.e).
    b. Lack of comprehensive drinking water (DW) monitoring data. NRDC 
contends that, because EPA used a model for calculating drinking water 
exposure, EPA does not have, as a definitional matter, ``reliable 
data'' for choosing a factor different than the 10X default value. 
Similar comments were made during the development of EPA's Children's 
Safety Policy. This issue was addressed at length in the response to 
the imidacloprid objections. (69 FR at 30058-30064, May 26, 2004). That 
response is incorporated herein and is summarized below.
    Although the availability of drinking water monitoring data has 
increased dramatically in the last several years, EPA still finds it 
necessary to rely for most pesticides upon various exposure models to 
estimate exposure levels in drinking water. These models are based on 
generic data regarding fate and transport of pesticides in the 
environment, and they operate by combining this generic data with 
pesticide-specific data on chemical properties to estimate exposure. 
EPA has primarily used its drinking water models to ``screen'' those 
pesticides that may pose unacceptable risks due to exposures in 
drinking water from pesticides not likely to result in such exposures. 
To accomplish this goal, the models are based on data from studies at 
sites that are highly vulnerable to runoff of pesticides to surface 
water or leaching of pesticides to ground water. If a pesticide fails 
this conservative (health-protective) screen, EPA would investigate 
whether the model is significantly overstating the residue levels that 
actually occur.
    EPA has developed models for estimating exposure in both surface 
water and ground water. EPA uses a two-tiered approach to modeling 
pesticide exposure in surface water. In the initial tier, EPA uses the 
FQPA Index Reservoir Screening Tool (FIRST) model. FIRST replaces the 
GENeric Estimated Environmental Concentrations (GENEEC) model that was 
used as the first tier screen by EPA from 1995-1999. If the first tier 
model suggests that pesticide levels in water may be unacceptably high, 
a more refined model is used as a second tier assessment. The second 
tier model is actually a combination of the models, Pesticide Root Zone 
Model (PRZM) and the Exposure Analysis Model System (EXAMS). For 
estimating pesticide residues in groundwater, EPA uses the Screening 
Concentration In Ground Water (SCI-GROW) model. Currently, EPA has no 
second tier groundwater model.
    Whether EPA assesses pesticide exposure in drinking water through 
monitoring data or modeling, EPA uses the higher of the two values from 
surface and ground water in assessing overall exposure to the 
pesticide. In most cases, pesticide residues in surface water are 
significantly higher than in ground water.
    In the Imidacloprid Order, EPA analyzed each of its water models 
extensively. Based on the results of design characteristics of the 
models, outside peer review of the models, validation of the models, 
and comparison between the models' predictions and extensive water 
monitoring data, EPA concluded that the models are based on reliable 
data and will produce estimates that are unlikely to underestimate 
exposure to pesticides in drinking water. (69 FR at 30065). 
Accordingly, EPA reaffirms its earlier conclusion that its drinking

[[Page 46727]]

water models provide a reliable basis for finding that exposure to 
pesticide residues in water are not underestimated.
    5. Missing exposure data - specific--a. Mepiquat. NRDC asserts that 
there is a data gap for side-by-side residue field trials for mepiquat. 
(Ref. 7 at 5). The tolerance in question covers both mepiquat chloride 
(N,N-dimethylpiperidinium chloride) and mepiquat pentaborate (N,N-
dimethylpiperidinium pentaborate) on cotton. A full toxicological and 
residue database was submitted on mepiquat chloride. As to mepiquat 
pentaborate, the petitioner relied on the mepiquat chloride data and a 
dissociation study demonstrating that ``pentaborate salt'' of mepiquat 
dissociates in water in an identical physical manner to the ``chloride 
salt'' of mepiquat. Based on this data, EPA concluded that the proposed 
foliar application of mepiquat pentaborate to cotton is not expected to 
result in residues of mepiquat per se greater than those resulting from 
the application of mepiquat chloride. (67 FR at 3114, January 23, 
2002). The required residue studies are confirmatory in nature. (Ref. 
62). Accordingly, EPA concludes it has reliable data on mepiquat 
residues in cotton.
    b. Bifenazate-assessment of drinking water exposure to bifenazate 
degradates. NRDC claims that EPA has failed to complete ``an assessment 
of drinking water exposure to bifenazate degradates.'' (Ref. 7 at 5). 
As the Federal Register notice establishing the contested tolerances 
for bifenazate reveals, however, EPA scientists considered 
environmental persistence of bifenazate and its two major degradates, 
D3598 (diazinecarboxylic acid, 2-(4-methoxy-[1,1'-biphenyl]-3-yl), 1-
methylethylester) and D1989 (4-methylethylester). Aqueous photolysis 
and soil metabolism studies demonstrated that the parent bifenazate and 
the D3598 degradate ``quickly metabolize under aerobic soil 
conditions.'' (67 FR at 4918, February 1, 2002). Noting the lack of 
persistence of these two compounds and the absence of any acute dietary 
endpoint, EPA focused its drinking water exposure assessment for 
bifenazate on the degradate that had a possibility of being present in 
drinking water. (Id.). Accordingly, NRDC is incorrect to assert that 
potential exposure to bifenazate degradates in drinking water was not 
assessed by EPA and hence, NRDC's assertion does not call into question 
EPA's decision concerning the children's safety factor for bifenazate.
    c. Zeta-cypermethrin--assessment of drinking water exposure zeta-
cypermethrin degradates. NRDC claims that EPA has ``failed to address 
drinking water exposure to zeta-cypermethrin degradates.'' (Ref. 7 at 
5). To the contrary, EPA has determined that DCVA need not be included 
in drinking water assessments for zeta-cypermethrin or other 
pyrethroids.
    DCVA is the hydrolysis product of several pyrethroids (permethrin, 
cypermethrin, zeta-cypermethrin, cyfluthrin). It is the acid portion of 
these insecticides (which are esters) and its full chemical name is 3-
(2,2-dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid. Although 
it is significantly more mobile than the parent pyrethroids, EPA has 
not included it in drinking water assessments for the following 
reasons.
    (1) Based on its structure (i.e., lacking the ester function in the 
parent insecticides), it would be devoid of the neurotoxic properties 
of the parent and thus, it would not be of significant concern with 
respect to the neurotoxicity endpoints on which the dietary risks of 
the pyrethroids are assessed.
    (2) Mutagenicity and acute toxicity data have been provided for 
DCVA. The submitted salmonella reverse mutation assay (Ames assay) 
conducted with DCVA indicated that the compound was negative in the 
presence and absence of metabolic activation in all five tester 
strains. The submitted acute oral toxicity study in rats conducted with 
DCVA concluded that the acute oral LD50 is 1,609 mg/kg for 
males and 1,192 mg/kg for females. These values are higher than those 
for the parent cypermethrin compounds (cypermethrin: LD50 = 
247 mg/kg for males, LD50 = 309 mg/kg for females; zeta-
cypermethrin: LD50 = 134.4 mg/kg for males, LD50 
= 86.0 mg/kg for females).
    (3) Although DCVA does contain the electrophilic dichlorovinyl 
group which raises a potential concern with carcinogenicity, it is not 
likely this compound is a carcinogen. The latter conclusion is based on 
the different toxicity profiles of the parent pyrethroids which produce 
DCVA in significant quantities. Cyfluthrin, permethrin, and zeta-
cypermethrin/cypermethrin are all extensively metabolized by cleavage 
of the ester linkages with formation of DCVA as shown by the amount and 
nature of the radioactivity appearing in urine of rats. In the case of 
cypermethrin, similar metabolism and pharmacokinetics are observed in 
mice and dogs. As a result, toxicological testing of the parent 
compounds results in testing of DCVA at approximately one-third of the 
dose of the parent on a weight basis. In spite of that fact, the parent 
compounds have markedly different profiles of toxicity. For example, 
using an earlier cancer classification system, cyfluthrin is a category 
E carcinogen (i.e., no evidence of carcinogenicity), zeta-cypermethrin 
is category C (i.e., possible human carcinogen), and permethrin is 
category C(q) (i.e., possible human carcinogen with sufficient evidence 
to quantify cancer risk). On this basis, the common metabolite DCVA is 
not likely to be carcinogenic.
    (4) Even though DCVA is more mobile than its parent compounds, it 
is expected to reach groundwater in very low levels. Exposure is 
further mitigated by the DCVA's high polarity and the likelihood of it 
being readily excreted from the body due to the presence of the 
carboxylic acid group.(Refs. 63, 64 and 65)
    d. Diflubenzuron--Residue data on two metabolites. NRDC states that 
there is a data gap for residue chemistry data on two diflubenzuron 
metabolites. (Ref. 7 at 6). As discussed in Unit VII.C.3.a. of this 
document, the only missing data at the time of the tolerance action was 
Agency validation of the analytical enforcement method. The Federal 
Register notice does note, however, that the analytical enforcement 
methods have been successfully validated independently, (67 FR at 7090; 
Ref. 66). The Agency validation has now been successfully completed. 
(Ref. 67). In any event, a second validation is conducted by EPA not 
for the purposes of refining its risk assessment but to insure that the 
procedures for conducting enforcement monitoring are adequately 
described so that accurate and reproducible results can be produced by 
enforcement personnel. Accordingly, this objection is without merit.
    e. Acetamiprid--oral exposure from residential uses. NRDC asserts 
that EPA is missing data bearing on oral exposure to acetamiprid from 
residential uses of the pesticide. (Ref. 9 at 6). The Federal Register 
notice on the contested acetamiprid tolerance notes that ``incidental 
oral exposure is an insignificant pathway of exposure'' for 
acetamiprid. (67 FR at 14657, March 22, 2004). Little or no incidental 
oral exposure is expected since acetamiprid's residential uses are 
limited to ornamentals, flowers, vegetable gardens, and fruit trees. 
Incidental oral exposure to pesticides can occur when young children 
engage in ``mouthing'' behavior (i.e. repeatedly placing their hands or 
other objects in their mouth) in a location where a pesticide is 
present. EPA assumes that incidental oral exposure to a pesticide

[[Page 46728]]

may occur when a pesticide is used to treat a home lawn because young 
children frequently play on home lawns. EPA, however, considers it 
unlikely that young children would spend an extended time in flower, 
vegetable, or ornamental gardens, and thus treatment of such gardens 
with a pesticide is not likely to lead to a significant exposure to 
children by the incidental oral route.
    EPA would note that NRDC was mistaken in its objections when it 
claimed that EPA estimated the MOE for short- and intermediate-term 
residential exposure to be 189 for adults and 239 for children aged 10-
12. (Ref. 9 at 9-10). As the Federal Register notice made clear the 
MOEs for these two groups are 1,858 and approximately 3,000, 
respectively, for pesticide exposures in food and 18,000 and 23,000, 
respectively for non-dietary pesticide exposures. (67 FR at 14657).
    6. Missing risk assessments. As to several of the pesticides, NRDC 
has claimed that there is a data gap for a specific type of risk 
assessment (e.g., short-term residential risk assessment) and that 
therefore the full 10X children's safety factor must be retained. There 
are two problems with this argument. First, a risk assessment is not 
data or information that is required to be submitted to EPA but rather 
an analysis of the data and information that is submitted. Thus, NRDC 
has mislabeled these allegedly missing risk assessments by calling them 
``data gaps.''
    Second, and more important, NRDC appears to have misread the 
relevant Federal Register notices in reaching the conclusion that 
various risk assessments are missing. In some cases, risk assessments 
that are claimed to be missing were performed and were described in the 
pertinent Federal Register notice. In other cases, NRDC may have been 
confused by language in Federal Register notices that states a certain 
risk assessment was not conducted or performed. In conducting the 
safety evaluation required by section 408, EPA performs various risk 
assessments depending on the types of risks posed by a pesticide and 
the varieties of exposure routes related to its use. The number and 
scope of risk assessments may vary considerably from pesticide to 
pesticide. Language that a risk assessment was not required or 
performed has been frequently used by EPA to indicate circumstances 
where a quantitative risk assessment was not needed either because the 
pesticide did not present a particular hazard (e.g., a quantitative 
acute risk assessment is not performed for a pesticide not judged to 
pose a risk due to a one-day or single exposure) or there was no 
exposure (e.g., a residential risk assessment is not performed when the 
pesticide does not have residential uses). As explained below, in each 
instance where NRDC objected to a ``missing'' risk assessment, EPA had 
either performed the risk assessment or determined that such risk 
assessment was not needed.
    a. Halosulfuron-methyl. NRDC claims that EPA, in evaluating 
halosulfuron, failed to conduct a cancer risk assessment, and short-
term and intermediate-term residential risk assessments for children 
and for adults. (Ref. 6 at 5). As an initial matter, EPA questions the 
relevance of this argument to the children's safety factor given the 
fact that EPA treats cancer as a non-threshold effect unless data show 
otherwise, and the children's safety factor only applies to threshold 
effects. (See 21 U.S.C. 346a(b)(2)(C)). NRDC has not contended that 
halosulfuron-methyl is a non-threshold carcinogen. In any event, based 
on its qualitative assessment of the data bearing on cancer, EPA 
concluded that halosulfuron-methyl was not likely to be a human 
carcinogen, and therefore did not conduct a quantitative risk 
assessment. (66 FR at 66338, Dec. 26, 2001). As to the missing short-
term and intermediate-term risk assessments, those risk assessments 
were performed and summarized on pages 66337 and 66338 of the Federal 
Register notice to which NRDC filed objections. (Id. at 66337-66338).
    b. Bifenazate. NRDC asserts there is a data gap for a developmental 
toxicity assessment for bifenazate. (Ref. 7 at 5). NRDC appears to be 
referring to language in the Federal Register notice establishing the 
contested bifenazate tolerances that states that ``a clear assessment 
of developmental toxicity was not possible'' in the range-finding study 
used to choose dose levels for the main developmental toxicity study in 
rabbits. (67 FR at 4915). The statement ``a clear assessment of 
developmental toxicity was not possible'' in the range finding study is 
an error in the Data Evaluation Record (Ref. 68) since a detailed 
assessment of developmental toxicity is not performed in the range 
finding study. The objective of this study is to demonstrate definite 
maternal toxicity and to guide selection of dose levels for the main 
study regarding development toxicity in rabbits. This main study was 
submitted and considered in conducting the risk assessment for 
bifenazate. (67 FR at 4914). The study showed no developmental toxicity 
at 200 mg/kg/day (highest dose tested). The doses tested in this study 
was judged to be adequate since abortions were seen at >=250 mg/kg/day 
and decreases in body weight seen at doses >=500 mg/kg/day in the 
range-finding study. This study provided a clear assessment of 
developmental toxicity in rabbits for bifenazate.
    c. Isoxadifen-ethyl. NRDC claims that short-term and intermediate-
term residential risk assessments are missing for isoxadifen-ethyl. 
(Ref. 9 at 6). As the relevant Federal Register notice notes, however, 
EPA determined these residential risk assessments were not necessary 
because isoxadifen-ethyl is not approved for any residential uses. (67 
FR at 33185).
    d. Propiconazole. NRDC argues that there is a data gap for all 
residential risk assessments for propiconazole. (Ref. 9 at 6). For 
propiconazole, EPA did quantitatively assess the short-term and 
intermediate-term residential risks resulting from the treatment of 
wood with propiconazole. (64 FR at 2999, January 20, 1999). EPA 
determined it was unnecessary to assess quantitatively short-term and 
intermediate-term residential risks connected with the turf use of 
propiconazole because of the unlikelihood of exposure. (Id.). EPA 
considered exposure to be minimal due to a combination of a number of 
factors: (1) Propiconazole is infrequently used on lawns; and (2) even 
when used, it is generally applied by lawn care operators rather than 
homeowners.
    e. Fenhexamid. NRDC claims that short-term and intermediate-term 
residential risk assessments are missing for fenhexamid. (Ref. 9 at 6). 
As the relevant Federal Register notice notes, however, EPA determined 
these residential risk assessments were not necessary because 
fenhexamid is not approved for any residential uses. (67 FR at 19118, 
April 18, 2002).
    f. Fluazinam. NRDC argues there is a data gap for a cancer risk 
assessment for fluazinam. (Ref. 9 at 6). As with its objection 
concerning the halosulfuron-methyl cancer risk assessment, EPA 
questions the relevance of this argument to the children's safety 
factor decision. NRDC has not contended that fluazinam is a non-
threshold carcinogen. In any event, EPA did qualitatively assess the 
cancer potential of fluazinam and found that the data showed, at most, 
suggestive evidence of carcinogenicity but that the evidence was not 
strong enough to warrant quantifying this risk. (67 at 19128, April 18, 
2002). This decision was based on the fact that there was equivocal/
some evidence of carcinogenicity in one species and one sex. Thyroid 
tumors were seen in male rats, but not in female rats, while liver 
tumors were seen in male mice but not

[[Page 46729]]

in female mice. In addition, fluazinam was negative in mutagenicity 
assays. (Ref. 69).
    g. 2,4-D. NRDC claims that short-term and intermediate-term 
residential assessments have not been completed for 2,4-D. (Ref. 8 at 
8). This claim is not supported by the record. The Federal Register 
notice associated with the challenged tolerances summarizes EPA's 
short-term residential risk quantitative assessment, (67 FR at 10629, 
March 8, 2002), and explains why no intermediate-term exposure, and 
hence no intermediate-term risk, is expected, (Id. at 10627).
    7. Conclusion on children's safety factor objections. After 
examining each of NRDC's objections, EPA has found no basis in the 
objections to revise its conclusions regarding the children's safety 
factor as to the 13 pesticides.

C. LOAEL/NOAEL

    NRDC argues that EPA cannot legally make the reasonable certainty 
of no harm finding for pymetrozine, mepiquat, zeta-cypermethrin, and 
fluazinam because EPA has relied on a LOAEL in assessing the safe level 
of exposure to the pesticide. NRDC claims EPA ``cannot lawfully 
establish tolerances in the absence of a no-observed-effect-level 
(NOEL).'' (Ref. 7 at 18). Implicit in this argument is that EPA cannot 
use a no-observed-adverse-effect-level (NOAEL) in making a safety 
finding. In later objections, NRDC confirmed that in fact it was 
contending that section 408's safety standard does not permit EPA to 
rely on a NOAEL in concluding a tolerance is safe. Rather, according to 
NRDC, EPA may only make a safety finding for a pesticide where EPA has 
determined the dose in animals at which no effects, adverse or 
otherwise, are elicited from exposure to the pesticide. (Ref. 7 at 17-
18). Below EPA identifies the flaws in NRDC's generic argument 
concerning LOAELs and NOAELs and addresses the pesticide-specific 
concerns NRDC raises with regard to use of a LOAEL as to pymetrozine, 
zeta-cypermethrin, and fluazinam.
    1. Generic legal argument. EPA believes that it can make a 
reasonable certainty of no harm finding based on a LOAEL from an animal 
study (where no NOAEL or NOEL was found) in appropriate circumstances. 
Whether or not a reasonable certainty of no harm finding can be made 
when only a LOAEL is identified in a study depends on whether EPA has 
sufficient toxicological evidence to estimate with confidence a 
projected NOAEL that is unlikely to be higher than the actual NOAEL. 
Typically, when a LOAEL but not a NOAEL has been identified by a study, 
EPA will, when the data support it, project a NOAEL for that study by 
dividing the LOAEL by a safety factor.
    There is nothing in the statutory safety standard explicitly 
addressing the use of NOELs, NOAELs, or LOAELs. Moreover, nothing in 
the phrase ``reasonable certainty of no harm'' legally precludes use of 
NOAELs or LOAELs to make a finding regarding the likelihood that harm 
will occur at a given dose. Whether a NOAEL or LOAEL provides a 
sufficient basis for a reasonable certainty of no harm finding is a 
question of scientific fact. EPA fully responded to the arguments 
raised by NRDC in the Imidacloprid Order, (69 FR at 30066-30067, May 
26, 2004), and incorporates that response herein.
    2. Objections pertaining to specific pesticides--a. Pymetrozine. 
NRDC asserts that EPA unlawfully relied upon a LOAEL in assessing both 
short-term risk and acute risks to pymetrozine. (Ref. 6 at 9). NRDC is 
correct that EPA used the LOAEL from an acute neurotoxicity study with 
pymetrozine to assess both the acute dietary risk and short-term 
residential risk for the general population. (Acute risk to the 
developing fetus, however, was based on the developmental study in the 
rabbit which had a NOAEL.) (Ref. 70). To ensure that there would be a 
reasonable certainty of no harm, EPA retained two additional 3X safety 
factors in assessing acute risk to the infants and children. (Id. at 
18). This decision was based both on the lack of a LOAEL from the acute 
neurotoxicity study and the absence of a required DNT study. The 
protectiveness of this approach is demonstrated by the fact that the 
LOAEL from the acute neurotoxicity study used for conducting the safety 
assessment for acute risk faced by the general population is only 
higher by a factor of 2 than the NOAEL from the subchronic 
neurotoxicity study. Retaining what is essentially a 10X safety factor 
results in a projected acute NOAEL five times lower than the NOAEL 
found in a subchronic study measuring the same endpoint. Thus, this 
projected NOAEL is more conservative for a single exposure than the 
measured result in the repeated exposure study (i.e., 13 weeks).
    Syngenta, the registrant for pymetrozine, defends EPA's reliance on 
a LOAEL here noting that the effects observed at the LOAEL ``were 
reversible and not of severe magnitude (for example, body temperature 
was decreased at the LOEL, but only by about 2 percent compared to 
controls).'' (Ref. 18 at 5). EPA agrees that the severity of the effect 
at the LOAEL should be considered in the weight of the evidence 
regarding a safety determination and relied on the lack of severity and 
reversibility in its determination on pymetrozine. (Ref. 71).
    b. Mepiquat. NRDC claims that for mepiquat EPA ``measured 
reproductive toxicity only on the basis of a LOAEL.'' (Ref. 7 at 18). 
NRDC was mislead, however, by the Federal Register notice's description 
of the rat reproduction study which states: ``The study did not 
establish a reproductive NOAEL; however, the systemic NOAEL of 1,500 
ppm would also be regarded as the reproductive NOAEL.'' (65 FR at 1792, 
January 12, 2000). This was an error by EPA in preparing the Federal 
Register notice. In fact, in the two-generation reproduction study, the 
NOAEL for reproductive toxicity was 5,000 ppm (highest dose tested); a 
LOAEL was not established. (Ref. 72).
    c. Zeta-cypermethrin. NRDC argues that EPA relied upon a LOAEL from 
a zeta-cypermethrin developmental toxicity study. (Ref. 7 at 18). NRDC, 
however, is mistaken. In the four developmental studies conducted with 
cypermethrin and zeta-cypermethrin in rats and rabbits, no 
developmental effects were observed at the highest dose tested. (Ref. 
73). Maternal toxicity was seen in all four studies. NRDC may have been 
mislead by an error in one of the data tables in the Federal Register 
that lists the NOAEL for one of the four developmental studies as <35 
mg/kg/day.'' (66 FR at 47981, September 17, 2001 (Table 2)). The table 
should have read >= 35 mg/kg/day. (Id.)
    d. Fluazinam. NRDC claims that for fluazinam EPA relied upon a 
LOAEL in assessing dermal toxicity and that only a LOAEL was achieved 
in dietary studies in mice and rats. (Ref. 9 at 18). NRDC is correct 
that a dermal NOAEL (as distinguished from a systemic NOAEL) was not 
found in the 21-day dermal toxicity study. (67 FR at 19121, April 18, 
2002). Nonetheless, EPA did not rely on the LOAEL from this study in 
setting the fluazinam tolerances because there are no residential uses 
for fluazinam and dermal toxicity is only relevant to exposure 
occurring in the residential setting. Moreover, the data were 
sufficient to set a systemic NOAEL from dermal exposure, as opposed to 
a NOAEL for dermal effects. (Ref. 58 at 14). A systemic NOAEL is the 
information needed to conduct an aggregate risk assessment. EPA had 
adequate data on oral toxicity for evaluating dietary exposure.
    As to not achieving a NOAEL in dietary studies with mice and rats, 
NRDC appears to be referring to a 4-week dietary range-finding study in

[[Page 46730]]

mice and a special 90-day liver study in rats. The lack of a NOAEL in 
these studies is irrelevant to the fluazinam risk assessment. The lack 
of a NOAEL in the mouse study is not a concern because it is a range 
finding study (i.e. a preliminary study used to gauge dosing for 
another study) and the LOAEL (555 mg/kg/day) is approximately 50-fold 
higher than the LOAEL (10.7 mg/kg/day) and the NOAEL (1.1 mg/kg/day) in 
the chronic mouse study which was used establishing the chronic RfD. 
(67 at 19121, April 18, 2002 (Table 1)). The 90-day study in rats was a 
special non-guideline study (not requested by EPA) that tested one 
relatively high dose level (500 ppm) to evaluate the hepatotoxic 
effects of fluazinam and determine their reversibility. It was not 
considered for the purpose of determining a NOAEL and a RfD. Because 
the study only resulted in the modest liver changes of questionable 
toxicologic significance it was of marginal value. (Refs. 74 and 75) 
Neither of these studies were used for overall risk assessments (Ref. 
46).
    e. Isoxadifen-ethyl, acetamiprid, propiconazole, furilazole, and 
fenhexamid. NRDC has lodged a blanket legal objection to the use of 
NOAELs in assessing the risk to isoxadifen-ethyl, acetamiprid, 
propiconazole, furilazole, and fenhexamid. (Ref. 9 at 18). NRDC has 
offered no factual evidence or argument as to why reliance on these 
specific NOAELs invalidates EPA's safety determination. Accordingly, 
EPA denies this objection for the reasons given above and in the 
Imidacloprid Order, (69 FR at 30066-30067, May 26, 2004), for rejecting 
the argument that EPA is barred, as a matter of law, from using NOAELs 
in assessing the safety of pesticide residues.

D. Aggregate Exposure

    1. Worker exposure. EPA has interpreted ``aggregate exposure'' to 
pesticide residues not to extend to pesticide exposure occurring at the 
workplace based on the language in section 408(b)(2)(D) explaining what 
exposures are included in the term ``aggregate exposure:''

    [T]he Administrator shall consider, among other relevant factors 
- . . . available information concerning the aggregate exposure 
levels of consumers (and major identifiable subgroups of consumers) 
to the pesticide chemical residue and to other related substances, 
including the dietary exposure under the tolerance and all other 
tolerances in effect for the pesticide chemical residue, and 
exposure from other non-occupational sources . . . .

This language quite plainly directs EPA to limit consideration of 
aggregate exposure of pesticide residues and other related substances 
to those exposures arising from non-occupational sources. NRDC's claim 
that EPA erred by not considering worker risks in making tolerance 
decisions under section 408 runs afoul of Congress' explicit mandate 
that such exposures not be included. Although there is some ambiguity 
as to precisely how the factors listed in section 408(b)(2)(D) relate 
to the safety finding described in section 408(b)(2)(A)(ii), for the 
reasons set forth in the Imidacloprid Order, (69 FR at 30067-30068, May 
26, 2004), NRDC's interpretation of the statutory language is 
unreasonable.
    2. Classification of farm children as a major identifiable 
population subgroup. NRDC points out that FFDCA section 408 directs EPA 
to consider not just the general population in assessing aggregate 
exposure but also ``major identifiable subgroups of consumers.'' (21 
U.S.C. 346a(b)(2)(D)(vi)). In this regard, NRDC argues that children 
living in agricultural communities should be treated as such a major 
identifiable subgroup. These children are an identifiable subgroup, 
according to NRDC, because of the allegedly heightened exposure to 
pesticides that they receive due to their proximity to farm operations 
and farm land and, for some, due to their contact with parents involved 
in agriculture. (Ref. 9 at 11-12). NRDC claims these children comprise 
a ``major'' subgroup citing statistics showing that ``320,000 children 
under the age of six live on farms in the United States[], . . . many 
hundreds of thousands of children play or attend schools on or near 
agricultural land, . . . [and] [t]he nation's 2.5 million farm workers 
have approximately one million children living in the United States.'' 
(Id.)
    Whether or not EPA attaches the label ``major identifiable 
subgroup'' to farm children, EPA's risk assessment approach to 
children, including the major identifiable subgroups of children used 
in its risk assessments, adequately takes into account any pesticide 
exposures to children - whether as a result of living close to 
agricultural areas or otherwise. For some time, EPA has treated infants 
and children grouped by ages (e.g., infants younger than 1 year, 
children 1 - 2 years) as major identifiable subgroups. These age 
groupings have been chosen to reflect different eating patterns of the 
age groups. In evaluating exposure to these or any other subgroup, 
however, EPA considers the range of exposures across the subgroup not 
just as a result of pesticide residues in food but from all non-
occupational exposures. If a significant number of any of the 
population subgroups of children have higher exposures due to a non-
food source (e.g., residential uses of a pesticide, proximity to 
agricultural areas), EPA believes that that exposure is appropriate to 
consider in evaluating the range of exposures for the subgroup. The 
fact that the children in the subgroup receiving the higher exposures 
are not themselves labeled a major identifiable subgroup in no way 
lessens EPA's consideration of their exposures. Further, EPA questions 
whether NRDC has properly characterized farm children as a major 
identifiable subgroup in that it is not at all clear that the members 
of this group are readily identifiable nor does the evidence support 
that this group consistently receives higher pesticide exposures. These 
issues are discussed in greater depth in the Imidacloprid Order and 
that discussion is incorporated herein. (69 FR at 30068-30069, May 26, 
2004).
    3. Adequacy of EPA's assessment of the aggregate exposure of 
children, including children in agricultural areas. EPA believes that 
it has adequately assessed the aggregate exposure of children to the 13 
pesticides (including both farm children and non-farm children), 
through its assessment of exposure through food, drinking water and 
residential use pathways. In support of its objection to this 
assessment, NRDC cites numerous studies for the proposition that other 
pathways (e.g., track-in) increase farm children's exposures, and it 
also cites information purportedly suggesting that volatilization and 
spray drift lead to higher exposures among farm children. For reasons 
discussed above (see Unit VII.B. and C.), and in the Imidacloprid 
Order, however, EPA does not believe that the epidemiological data 
relied upon demonstrate that the pathways asserted, to the extent they 
exist, lead to farm children experiencing pesticide exposure levels 
significantly higher than those experienced by other children. Rather, 
these studies are largely inconclusive, and to the extent they show 
anything, tend to suggest that farm children and non-farm children 
generally receive similar levels of exposure.
    Further, EPA's evaluation of the potential additional exposure to 
the 13 pesticides challenged in these objections from spray or 
volatilization drift showed little likelihood of significant exposure. 
In any event, an overly conservative (health-protective) estimate of 
overall drift, food, water, and residential exposures shows no safety 
concerns for any of these pesticides.

[[Page 46731]]

    4. Residential exposure as a result of use requiring a tolerance. 
NRDC also argues that EPA has erred in not assuming that additional 
residential exposure occurs each time an additional agricultural use is 
added. The reasons explained above as to why any additional exposure to 
children as a result of their proximity to farming operations is 
expected to be insignificant as regards the 13 pesticides apply with 
equal or more force as to this contention.
    5. Anticipated residues/exposures due to purchase of food at farm 
stands. NRDC claims that EPA has underestimated aggregate exposure for 
several of the pesticides because EPA used ``anticipated residues'' for 
estimating exposure rather than assuming residues would be at the 
tolerance level. NRDC argues that ``EPA must ensure that the legal 
level of pesticide chemical residue - the established tolerance levels 
- are themselves safe.'' (Ref. 9 at 20). Additionally, NRDC asserts 
that using ``anticipated residues'' does not take into account the 
``significant number of consumers who purchase produce at farmers 
markets, farm stands, and `pick-your-own' farming operations.'' (Ref. 9 
at 19). NRDC cites information from the National Association of 
Farmers' Market Nutrition Programs indicating that 1.9 million people 
purchase food from farm stands.
    NRDC is wrong in its assertion that EPA must assume all residues in 
food are at tolerance levels in assessing the safety of tolerances. The 
statute is quite clear that EPA may consider data on anticipated or 
actual pesticide residue levels in establishing tolerances. (21 U.S.C. 
346a(b)(2)(E)). This statutory provision essentially codifies EPA 
practice developed and implemented over the last 20 years.
    EPA's approach to estimating exposure for tolerance risk 
assessments, at least as far back as the late 1980's, is to first make 
a worst case assessment of the exposure, and then, only if this worst 
case exposure assessment indicates that there might be risk concerns 
would EPA undertake a more sophisticated assessment using more 
realistic data such as data on ``anticipated residues.'' (See Ref. 76). 
Worst case exposure was designated by EPA as the Theoretical Maximum 
Residue Level (TMRC) and was calculated by assuming all foods covered 
by tolerances had residues at the tolerance level. (See, e.g., 59 FR 
54818, 54820, November 2, 1994; (metalaxyl tolerance); 50 FR 26683, 
June 27, 1985; (chlorpyrifos-methyl tolerance)). When such an 
assessment shows no risks of concern, EPA's resources are conserved 
because a more complex risk assessment is avoided and regulated parties 
are spared the cost of any additional studies that may be needed.
    If, however, a first tier assessment suggests there could be a risk 
of concern, EPA then attempts to refine its exposure assumptions to 
yield a more realistic picture of residue values through use of data on 
the percent of the crop actually treated with the pesticide and data on 
the level of residues that may be present on the treated crop. These 
latter data are used to estimate what has been traditionally referred 
to by EPA as ``anticipated residues.'' (Ref. 76 at 1; see, e.g., 54 FR 
33044, 33045, August 11, 1989) (iprodione tolerance)).
    Use of percent crop treated data and anticipated residue 
information is appropriate because EPA's worst case assumptions of 100 
percent treatment and residues at tolerance value significantly 
overstate residue values. There are several reasons this is true. 
First, all growers of a particular crop would rarely choose to apply 
the same pesticide to that crop; generally, the proportion of the crop 
treated with a particular pesticide is significantly below 100 percent. 
For example, the 2001 USDA Agricultural Chemical Usage survey notes 14 
insecticides used on tomatoes with percent crop treated values ranging 
from 2 to 26 percent, including 9 insecticides used on less than 10 
percent of the crop. In another example, the survey notes 39 herbicides 
used on corn with percent crop treated values ranging from less than 1 
to 68 percent, including 32 herbicides used on less than 10 percent of 
the crop. (Refs. 77 and 78). Obviously, if a portion of a crop is not 
treated, food from that portion of the crop will not contain residues.
    Second, for that portion of the crop that is treated, residues on 
most treated commodities are likely to be significantly lower than the 
tolerance value, even when the pesticide is applied in the manner and 
amount permitted by the label that is likely to yield the highest 
possible residue [hereinafter referred to as a ``maximum residue 
application'']. EPA's general practice is to set tolerance values just 
slightly above the highest value observed in crop field trials 
conducted using maximum residue applications. For example, based on the 
hypothetical pesticide residue data set in Figure 1, EPA would set the 
tolerance value at 4 ppm or slightly higher. As Figure 1 illustrates, 
there may be some commodities from a treated crop that approach the 
tolerance value where the maximum residue applications are followed, 
but most commodities generally fall significantly below. In fact, EPA's 
experience is that crop field trial data generally does not sort out 
into a normal, bell-shaped distribution; rather, the distribution when 
plotted based on frequency/probability (Y axis) and level of residues 
(X axis) is generally ``log-normal'' or ``right-skewed'' - that is, 
there is a clumping of values close to, or on, the Y axis (i.e. 
approaching non-detectable residues) with a few higher values out 
farther on the X axis (i.e. approaching the tolerance value) resulting 
in a long ``tail'' stretching out to the right. (Ref. 4 at 12, Ref. 79 
and Ref. 80 at 10). Figure 1 presents a hypothetical example of how 
residue data generally fall in a right-skewed curve.

[[Page 46732]]

[GRAPHIC] [TIFF OMITTED] TR10AU05.066

    Third, if less than the maximum residue application is followed 
(e.g., lower than the maximum amount applied, applications are not as 
frequent as allowed, the pre-harvest interval after the last 
application exceeds thelegal minimum), residues will be even lower than 
measured by crop field trials using maximum residue applications. 
Essentially, the entire distribution curve illustrated in Figure 1 
shifts to the left. Finally, residue levels measured in the field do 
not take into account the lowering of residue values that frequently 
occurs as a result of degradation over time and through food processing 
and cooking. (Ref. 4 at 14, and Ref. 79).
    EPA uses several techniques to refine residue value estimates from 
worst case levels to more realistic levels. (See Ref. 1 at 10-12). 
First, where appropriate, EPA may take into account all the residue 
values reported in the crop field trials, either through use of an 
average or individually. Second, EPA may consider data showing what 
portion of the crop is not treated with the pesticide. Third, data may 
be produced showing pesticide degradation and decline over time, and 
the effect of commercial and consumer food handling and processing 
practices. Finally, EPA may consult monitoring data gathered by FDA, 
the US Department of Agriculture, or pesticide registrants, on 
pesticide levels in food at points in the food distribution chain 
removed from the farm, including retail food establishments. EPA's 
experience has been that, even without the use of probabilistic risk 
assessment techniques discussed below, reliance on these refinements, 
and particularly use of food monitoring data, reduces exposure and risk 
estimates by over a order of magnitude. (See 55 FR 20416, 20422, May 
16, 1990) (``Earlier registrant residue monitoring studies and FDA and 
State monitoring studies indicate that [EBDC] residues may be 1 to 2 
orders of magnitude lower than the Agency's current residue 
estimates.''); 54 FR 22558, 22565, May 24, 1989) (using a residue value 
of 1 ppm from market basket survey to assess risk of daminozide on 
apples; tolerance value was 20 ppm, 40 CFR 180.246(b)(1989)); (Ref. 
79).
    In the FQPA, Congress essentially adopted EPA's approach, including 
EPA's terminology with the slight change that it labeled one category 
of anticipated residue data, monitoring results, as ``actual residue 
data.'' (See 21 U.S.C. 346a(b)(2)(E)(1) (designating that data on 
actual residues measured in food ``includ[es] reside data collected by 
the Food and Drug Administration'')).
    That Congress was codifying existing practice is confirmed by the 
legislative history of the FQPA. EPA's use of anticipated residue data 
had been questioned by some and several bills were introduced that 
essentially prohibited EPA from using its traditional risk assessment 
approach. For example, H.R. 1725, a bill introduced in the 101st 
Congress, directed that ``in calculating dietary exposure to the 
pesticide chemical residue in or on the raw agricultural commodity or 
processed food for which the tolerance is proposed or is in effect, the 
Administrator shall consider the level of exposure to be the amount of 
exposure that would occur if all the commodities and food for which the 
pesticide chemical residue has a tolerance have amounts of pesticide 
chemical residues equal to their respective tolerances. . . .'' (H.R. 
1725, 101st Cong. section 4 (establishing a new section 
408(b)(2)(C)(ii)) (1989) (an exception to this bar on the use of 
anticipated residue data was allowed if a second tolerance was 
established to insure residue levels did not exceed the levels used to 
calculate dietary exposure); see S. 722, 101st Cong. section 4 
(establishing a new section 408(b)(2)(C)(ii)) (1989) (same)). A similar 
approach was taken in the Clinton Administration proposal in 1994. 
(H.R. 4362, 103d Cong. section 3 (establishing a new section 
408(b)(2)(B)(i)) (the Administrator shall assume that the food bears or 
contains residues of the pesticide chemical equal to the level 
established by the tolerance set at the point closest to the time the 
food is purchased); see also S. 2084, 103d Cong., section 3 
(establishing a new section 408(b)(2)(B)(i)) (same)). However, this 
approach was not included in the bill passed in 1996 as the FQPA. 
Rather, Congress specifically authorized EPA to consider ``anticipated 
residues,'' terminology EPA had long regarded as describing evidence 
demonstrating the residues were below tolerance levels.
    NRDC is also incorrect in its claim that failure to focus on food 
purchased at farm stands will vastly underestimate dietary exposure to 
pesticides. This underestimation occurs, according to NRDC because EPA 
does not take into account that a significant number of consumers buy 
produce at farm stands. Even assuming that food consumed as a result of 
purchases at farm stands

[[Page 46733]]

constitute more than a negligible amount of the diet, NRDC's claims 
here are inaccurate whether EPA is relying on anticipated residues 
estimated based on crop field trials or monitoring data. Crop field 
trials measure residue levels at harvest after use of application rates 
and procedures that will produce maximum residues under the currently-
approved pesticide label. Thus, anticipated residue values from crop 
field trials, if anything, will overstate the values found at farm 
stands or U-pick farms. Even where EPA uses monitoring data it is 
likely to differ little from the values at farm stands or U-pick farms. 
The monitoring data EPA relies upon most frequently is from the 
Pesticide Data Program (PDP) run by USDA. PDP data is extensive and 
covers a wide spectrum of residue values. Samples are generally 
collected at wholesale and central distribution points prior to 
distribution to supermarkets and grocery stores. For fresh produce, the 
type of food most likely to be found at a farm stand or U-pick farm, 
rapid distribution is critical and thus central food distribution 
points are likely to very close to the farm in terms of time from 
harvest. This would be particularly true for those commodities which 
are transported quickly from farm to distribution center under 
controlled-environment conditions (e.g., strawberries, blueberries). 
For all of these reasons, EPA concludes that its exposure estimates are 
not likely to understate exposure without use of specific data on 
residue levels at farm stands and U-pick farms.
    6. Population percentile used in aggregate exposure estimates--a. 
In General. NRDC contends that EPA in making the reasonable certainty 
of no harm finding must make such a finding as to ``all children'' --
that is, EPA must find that ``no children will be harmed'' by exposure 
to the pesticide. Although EPA is somewhat uncertain as to precisely 
what approach to risk assessment and safety findings NRDC is 
advocating, EPA believes that its approach to implementing the 
reasonable certainty of no harm standard is consistent with the 
statutory framework. As specified in the statute, EPA focuses its risk 
assessment and safety findings on major identifiable population 
subgroups. (21 U.S.C. 346a(b)(2)(D)(vi)). For children EPA has 
identified the following subgroups: nursing infants (0-6 months); non-
nursing infants (6 months - year); 1-2 year-olds; 3-5 year olds; 6-12 
year olds; and 13-19 year olds. EPA evaluates each of these subgroups 
to determine if it can be determined that there is a reasonable 
certainty of no harm for individuals in these subgroups. (See Refs. 2 
at 40; and 1 at 14).
    b. Choice of population percentile. NRDC asserts that EPA erred by 
allegedly making its safety decision as to the acute risk posed by 
pymetrozine, mepiquat, isoxadifen-ethyl, acetamiprid, and furilazole 
based on only a portion of the population, leaving the rest of the 
population unprotected. According to NRDC, EPA only considered 95 
percent of the affected population. This argument was rejected in the 
Imidacloprid Order, and EPA incorporates the reasoning used there. (69 
FR at 30070-30071, May 26, 2004).
    EPA relies on population percentages as one of several inputs in 
estimating the full range of exposures in each population subgroup and 
not because it has concluded that a certain percentage of the 
population is unworthy of protection. As EPA explained in its 
Imidacloprid Order:

    the use of a particular percentile of exposure is a tool to 
estimate exposures for the entire population and population 
subgroups and not a means to eliminate protection for a certain 
segment of a subgroup. When inputs for pesticide residue values in 
the exposure estimate are high end (e.g., assuming all food contains 
tolerance level residues), a lower percentile of exposure (e.g., 95 
percent) is thought to be representative of exposure to the overall 
population as well as subgroups. As increasingly realistic residue 
values are used (e.g., information from pesticide residue 
monitoring), a higher percentile of exposure (e.g., 99.9 percent) is 
generally necessary to be protective of the overall population and 
its subgroups.

(69 FR at 30070). As EPA pointed out, a risk assessment using the 95th 
population percentile and worst case residue values is likely to 
estimate much higher exposure levels than an assessment using the 
99.9th population percentage and residue values from monitoring 
studies. (Id. at 30071).
    For each of the pesticides as to which NRDC raised concerns with 
the use of the 95th population percentile for estimating exposure, EPA 
estimated exposure using the gross overestimate of all crops covered by 
the tolerance containing residues at tolerance levels. (66 FR at 66788, 
December 27, 2001 (pymetrozine); 65 FR at 1790, 1792-93, January 12, 
2000 (mepiquat); 66 FR 33179, 33184, June 21, 2001 (isoxadifen-ethyl); 
67 FR at 14653, March 27, 2002 (acetamiprid); 67 FR at 15731, April 3, 
2002 (furilazole)). Thus, EPA concludes it reasonably estimated 
exposure in making its reasonable certainty of no harm finding for 
these pesticides.
    7. Alleged inadequacies pertaining to specific pesticides--a. 
Pymetrozine. NRDC argues the EPA has underestimated aggregate exposure 
to pymetrozine because (1) ``EPA assumes that a toddler's hand-to-mouth 
exposure occurs very few times per hour;'' (2) EPA fails to consider 
that children put other objects in their mouths beside their hands; and 
(3) EPA ignores children's consumption of ```feral' food - food that 
has been dropped on the floor and which picks up residues from 
contaminated surfaces.'' (Ref. 6 at 8). NRDC is incorrect. First, 
several years ago EPA modified its estimate of hand-to-mouth exposures 
from 1.28/hour to 20/hour, a 90th percentile value. (Ref. 81). As to 
the other types of oral exposures cited by NRDC, EPA's experience has 
shown that any exposures that occurs in such a manner is 
inconsequential beside the non-dietary oral exposures EPA estimates 
through its models. In modeling toddler exposure, EPA assumes that the 
toddler plays in the treated area engaging in repeated mouthing 
behavior immediately after treatment. NRDC is referencing potential 
exposures that may occur occasionally in areas inside the home and thus 
well-separated from the treatment area (the lawn).
    b. Bifenazate. NRDC claims that EPA relied upon ``unsupported and 
apparently arbitrary processing factors to reduce estimates of dietary 
exposure to bifenazate on apples and grapes.'' (Ref. 7 at 16). Further, 
NRDC alleges that despite the fact that bifenazate is registered for 
use on landscape ornamentals, EPA ignores this source of exposure. 
(Ref. 7 at 17).
    EPA's default processing factors are neither unsupported nor 
arbitrary. EPA uses all available data and analyzes it in a manner to 
ensure that the application of default processing factors will not 
understate pesticide exposure. In fact, EPA's manner of applying 
default processing factors tends to exaggerate greatly exposure levels 
in processed food compared to the level of residues that is actually 
present.
    Default processing factors are a numerical measure of the potential 
of pesticide residues to concentrate in processed foods when a raw food 
is partitioned into its component fractions. They are derived from the 
weight-to-weight ratio of raw and processed commodities and intended to 
reflect the highest potential concentration of pesticide residue that 
can occur. In calculating default processing factors EPA assumes that 
concentration will be inversely proportional to the reduction of weight 
(mass) that occurs during processing (e.g., if processing reduces

[[Page 46734]]

the mass of processed commodity proportional to the raw commodity by 50 
percent, the default processing factor would be 2X). Importantly, EPA 
applies default processing factors using the worst case assumption that 
all pesticide residue in the raw commodity remains in any commodity 
processed from such raw commodity. Thus, if the raw food contains 2 ppm 
of a pesticide and the default processing factor for a processed 
commodity from such raw food is 2X, EPA will assume that the processing 
commodity contains 4 ppm of the pesticide. The 4 ppm estimate should be 
regarded as a theoretical upper bound level, however, because actual 
processing data generally shows residues are reduced during processing, 
or at least not concentrated at EPA's theoretically-derived default 
level (i.e., the inverse proportion of reduction in mass of the 
processed commodity). EPA's use of default processing factors further 
exaggerates residue estimates in processed food because EPA assumes 
that each processed commodity from a raw food contains all of the 
pesticide present in the raw food (with the precise level being 
estimated by the default processing factor). (Refs. 82 and 83)
    Several examples will help to elucidate how EPA calculates and 
applies default processing factors. Perhaps the simplest example of how 
EPA calculates default processing factors involves potatoes and dried 
potato flakes. The default processing factor for potatoes is calculated 
by determining the weight-to-weight ratio of whole potatoes to dried 
potatoes. This ratio is assumed to be the concentration factor of the 
pesticide in the dried potato. USDA information indicates that it takes 
6.5 pounds of fresh potatoes to produce 1 pound of dried potato flakes. 
Thus, the default processing factor for potato flakes is 6.5X and this 
factor is multiplied times the residue level found in fresh potatoes to 
estimate residues in potato flakes. This approach produces a worst case 
estimate because it assumes that the processing process does not result 
in any loss or degradation of the pesticide residues in or on the 
potato - i.e, that the washing, peeling, heating, and drying that 
occurs in the processing of fresh potatoes into potato flakes does not 
result in any reduction in total pesticide residues.
    The processing of potatoes also is a good example of how EPA 
applies default processing factors in a manner that will exaggerate 
estimates of pesticide levels in processed food. With potato 
processing, EPA assumes that all of the pesticide residue in the raw 
potato not only is translocated to the dried potato flakes but also is 
present in the potato peel which is a byproduct of processing dried 
potato flakes and is used as an animal feed. The level of residue 
assumed for the peel is based, like the level for the flakes, on the 
level of residue in the raw potato multiplied by the appropriate 
default processing factor. Obviously, it is physically impossible for 
all of the pesticide in the raw potato to be translocated to both the 
dried flakes and the peel but in the absence of more specific data on 
how the pesticide is distributed in the raw potato, EPA's approach is a 
reasonable, health-protective measure. Similar methodology is employed 
with other commodities that have a peel that itself is an edible 
commodity for animals or humans, such as citrus.
    A slightly different approach is used for deriving the default 
processing factor for pome fruit, such as apples. For these 
commodities, the default processing factor is calculated by dividing 
the mass of the commodity that constitutes the processed commodity in 
question into the mass of the entire commodity. For example, USDA data 
indicates that the mass of a typical apple consists of 12.5 percent 
solids and 87.5 percent intrinsic (biological) water. To calculate the 
processing factor for apple juice, thus, the mass of the water (juice) 
portion of the apple is divided into the mass of the entire apple 
yielding a processing factor of 1.14X. Performing the same operation 
for dried apple commodities, yields a processing factor of 8X. Like 
with other raw commodities, to estimate residues in the processed 
commodities derived from apples (apple juice, dried apple pomace), EPA 
assumes all residue in the raw apple is translocated to each processed 
commodity and estimates residue levels by multiplying the appropriate 
default processing factor times the level of residue found in the fresh 
apples.
    Thus, NRDC is mistaken in its conclusion that EPA uses default 
processing factors to reduce exposure estimates. To the contrary, EPA's 
derivation and use of default processing factors will generally 
overstate residue levels in processed commodities. NRDC's objection 
here is not well taken.
    EPA concluded that no significant residential exposure would occur 
to the homeowner and family members as a result of the landscape 
ornamental use because (1) application of the pesticide at this site is 
restricted to commercial applicators; and (2) post-application exposure 
is unlikely where the application is limited to ornamentals (e.g., 
bushes, shrubs). EPA routinely assumes post-application exposure may 
occur with residential uses in such areas as on lawns or in vegetable 
gardens where there is the potential for homeowners and family members 
(other than young children as concerns vegetable gardens) to have 
significant contact with the treated plant. Although in the past EPA 
has occasionally conducted post-application exposure assessments for 
ornamental uses, EPA's current view is that any post-application 
exposure from such a use is likely to be minimal.
    c. Zeta-cypermethrin. As to zeta-cypermethrin, NRDC claims that EPA 
``wrongly ignores indoor and outdoor residential uses of cypermethrin 
(which the agency states is toxicologically identical to zeta-
cypermethrin for the purposes of these tolerances).'' (Ref. 7 at 17). 
NRDC, however, is mistaken in this allegation. EPA made clear in the 
Federal Register notice associated with the challenged zeta-
cypermethrin tolerances that EPA combines residential exposures from 
these two pesticides. As EPA explained:

    The analytical method does not distinguish cypermethrin from 
zeta-cypermethrin, and the toxicological endpoints are the same. 
Therefore, dietary and non-dietary residential aggregate risk 
assessment is conducted by adding the uses of the two chemicals.
(67 FR at 6426, 6427, February 12, 2002).
    d. Diflubenzuron. NRDC asserts that EPA has underestimated 
aggregate exposure to diflubenzuron because EPA concluded that 
application of diflubenzuron to tree canopies would result in 
negligible residential exposure to diflubenzuron. After review, 
however, EPA reaffirms that these potential exposures are expected to 
be limited. The label states that ``applications should be made during 
periods of minimal use'' and requires users to ``Notify persons using 
recreational facilities or living in the area to be sprayed before 
application.'' Diflubenzuron is only applied by commercial applicators 
to the tree canopy for control of gypsy moths and mosquitoes. Generally 
applied by helicopter, these sprays are not aerosols or ultra low 
volume sprays designed as space sprays, but are rather directed to the 
tree canopy and designed to impinge on the tree tops where they would 
be effective in pest control. The sprays designed for application to 
tree canopies utilize much larger droplet sizes which are essentially 
nonrespirable; therefore, minimal inhalation exposure to bystanders is 
expected. Additionally, due to a low dermal absorption rate (0.5 
percent), the potential for dermal exposure to bystanders is expected 
to be minimal.

[[Page 46735]]

    In any event, EPA would note that the results of the chronic 
dietary analysis indicated that the estimated chronic dietary risk 
associated with the proposed use of diflubenzuron was well below the 
Agency's level of concern for the general U.S. population. In fact, the 
highest exposed population subgroup (all infants <1 year of age) using 
a very conservative (health-protective) estimate of exposure is 5.5 
percent of the safe dose. An acute dietary exposure risk assessment was 
not conducted since no hazard was identified for any population, 
including infants and children, following a single exposure to 
diflubenzuron (i.e., no hazard was identified, therefore, 
quantification of risk is not appropriate).
    e. 2,4-D. NRDC claims that ``EPA deliberately ignores known 
residential uses in establishing new tolerances for 2,4-D . . . [by] 
fail[ing] to assess and incorporate those residential uses as a source 
of aggregate exposure, in violation of the FQPA.'' (Ref. 8 at 18). NRDC 
cites to several studies allegedly demonstrating that when 2,4-D is 
applied to turf, residues are tracked indoors and can lead to 
``significant'' exposures. Citing a rat study, NRDC also claims that 
children can be exposed to 2,4-D through mother's milk.
    Contrary to NRDC's assertions, however, EPA did aggregate 
residential exposures with food and water exposures to 2,4-D in 
assessing its safety. EPA's quantitative aggregate assessment of the 
short-term risk from residential uses appears at page 10629 of the 
Federal Register notice establishing the challenged tolerance. (67 FR 
at 10629, March 29, 2002). EPA did not aggregate residential exposures 
in conducting an intermediate-term residential risk assessment because 
data showed that intermediate-term exposure as a result of residential 
uses was very low. (ID. at 10626.)
    As to the study cited by NRDC on track-in exposures, EPA concludes 
that, at most, these data indicated some degree of elevated seasonal 
exposure but such exposure was minimal. (Ref. 33). The cited study 
noted that its estimate of the combined exposure for all routes for a 
10 kg child, whether looking at the maximum (8.871 micrograms/day 
([mu]g/day) ) or median values (2.421 [mu]g/day), was well below safe 
levels. By comparison, the exposure assessment for 2,4-D described in 
Unit VII.B.2.a. estimates a 10 kg child would be exposed to 503 [mu]g/
day (excluding drift) and 756 [mu]g/day (including drift). EPA's 
estimated exposure for a 10 kg child due to residential uses alone is 
473 [mu]g/day. (Ref. 33 at 9). Thus, the cited study does not suggest 
EPA is underestimating exposure. To the contrary, it demonstrates that 
EPA's asssessment approach is very conservative (health-protective).
    NRDC also expressed concern that nursing infants could be exposed 
to 2,4-D in breast milk. (Ref. 8 at 7) NRDC cites to a study in rats 
that showed 2,4-D in breast-fed neonates. (Ref. 84). EPA is aware, as a 
result of animal feeding studies using exaggerated doses, that 2,4-D 
may be present in milk. It is not surprising that the study relied upon 
by NRDC suggests that 2,4-D is transmitted in breast milk given the 
massive doses of 2,4-D in that study of 50, 70, 700 milligrams/kilogram 
of body weight/day (mg/kg/day). By comparison, EPA estimates that the 
maximum dietary exposure from food to human females ages 13-50 is 
0.01018 mg/kg/day and the average exposure is 0.000642 mg/kg/day. (Ref. 
61). These values range from 4,900 to 1 million times lower than the 
values in the cited rat study.
    Further, EPA's manner of doing risk assessment for infants is 
protective of any pesticide exposure to infants from human breast milk 
because the exposure values EPA assumes for pesticides in cow's milk 
greatly exceed the values that could be present in breast milk. The 
diet of non-nursing infants less than 1 year old still contains milk as 
a primary component. Importantly, dairy cows exposure to pesticides 
tend to be significantly higher than humans because residues in grass 
forage are generally higher than in human foods. For example, the 
tolerance for pastureland grass for 2,4-D is 1,000 ppm while the 2,4-D 
tolerances for various human foods are all in the single digits. (See 
40 CFR 180.142). Additionally, EPA tends to use very conservative 
methods for calculating tolerance values and exposure levels in meat 
and milk in cattle (e.g., relying on exaggerated feeding studies, use 
of worst case diets) which overstate exposure.
    For the 2,4-D risk assessment, EPA assumed that 2,4-D would be 
present in milk at 0.004 ppm for both acute and chronic exposure. (Ref. 
85). This value represents half of the level of detection from the 
analytical method used in studies monitoring milk for 2,4-D residues. 
No 2,4-D residues were detected in these studies, and in that 
circumstance it is common practice to estimate exposure at half of the 
level of detection. (Refs. 80 and 86). The conservative (health-
protective) nature of this exposure value can be seen by considering 
data from a 2,4-D feeding study in cattle and what those data suggest 
regarding the levels of 2,4-D present in rat milk in the cited study 
and in human breast milk. What the cattle study showed was that cattle 
fed a diet of 1,500 ppm 2,4-D had residues of 2,4-D in their milk at 
the level of 0.07 ppm. (Ref. 87). Extrapolating from these figures, 
2,4-D levels in rat milk in the cited study would have ranged from 0.05 
ppm to 0.65 ppm. Taking into account that the dose levels in the rat 
study were approximately 4,900 to 70,000-fold higher (50 mg/kg/day), 
and 69,000 to one million-fold higher (700 mg/kg/day) than the 
estimated maximum and average female 13-50 dietary exposure (0.01018 
mg/kg/day and 0.000642 mg/kg/day), it is striking that the estimated 
milk residue used to estimate dietary exposure to infants (0.004 ppm) 
is only approximately 12-fold lower than the rat milk residue estimated 
for the 4,900 - 78,000X exaggerated dose, and 162-fold less than the 
rat milk residue estimated for the 69,000 - 1,000,000X exaggerated 
dose. As to human breast milk, what the cattle study shows is that 
given the maximum and average exposure levels of females ages 13-50 to 
2,4-D, the expected maximum and average levels in breast milk are 
roughly 200 and 4,000 times lower, respectively, than the exposure 
value used for cow's milk. (Ref. 88). Thus, EPA concludes that its 
aggregate exposure assessment was protective for all children, 
including nursing infants.
    f. Isoxadifen-ethyl, acetamiprid, fluazinam. Repeating the 
allegations made as to bifenazate, NRDC argues that EPA relied upon 
``unsupported and apparently arbitrary processing factors to reduce 
estimates of dietary exposure'' for isoxadifen-ethyl, acetamiprid, and 
fluazinam. (Ref. 9 at 16). For the reasons described above in Unit 
VII.D.7.b., EPA denies these objections.

E. Human Testing

    NRDC claims that EPA used a human study to assess exposure to turf 
use of 2,4-D in violation of EPA's policy on use of human studies as 
announced in a press release on December, 14, 2001, and in violation of 
``the Nuremberg Code, the Helsinki Declaration, and EPA's common 
rule.'' (Ref. 8 at 21-22). NRDC states that EPA has not clarified 
whether the human study in question was an epidemiology study or 
involved third-party human testing. If the study falls in the latter 
category, according to NRDC, EPA's consideration of it would violate 
its own policy as well as the other cited authorities.
    EPA disagrees with NRDC's claim that it was improper for EPA to 
consider the study in question in assessing the risk posed by 2,4-D. To 
clarify, the study is not an epidemiology study; rather it is a 
biomonitoring study conducted by the

[[Page 46736]]

Canadian Centre for Toxicology. (Ref. 89). Because it was not conducted 
or supported by a department or agency of the U.S. Government, EPA 
refers to it as a ``third-party'' study. In this biomonitoring study, 
adult male and female volunteers were selected from the faculty, staff, 
and students of the University of Guelph. The study participants ``were 
supplied with written information outlining the possible risks they 
would be taking to participate in the study. . . . Consent forms were 
signed before the initiation of the study.'' (Ref. 89 at 12). In 
addition, ``[t]he protocol was appraised and approved by the University 
of Guelph Ethical Review Board.'' (Id.) Volunteers were exposed to 2,4-
D while performing activities specified by the researchers (walking, 
sitting, and lying) for one hour on turf previously treated (consistent 
with product's label instructions) with 0.88 lb acid equivalent/acre 
2,4-D. The product did not specify any restricted entry interval or 
require that people entering treated areas wear any special personal 
protective equipment. The researchers measured the amount of 2,4-D 
detectable in urine collected from the human participants for a period 
of 96 hours following this exposure.
    NRDC's objection appears to be based on their belief that the 2,4-D 
biomonitoring study was unethical and that the decision to rely on the 
data violated existing international standards (the Nuremberg Code and 
the Helsinki Declaration), as well as Agency regulations (the Common 
Rule) and policy (presumably the position announced in a December 14, 
2001 press release). Each of these is discussed below.
    The Nuremberg Code contains basic, broad ethical precepts to guide 
all types of scientific research with human subjects. The text of the 
Code was developed in 1949 and is available at: http://ohsr.od.nih.gov/guidelines/nuremberg.html. The Code indicates that for a human study to 
be considered ethical the subjects must participate voluntarily, they 
should be informed of the nature and purpose of the research, and they 
should be allowed to withdraw at any time. Also, the study should be 
designed to produce scientifically useful information and be conducted 
by appropriately qualified researchers. The Code also indicates 
researchers should take measures to protect the subjects and must 
terminate the research if continuation of the study would result in 
injury to a participant.
    The Agency has reviewed the ethical conduct of the 2,4-D 
biomonitoring study using the principles in the Nuremberg Code. While 
the available information on the biomonitoring study does not address 
each of the paragraphs in the Code, the information does indicate that 
the study complied with the broad principles of the Code. EPA is aware 
of no information to indicate that any of the Code's principles was not 
followed.
    The international medical research community has developed and 
maintains ethical standards documented in the Declaration of Helsinki, 
first issued by the World Medical Association in 1964 and revised 
several times since then. The latest version of the Declaration is 
available at: http://www.wma.net/e/policy/b3.htm . These standards are 
available to guide research on matters relating to the diagnosis and 
treatment of human disease, and to research that adds to understanding 
of the causes of disease and the biological mechanisms that explain the 
relationships between human exposures to environmental agents and 
disease. Because the 2,4-D biomonitoring study did not involve research 
on matters relating to the relationship between human exposure to 
environmental agents and human disease, or otherwise fall within the 
scope of the Declaration of Helsinki, the Declaration does not apply to 
this research.
    The Agency's rules for ``Protection of Human Subjects,'' generally 
referred to as the ``Common Rule,'' apply to ``all research involving 
human subjects conducted [or] supported . . . by any Federal department 
or agency.'' (40 CFR 26.101). Because the 2,4-D biomonitoring study was 
not conducted or supported by an agency or department of the U.S. 
Government, it was not subject to the Common Rule.
    At the time EPA prepared its risk assessment for the 2,4-D soybean 
tolerance, the Agency had a general practice of using ``third-party'' 
human studies, unless the studies involved intentional dosing of human 
subjects for the purpose of identifying or quantifying a toxic effect. 
(Ref. 90). This policy or practice (as described in the December, 2001 
Press release) applied only to intentional dosing studies conducted to 
identify or quantify a toxic effect and the 2,4-D biomonitoring study 
was not such a study.
    It should be noted that the approach described in the 2001 press 
release has been set aside. In early 2002 various parties from the 
pesticide industry filed a petition with the U. S. Court of Appeals for 
the District of Columbia for review of EPA's December 2001 press 
release. These parties argued that the Agency's interim approach 
constituted a ``rule'' promulgated in violation of the procedural 
requirements of the Administrative Procedure Act and the Federal Food, 
Drug, and Cosmetic Act. On June 3, 2003, the Court of Appeals concluded 
that:

    For the reasons enumerated above, we vacate the directive 
articulated in EPA's December 14, 2001 Press Release for a failure 
to engage in the requisite notice and comment rulemaking. The 
consequence is that the agency's previous practice of considering 
third-party human studies on a case-by-case basis, applying 
statutory requirements, the Common Rule, and high ethical standards 
as a guide, is reinstated and remains in effect unless and until it 
is replaced by a lawfully promulgated regulation.

Crop Life America v. EPA, 329 F.3d 876, 884 - 85 (D.C. Cir. 2003)).
    In sum, the information available to EPA does not suggest that the 
2,4-D human biomonitoring study was performed in an unethical manner 
and therefore should not have been considered by the Agency. Rather, 
the researchers in the 2,4-D study informed the participants of 
potential risks from participating in the study and obtained their 
written consent. In addition, the researchers obtained an assessment by 
an independent ethical review board of the proposed study design prior 
to conducting the study. While the Journal article describing the 2,4-D 
biomonitoring study does not reference any applicable ethical framework 
as governing its conduct, these measures - a prior ethics review by an 
independent board and informed consent - are the principal protections 
required by the Common Rule adopted in the United States in 1991. 
Accordingly, EPA has determined that the 2,4-D biomonitoring study is 
not significantly deficient relative to the ethical standards 
prevailing when the study was conducted, some time prior to 1992. EPA 
has also determined that the study is not fundamentally unethical. 
Moreover, EPA notes that this study is not subject to the Helsinki 
Declaration, EPA's Common Rule, or EPA's now overturned December 2001 
policy on third-party human testing. Finally, NRDC provided no specific 
information or argument to support its objection. Therefore, EPA 
concludes that it properly considered the data from the 2,4-D 
biomonitoring study.

F. Conclusion on Objections

    For the reasons stated above, all of the NRDC's objections are 
hereby denied.

VIII. Response to Comments on NRDC's Objections

    EPA has responded to many of the comments that pertained 
specifically to

[[Page 46737]]

the individual pesticides and pesticide tolerances in Unit VII. The 
more general comments filed by the IWG, IR-4, and the public were 
responded to in the Imidacloprid Order. That response is adopted 
herein. (69 FR at 30072-30074, May 26, 2004). Other comments are 
addressed below.
    ISK Biosciences noted that the challenged fluazinam tolerance 
applied to wine grapes and children do not usually consume wine. 
Although this is true, section 408(b) requires EPA to consider 
aggregate exposure to a pesticide and not just exposure under the 
specific tolerance at issue. Further, ISK Biosciences argues that EPA's 
assessment of exposure to fluazinam in wine is very conservative. EPA 
generally agrees with this comment.
    FMC Corporation argues that because a data call-in has not been 
issued for a DNT study on zeta-cypermethrin there can be no data gap 
and the database must be complete. In response, EPA would note that the 
``completeness'' inquiry in the children's safety factor provision is 
not a formalistic exercise turning on whether mandatory data call-ins 
have been issued. As EPA stated in its Children's Safety Policy:

    the ``completeness'' inquiry should be a broad one that takes 
into account all data deficiencies. In other words, the risk 
assessor should consider the need for traditional uncertainty 
factors not only when there are inadequacies or gaps in currently 
required studies on pesticides, but also when other important data 
needed to evaluate potential risks to children are missing or are 
inadequate.

(Ref. 2 at 20).
    Bayer CropScience states that historical control information 
relating to effects seen in a rat teratology study submitted to EPA 
demonstrates that the young do not have increased sensitivity to 
isoxadifen-ethyl. After reviewing this historical control data, EPA has 
again concluded that the developmental effects seen at the mid- and 
high-doses in the rat teratology study were statistically significant 
and treatment-related. (Ref. 9)

IX. Regulatory Assessment Requirements

    As indicated previously, this action announces the Agency's final 
order regarding objections filed under section 408 of FFDCA. As such, 
this action is an adjudication and not a rule. The regulatory 
assessment requirements imposed on rulemaking do not, therefore, apply 
to this action.

X. Submission to Congress and the Comptroller General

    The Congressional Review Act, (5 U.S.C. 801 et seq.), as added by 
the Small Business Regulatory Enforcement Fairness Act of 1996, does 
not apply because this action is not a rule for purposes of 5 U.S.C. 
804(3).

XI. Time and Date of Issuance of This Order

    The time and date of the issuance of this Order shall, for purposes 
of 28 U.S.C. 2112, be at 1 p.m. eastern time (daylight savings time) on 
the date that is 2 weeks after the date when the document is published 
in the Federal Register.

XII. References

    1. Office of Pesticide Programs, U.S. EPA, Available Information on 
Assessing Pesticide Exposure From Food: A User's Guide (June 21, 2000) 
(available at http://www.epa.gov/ fedrgstr/EPA-PEST/2000/July/Day-12/
6061.pdf).
    2. Office of Pesticide Programs, US EPA, Determination of the 
Appropriate FQPA Safety Factor(s) in Tolerance Assessment [hereinafter 
cited and referred to in the text as the ``Children's Safety Factor 
Policy''] (January 31, 2002) (available at http://www.epa.gov/oppfead1/trac/science/determ.pdf).
    3. Office of Pesticide Programs, US EPA, General Principles for 
Performing Aggregate Exposure and Risk Assessments (November 28, 2001) 
(available at http://www.epa.gov/pesticides/trac/science/aggregate.pdf).
    4. Office of Pesticide Programs, US EPA, Choosing a Percentile of 
Acute Dietary Exposure as a Threshold of Regulatory Concern 
[hereinafter referred to and cited as ``Percentile Policy''] (March 16, 
2000) (available at http://www.epa.gov/pesticides/trac/science/trac2b054.pdf).
    5. Petition For A Directive That the Agency Designate Farm Children 
as a Major Identifiable Subgroup and Population at Special Risk to Be 
Protected under the Food Quality Protection Act 2 (October 22, 1998).
    6. Objections to the Establishment of Tolerances for Pesticide 
Chemical Residues: Halosulfuron-methyl and Pymetrozine Tolerances 
(filed February 25, 2002).
    7. Objections to the Establishment of Tolerances for Pesticide 
Chemical Residues: Imidacloprid, Mepiquat, Bifenazate, Zeta-
cypermethrin, and Diflubenzuron Tolerances (filed March 19, 2002).
    8. Objections to the Establishment of Tolerances for Pesticide 
Chemical Residues: 2,4-D Tolerances (filed May 7, 2002).
    9. Objections to the Establishment of Tolerances for Pesticide 
Chemical Residues: Isoxadifen-ethyl, Acetamiprid, Propiconazole, 
Furilazole, Fenhexamid, and Fluazinam Tolerances (filed May 20, 2002).
    10. FQPA Implementation Working Group, Response to Objections of 
the Natural Resources Defense Council to Regulations Establishing 
Tolerances for Residues of Various Pesticide Chemicals In or On Food 
Items (October 16, 2002).
    11. Inter-Regional Research Project Number 4, Response to Natural 
Resources Defense Council Objection to Tolerances Established for 
Certain Pesticide Chemicals (October 15, 2002).
    12. ISK Biosciences, NRDC Objection to the Establishment of 
Tolerances for Fluazinam (October 14, 2002).
    13. Bayer CropScience, Comments to the May 20, 2002 NRDC Letter to 
the EPA Objecting to the Establishment of Tolerances for Isoxadifen-
ethyl (October 16, 2002).
    14. Peter Hertl, et al., Poster Session, 10th IUPAC International 
Congress on Chemistry of Crop Protection, Basel, Switzerland (2002).
    15. Aventis CropScience, Comments to the May 20, 2002 NRDC Letter 
to the EPA Objecting to the Establishment of Tolerances for Acetamiprid 
2 (October 11, 2002).
    16. FMC Corporation, Comments on NRDC Objections to EPA 
Establishment of Certain Pesticide Tolerances 5 (October 15, 2002).
    17. Crompton Corporation, Comments of Crompton Corporation to NRDC 
objections to Bifenazate and Diflubenzuron Tolerances 9 (October 15, 
2002).
    18. Syngenta Crop Protection, Comments on Objections to Tolerances 
Established for Certain Pesticide Chemicals, 2 (October 16, 2002) 
(citing Dourson, M.L., Fetter, S.P., and Robinson, D., Evaluation of 
Science-Based Uncertainty Factors in Non-Cancer Risk Assessment, 
Regulatory Toxicoloty and Pharmacology. 24(2), 108-120 (1996)).
    19. BASF Corporation, Docket Identification (ID) Number OPP-2002-
0057 (October 16, 2002).
    20. Industry Task Force II on 2,4-D Research Data, Response to 
Objections of the Natural Resources Defense Council to the 
Establishment of a Tolerance for Pesticide Chemical Residues of 2,4-
Dichlorophenoxyacetic Acid (2,4-D) (October 16, 2002).
    21. U.S. EPA, A Pilot Study of Children's Total Exposure to 
Persistent Pesticides and Other Persistent Organic Pollutants (CTEPP) 
(2005).

[[Page 46738]]

    22. National Exposure Research Laboratory, U.S. EPA, Memorandum 
from Kent Thomas to Ruth Allen, Transmittal of Agricultural Health 
Study/Pesticide Exposure 2,4-D Urinary Biomarker Measurement Results in 
Support of Response to Public Comments on the Draft 2,4-D Risk 
Assessment (November 9, 2004).
    23. Mandel, J.S., and Alexander, B.H., Measurement of Pesticide 
Exposure of Farm Residents Associated With the Agricultural Use of 
Pesticides Glyphosate, 2,4-D, Chlorpyrifos: The Farm Family Exposure 
Study (June 18, 2004).
    24. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Timothy C. Dole to Katie Hall, 2,4-D: Response to 
Public Comments (December 16, 2004).
    25. Pesticide Registration Notice 90-3 (April 6, 1990) (available 
at http://www.epa.gov/opppmsd1/PR_Notices/pr90-3.htm).
    26. Hewitt, Andrew J., Johnson, David R., Fish John D., Hermansky, 
Clarence G., and Valcore, David L., Development of the Spray Drift Task 
Force Database for Aerial Applications, 21(3) Environmental Toxicology 
and Chemistry, 648-658 (2002).
    27. Bird, Sandra L., Perry, Steven G., Ray, Scott L., and Teske, 
Milton E, Evaluation of the AgDISP Aerial Spray Algorithms in the 
AgDRIFT Model, Environmental Toxicology and Chemistry, Vol. 21, No.3, 
pp. 672-681 (2002).
    28. Teske, Milton E., Bird, Sandra L., Esterly, David M., 
Curbishley, Thomas B., Ray, Scott L., and Perry, Steven G., AgDRIFT: 
AModel for Estimating Near-field Spray Drift from Aerial Applications, 
21 Environmental Toxicology and Chemistry 659-671 (2002).
    29. U.S. EPA, Guidelines for Exposure Assessment. 57 FR 22888 
(1992).
    30. Bilanin, A.J., M.E. Teske, J.W. Barry, and R.B. Ekblad (1989). 
AGDISP: The aircraft dispersion model, code development and 
experimental validation. Trans. A.S.A.E. 32:327-334.
    31. Bird, Sandra L., Steven G. Perry, Scott L. Ray, Milton E. 
Teske, Peter N. Scherer. (1996) An Evaluation of AgDRIFT 1.0 for Use in 
Aerial Applications. Ecosystems Research Division, National Exposure 
Research Laboratory, Office of Research and Development, USEPA, Athens 
GA, 30605.
    32. Bird, Sandra L., David M. Esterly, and Steven G. Perry (1996). 
Off-target Deposition of Pesticide from Agricultural Aerial Spray 
Applications. Journal of Environmental Quality. 25:1095-1104.
    33. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jeff Evans to Betty Shackleford, Estimates of 
Residential Bystander Exposure (August 1, 2004).
    34. Californians for Pesticide Reform, Secondhand Pesticides: 
Airborne Pesticide Drift in California (2003).
    35. See Lee, S., McLaughlin, R., Harnly, M., Gunier, R., Kreutzer, 
R., Community Exposures to Airborne Agricultural Pesticides in 
California: Ranking of Inhalation Risks, 110 Environmental Health 
Perspectives 1175 (December 2002).
    36. Camann, D.E., Geno, P.W., Harding, H, Jac, Giardino, N.J. and 
Bond, A.E., Measurements to assess exposure of the farmer and family to 
agricultural pesticides, U.S. EPA (Contract 68D10150). pp. 712 - 717 
(1993).
    37. Segawa, R.T., Sitts, J.A., White, J.H., Marade, S.J., Powel, 
S.A. Environmental monitioring of malathion aerial applications used to 
eradicate Mediterranean fruit flies in Southern California. EH 91-03 
California Department of Pesticide Regulation, Sacramento, California.
    38. Nishioka, M.G., Burkholder, H.M, Brinkman, M.C., and Lewis, 
R.G., Distribution of 2,4-Dichlorophenoxyacetic Acid in Floor Dust 
Throughout Homes Following Homeowner and Commercial Lawn Applications: 
Quantitative Effect of Children, Pets, and Shoes, 33 Environmental 
Science and Technology 1359-1365 (1999).
    39. Solomon, K.R., Harris, S.A. and Stephenson, G.R., Applicator 
and Bystander Exposure to Home Garden and Landscape Pesticides, 
American Chemical Society, Pesticides in Urban Environments, Chapter 
22, pp. 262-274 (Eds. Racke and Leslie) (1993).
    40. U.S. EPA, Pesticide Exposure and Potential Health Effects in 
Young Children Along the U.S.-Mexico Border (EPA 600/R-02/085, 
November, 2002).
    41. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jeff Evans to Betty Shackleford, Potential 
Bystander Exposure to Volatile Pesticides (August 1, 2005).
    42. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Margaret J. Stasikowski to Health Effects Division 
Staff, Guidance: Waiver Criteria for Multiple-Exposure Inhalation 
Toxicity Studies (August 15, 2002) (citing references).
    43. ISK Biosciences, Label for Omega 500F (fluazinam) (June 11, 
2003)
    44. BASF, Label for Pentia plant regulator (mepiquat pentaborate) 
(March 17, 2005); BASF, Label for BAS 130 03W plant regulator (mepiquat 
pentaborate) (January 25, 2002).
    45. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Interim Reregistration Eligibility Decision for Chlorpyrifos 
(February 2002).
    46. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from William D. Cutchin to Cynthia Giles-Parker/CP 
Moran, Addendum to Human Health Risk Assessment for the Use of 
Fluazinam on Peanuts, Potatoes, and Wine Grapes. 5 (10/23/01).
    47. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Margarita Collantes to Janet Whitehurst/Cynthia 
Giles-Parker, PP#1F03955. Mepiquat Chloride in/on Grapes and Raisins. 
Human Health Risk Assessment. 25 (11/22/1999).
    48. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Deborah Smegal to Mark Hartman, Occupational/
Residential Handler and Postapplication Residential/Non-Occupational 
Risk Assessment for Chlorpyrifos. DP Barcode: D266562. Case No. 818975. 
PC Code: 059101. Submission: S568580. 6 (June 20, 2000).
    49. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jihad Alsadek to Jeff Evans, Usage Report in 
Support of Chlorpyrifos, an Insecticide, and Mepiquat, a Plant Growth 
regulator (April 25, 2005).
    50. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, PHED Surrogate Exposure Guide: Estimates of Worker Exposure from 
The Pesticide Handler Exposure Database Version 1.1. (August 1998).
    51. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Tim Leighton to Debbie Smegal, Agricultural and 
Occupational Exposure Assessment and Recommendations for the 
Reregistration Eligibility Decision Document for Chlorpyrifos. 31 (June 
19, 2000).
    52. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Deborah Smegal to Steve Knizner, Chlorpyrifos - 
Reevaluation Based on Phase 3 (Public Comments) of the TRAC Process. 
Report of the Hazard Identification Assessment Review Committee (April 
6, 2000) (HED Doc. No. 014088) (available at http://www.epa.gov/ 
oppsrrd1 /op/chlorpyrifos/ reevaluation.pdf.
    53. Makris, Susan et al., A Retrospective Analysis of Twelve 
Developmental Neurotoxicity Studies

[[Page 46739]]

Submitted to the USEPA Office of Prevention, Pesticides, and Toxic 
Substances (draft November 12, 1998) (available at http://www.epa.gov/scipoly/sap/1998/index.htm#december8).
    54. U.S. EPA, Response to Petition to Compel the U.S. EPA to Repeal 
Its Test Guidelines for Developmental Neurotoxicity (January 3, 2005) 
(available at http://docket.epa.gov/edkpub/do/EDKStaffCollectionDetailView?objectId=0b0007d480525f44 =0b0007d480525f44).
    55. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jess Rowland to Betty Shackleford, Effect of 
Developmental Neurotoxicity Studies on Endpoint Selection - Preliminary 
Results (July 28, 2005).
    56. U.S. EPA, Toxicology data requirements for assessing risks of 
pesticide exposure to children's health. Report of the Toxicology 
Working Group of the 10X Task Force 31 (draft April 28, 1999) 
(Available at http://www.epa.gov/scipoly/sap/1999/may/10xtx428.pdf).
    57. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from George F. Kramer to Shaja Brothers/Robert Forrest, 
PP#: 0E06167. Diflubenzuron in/on Pears (Dimilinr 2L, EPA Reg #400-461& 
Dimilinr 25W, EPA Reg # 400-464). Health Effects Division (HED) Risk 
Assessment. PC Code 108201. DP Barcode: D271495. Case: 293100. 
Submission S590172. (September 27, 2001).
    58. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Edwin R. Budd to William Cutchin, Fluazinam - 
Report of the Hazard Identification Assessment Review Committee 28 
(February 13, 2001).
    59. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jessica Kidwell to Jessica Kidwell, MON 13900: 
Data Waiver Request - Report of the Hazard Identification Assessment 
Review Committee (November 14, 2000); Memorandum from Guruva B. Reddy 
to George Kramer, MON 13900 - Report of the Hazard Identification 
Assessment Review Committee (December 4, 2001).
    60. Garabrant DH, Philbert MA, Review of 2,4-dichlorophenoxyacetic 
acid (2,4-D) epidemiology and toxicology, Crit Rev Toxicol. 2002 
Jul;32(4):233-57 (``there is no convincing evidence in the literature 
that 2,4-D is associated with human reproductive toxicity.``).
    61. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from G. Jeffrey Herndon to Dan Kenny/Joanne Miller, 
2,4-D. Extension of Time-Limited Tolerance on Soybean Seed. Request 
from Registration Division (RD) for an Updated Human Health Risk 
Assessment. 10-11 (January 31, 2002).
    62. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from HED Chemistry Science Advisory Council to HED 
Chemistry Interest Group, Minutes of 5/16/01 ChemSAC meeting (June 15, 
2001).
    63. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Sherrie L. Kinard to Yan Donovan, Permethrin. 
Metabolism Assessment Review Committee Memorandum (July 6, 2004) (TXR 
NO. 0052775).
    64. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Yan Donovan to George Kramer, Cypermethrin and 
Zeta-Cypermethrin -- Conclusions of the Meeting of Metabolism 
Assessment Review Committee (10/10/00) (November 03, 2000) 
(TXR 0050106).
    65. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Richard Loranger to Yan Donovan, MARC Decision 
Memo for 5/22/02 Meeting on Cyfluthrin: Residues of Concern in Drinking 
Water; Chemical #128831; DP Barcode D283553; Submission #S549586 (June 
13, 2002) (TXR NO. 0050805).
    66. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Jennifer E. Rowell to Donald A. Marlow, PP#8F4925. 
Diflubenzuron (Dimilinr 2L, EPA Reg #400-461) on Rice. Request for 
Petition Method Validation (PMV). MRID # s 44399303, 44399306, 
44695001, and 44695002. Chemical 108201. Barcode D251484. Case 289260. 
Submission # S539585. (December 15, 1998).
    67. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from George F. Kramer to Rita Kumar, PP # 8F4925. 
Diflubenzuron (Dimilinr 2L, EPA Reg #400-461) on Rice. Results of 
Petition Method Validation (PMV) MRID #s 443993-03 and -06. Barcode 
D261060. Chemical No 108201. Case 289260. Submission S571149. 
(September 6, 2002).
    68. Office of Prevention, Pesticides, and Toxic Substances, Data 
Evaluation Report: Bifenazate; Study Type: Developmental Toxicity- 
Rabbit (83-3B) TXR No 013403 (undated).
    69. Cancer Assessment Review Committee, Health Effects Division, 
Office of Pesticide Programs, U.S. EPA, Evaluation of the Carcinogenic 
Potential of Fluazinam (March 29, 2001).
    70. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Michael Doherty to Daniel Peacock, PPs 8F4984, 
8F5031, and 0F6141. Human Health Risk Assessment for the Use of 
Pymetrozine on Cotton, Hops, Pecans, Leafy Vegetables (Except Brassica 
Vegetables), Head and Stem Brassica, Leafy Brassica Greens, Turnip 
Greens, Cucurbits, and Fruiting Vegetables 3 (December 20, 2001)
    71. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from John Doherty to Mike Ioannou, Pymetrozine - Report 
of the Hazard Identification Assessment Review Committee 5 (March 15, 
1999).
    72. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Alan Levy to Margarita Collantes, Mepiquat 
Chloride: - Report of the Hazard Identification Assessment Review 
Committee 16 (October 21, 1999).
    73. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Yan Donovan to A. Layne/L. Deluise, PP# 4F3012, 
9F6040, 8F4970, 9F6037, and 4F4399. FQPA Human Health Risk Assessment 
for the Use of Z-Cypermethrin on Sweet Corn, Rice, Leafy Vegetables 
(Except Brassica), Brassica Leafy Vegetables, Sugar Beets, Sugarcane, 
Corn (Field, Seed, Pop), Green Onions, and Alfalfa. (July 11, 2001).
    74. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Edwin Budd to Cynthia Giles-Parker/C.P. Moran, 
Fluazinam. PP# 9F05079. EPA File Symbol 71512-R. New Reduced Risk 
Active Ingredient. Toxicology Disciplinary Chapter for the Registration 
Support Document and Data Evaluation Records (DERs) for All Recently 
Submitted Toxicology Studies, Toxicology Studies Not Previously 
Reviewed, and Previously Reviewed Toxicology Studies for Which Amended 
DERs or Updated Executive Summaries Have Been Prepared. (June 18, 
2001).
    75. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Data Evaluation Report Fluazinam Study Type: Subchronic Oral Liver 
Toxicity - Rat (Non-Guideline) (June 18, 2001)
    76. U.S. EPA, Guidelines for the Use of Anticipated Residues in 
Dietary Exposure Assessment (March 25, 1991).
    77. U.S. Department of Agriculture, Agricultural Chemical Usage, 
Vegetable Summary 2000(July 2001) (available at http://usda.mannlib.cornell.edu/reports/nassr/other/pcu-bb/).
    78. U.S. Department of Agriculture, Agricultural Chemical Usage, 
Field Crop Summary 2000 (July 2001) (available at

[[Page 46740]]

http://usda.mannlib.cornell.edu/reports/nassr/other/pcu-bb/).
    79. Office of Pesticide Programs, U.S. EPA, Use of the Pesticide 
Data Program (PDP) in Acute Risk Assessment (May 5, 1999-DRAFT) (citing 
studies).
    80. Office of Pesticide Programs, U.S. EPA, Assigning Values to 
Nondetected/non-quantified Pesticide Residues in Human Health Food 
Exposure Assessments (March 23, 2000) (available at http://www.epa.gov/pesticides/trac/science/trac3b012.pdf).
    81. Office of Pesticide Programs, U.S. EPA, Office of Pesticide 
Programs Science Advisory Council for Exposure, Policy Number 12, 
Recommended Revisions to the Standard Operating Procedures (SOPs) for 
Residential Exposure Assessments (Revised: February 22, 2001)
    82. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Residue Chemistry Test Guidelines: OPPTS 860.1520 Processed Food/
Feed (August 1996) (available at http://www.epa.gov/OPPTS_Harmonized/
).
    83. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Sheila Piper to Betty Shackleford, Information on 
Default Processing Factors For Commodities Which Appear in DEEM (Draft: 
July 29, 2005).
    84. Sturtz N, Evangelista de Duffard AM, Duffard R., Detection of 
2,4-dichlorophen oxyacetic acid (2,4-D) residues in neonates breast-fed 
by 2,4-D exposed dams, Neurotoxicology. 2000 Feb-Apr;21(1-2):147-54.
    85. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from William H. Donovan to PV Shah, 2,4-
Dichlorophenoxyacetic Acid - Dietary Exposure Analysis for 2,4-
Dichlorophenoxyacetic Acid in/on Hops (00WA0033). Chemical #: 030001. 
DP Barcode: D266939. Case #: 293138. Submission #: S580138. 3 (July 6, 
2000).
    86. Office of Prevention, Pesticides, and Toxic Substances, 
Memorandum from William J. Hazel to William J. Hazel, 2,4-D. Acute and 
Chronic Dietary Exposure Assessments for Reregistration Eligibility 
Decision 2 (March 1, 2004).
    87. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, 2,4-D, PC Code No. 030001, Case No. 0073 DP Barcode D287660, 
Reregistration Eligibility Decision, Residue Chemistry Considerations 
15 (July 8, 2003).
    88. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Elizabeth Mendez to Jonathan Fleuchaus, 2,4-D; 
Exposure Issues from Breast Milk Residues (May 12, 2005).
    89. Harris and Solomon, 1992, Human Exposure to 2,4-D Following 
Controlled Activities on Recently Sprayed Turf, Journal of 
Environmental Science and Health, B27 (1), 9-22 (1992).
    90. U.S. EPA Press Release (December 14, 2001) (available at: 
http://yosemite.epa.gov/opa/admpress.nsf/b1ab9f485b098972852562e7004dc686/c232a45f5473717085256b2200740ad4?OpenDocument).
    91. Office of Prevention, Pesticides, and Toxic Substances, U.S. 
EPA, Memorandum from Brenda Tarplee to William Donovan, Isoxadifen-
ethyl - 2nd Report of the Hazard Identification Assessment Review 
Committee 4 (March 23, 2003).

List of Subjects

    Environmental protection, pesticides and pest.


    Dated: August 3, 2005.
James Jones,
Director, Office of Pesticide Programs.

[FR Doc. 05-15840 Filed 8-9-05; 8:45 am]
BILLING CODE 6560-50-S