[Federal Register: July 23, 2008 (Volume 73, Number 142)]
[Rules and Regulations]               
[Page 42683-42713]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr23jy08-6]                         

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2002-0302; FRL-8372-5]

 
Dichlorvos (DDVP); Order Denying NRDC's Objections and Requests 
for Hearing

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final Order.

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SUMMARY: In this order, EPA denies objections to, and requests for 
hearing on, a prior order denying a petition requesting that EPA revoke 
all pesticide tolerances for dichlorvos under section 408(d) of the 
Federal Food, Drug, and Cosmetic Act. The objections and hearing 
requests were filed on February 1, 2008, by the Natural Resources 
Defense Council (``NRDC''). The Original petition was also filed by 
NRDC.

DATES: This order is effective July 23, 2008.

ADDRESSES: EPA has established a docket for this action under docket 
identification (ID) number EPA-HQ-OPP-2002-0302. To access the 
electronic docket, go to http://www.regulations.gov, and search for the 
docket number. Follow the instructions on the regulations.gov website 
to view the docket index or access available documents. All documents 
in the docket are listed in the docket index available in 
regulations.gov. Although listed in the index, some information is not 
publicly available, e.g., Confidential Business Information (CBI) or 
other information whose disclosure is restricted by statute. Certain 
other material, such as copyrighted material, is not placed on the 
Internet and will be publicly available only in hard copy form. 
Publicly available docket materials are available in the electronic 
docket at http://www.regulations.gov, or, if only available in hard 
copy, at the OPP Regulatory Public Docket in Rm. S-4400, One Potomac 
Yard (South Bldg.), 2777 S. Crystal Dr., Arlington, VA. The Docket 
Facility is open from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays. The Docket Facility telephone number is (703) 
305-5805.

FOR FURTHER INFORMATION CONTACT: Susan Bartow, Special Review and 
Reregistration Division (7508P), Office of Pesticide Programs, 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460-0001; telephone number: 703-603-0065; e-mail 
address: bartow.susan@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    In this document EPA denies objections and hearing requests by the 
Natural Resources Defense Council (``NRDC'') concerning EPA's denial of 
NRDC's petition to revoke pesticide tolerances. This action may also be 
of interest to agricultural producers, food manufacturers, or pesticide 
manufacturers. Potentially affected entities may include, but are not 
limited to those engaged in the following activities:
     Crop production (North American Industrial Classification 
System (``NAICS'') code 111), e.g., agricultural workers; greenhouse, 
nursery, and floriculture workers; farmers.
     Animal production (NAICS code 112), e.g., cattle ranchers 
and farmers, dairy cattle farmers, livestock farmers.
     Food manufacturing (NAICS code 311), e.g., agricultural 
workers; farmers; greenhouse, nursery, and floriculture workers; 
ranchers; pesticide applicators.
     Pesticide manufacturing (NAICS code 32532), e.g., 
agricultural workers; commercial applicators; farmers; greenhouse, 
nursery, and floriculture workers; residential users.
    This listing is not intended to be exhaustive, but rather to 
provide a guide for readers regarding entities likely to be affected by 
this action. Other types of entities not listed in this unit could also 
be affected. The NAICS codes have been provided to assist you and 
others in determining whether this action might apply to certain 
entities. If you have any questions regarding the applicability of this 
action to a particular entity, consult the person listed under FOR 
FURTHER INFORMATION CONTACT.

B. How Can I Access Electronic Copies of this Document?

    In addition to accessing an electronic copy of this Federal 
Register document through the electronic docket at http://
www.regulations.gov, you may access this Federal Register document 
electronically through the EPA Internet under the ``Federal Register'' 
listings at http://www.epa.gov/fedrgstr. You may also access a 
frequently updated electronic version of EPA's tolerance regulations at 
40 CFR part 180 through the Government Printing Office's pilot e-CFR 
site at http://www.gpoaccess.gov/ecfr.

C. Acronyms

    The following is a list of acronyms used in this order:
CSFII - Continuing Survey of Food Intakes by Individuals
CNS - Central Nervous System
DDVP - dichlorvos
EDSTAC - Endocrine Disruptor Screening and Testing Advisory 
Committee
EPA - Environmental Protection Agency
FACA - Federal Advisory Committee Act
FDA - Food and Drug Administration
FIFRA - Federal Insecticide, Fungicide, and Rodenticide Act
FFDCA - Federal Food, Drug, and Cosmetic Act
FQPA - Food Quality Protection Act of 1996
HSRB - Human Studies Review Board
IRED - Interim Reregistration Eligibility Decision
LOAEL - Lowest Observed Adverse Effect Level
MOE - Margin of Exposure
MRID - Master Record Identification
NOAEL - No Observed Adverse Effect Level
NRDC - Natural Resources Defense Council
OECD - Organisation for Economic Co-operation and Development
PAD - Population Adjusted Dose
ppm - parts per million
RBC - red blood cell
RED - Reregistration Eligibility Decision
RfD - Reference Dose
SDWA - Safe Drinking Water Act
SOP - Standard Operating Procedure
USDA - United Stated Department of Agriculture

II. Introduction

A. What Action Is the Agency Taking?

    In this order, EPA denies objections, and requests for a hearing on 
those objections, to an earlier EPA order, (72 FR 68662 (December 5, 
2007)), denying a petition to revoke all tolerances established for the 
pesticide dichlorvos (``DDVP'') under the Federal Food, Drug, and 
Cosmetic Act (``FFDCA''), 21 U.S.C. 346a. (Refs. 1 and 2). Both the 
objections and hearing requests, as well as the petition, were filed 
with EPA by NRDC.
    NRDC's petition, filed on June 2, 2006, pursuant to FFDCA section 
408(d)(1), asserted numerous grounds as to why the DDVP tolerances 
allegedly fail to meet the FFDCA's safety standard. This petition was 
filed as EPA was completing its reassessment of the safety of the DDVP 
tolerances pursuant to FFDCA section 408(q). (Ref. 3). In response to 
the petition, EPA undertook an extensive review of its DDVP safety 
evaluation in the tolerance reassessment decision. Based on certain 
concerns raised by NRDC, EPA determined it was necessary to incorporate 
updated data on numerous points and to adopt revised and more 
conservative assumptions, in its DDVP risk assessments. This led to 
complete revisions of both EPA's assessments of

[[Page 42684]]

dietary and residential risks from exposure to DDVP. (72 FR at 68678, 
68687-68691). Nonetheless, EPA concluded that its revised risk 
assessments demonstrated that DDVP met the FFDCA safety standard and, 
therefore, denied the petition. (Id. at 68695). EPA's denial was issued 
in the form of an order under FFDCA section 408(d)(4)(iii). (21 U.S.C. 
346a(d)(4)(iii)).
    NRDC then filed objections with EPA to the petition denial order 
and requested a hearing on its objections. These objections and hearing 
requests were filed pursuant to the procedures in the FFDCA section 
408(g)(2). (21 U.S.C. 346a(g)(2)). The objections narrowed NRDC's 
claims to two main topics - that, in assessing the risk to DDVP, EPA 
unlawfully reduced the statutory safety factor for the protection of 
infants and children and EPA unlawfully relied on a human toxicity 
study. As to these claims, NRDC largely repeats the arguments as 
presented in its petition without addressing EPA's substantial 
revisions to the DDVP risk assessment and proffers little to no 
evidence in support of its requests for a hearing. After carefully 
reviewing the objections and hearing requests, EPA has determined that 
NRDC's hearing requests do not satisfy the regulatory requirements for 
such requests and that its substantive objections are without merit. 
Therefore, EPA, in this final order, denies NRDC's objections and its 
requests for a hearing on those objections.

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

    NRDC petitioned to revoke the DDVP tolerances pursuant to the 
petition procedures in FFDCA section 408(d)(1). (21 U.S.C. 346a(d)(1)). 
Under section 408(d), EPA may respond to such a petition by either 
issuing a final or proposed rule modifying or revoking the tolerances 
or issuing an order denying the petition. (21 U.S.C. 346a(d)(4)). Here, 
EPA responded by issuing an order under section 408(d)(4)(iii) denying 
the petition. (72 FR 68622 (December 5, 2007)).
    Orders issued under section 408(d)(4)(iii) are subject to a 
statutorily-created administrative review process. (21 U.S.C. 
346a(g)(2)). Any person may file objections to a section 408(d)(4)(iii) 
order with EPA and request a hearing on those objections. (Id.). EPA is 
required by section 408(g)(2)(C) to issue a final order resolving the 
objections to the section 408(d)(4)(iii) order. (21 U.S.C. 
346a(g)(2)(C)).

III. Statutory and Regulatory Background

    In this Unit, EPA provides background on the relevant statutes and 
regulations governing NRDC's objections and requests for hearing as 
well as on pertinent Agency policies and practices. As noted, NRDC's 
objections and requests for hearing raise two main claims: (1) that EPA 
has unlawfully failed to retain the full tenfold safety factor for the 
protection of infants and children; and (2) that it was unlawful for 
EPA to rely on a toxicity study for DDVP that was conducted with 
humans. The children's safety factor claim is based on assertions 
regarding DDVP's potential endocrine effects and the adequacy of EPA's 
data and risk assessments pertaining to exposure to DDVP in food as a 
result of the use of DDVP (and similar pesticides) in agriculture or 
food storage and through use of DDVP in residential settings. The human 
studies claim involves a challenge to the EPA regulation governing 
reliance on human studies as well as to EPA's application of that rule 
to a particular human study. The human study in question measured 
cholinesterase inhibition in humans resulting from administration of 
DDVP. Background information on each of these topics is included in 
this Unit.
    Unit III.A. summarizes the requirements and procedures in section 
408 of the FFDCA and applicable regulations pertaining to pesticide 
tolerances, including the procedures for petitioning for revocation of 
tolerances and challenging the denial of such petitions and the 
substantive standards for evaluating the safety of pesticide 
tolerances. This unit also discusses the closely-related statute under 
which EPA regulates the sale, distribution, and use of pesticides, the 
Federal Insecticide, Fungicide, and Rodenticide Act (``FIFRA''), (7 
U.S.C. 136 et seq.).
    Unit III.B. provides an overview of EPA's risk assessment process. 
It contains an explanation of how EPA identifies the hazards posed by 
pesticides, how EPA determines the level of exposure to pesticides that 
pose a concern (``level of concern''), how EPA measures human exposure 
to pesticides, and how hazard, level of concern conclusions, and human 
exposure estimates are combined to evaluate risk. Further, this unit 
presents background information on two Agency policies with particular 
relevance to this action, EPA's policy with regard to the statutory 
safety factor for the protection of infants and children and its policy 
with regard to cholinesterase inhibition.
    Unit III.C. summarizes EPA's program for implementing the statutory 
requirement to screen pesticides for potential endocrine effects. Unit 
III.D. describes the EPA regulation on use of human studies.

A. FFDCA/FIFRA and Applicable Regulations

    1. In general. 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''). Section 408 was substantially rewritten by the 
Food Quality Protection Act of 1996 (``FQPA''), which added the 
provisions discussed below establishing a detailed safety standard for 
pesticides, additional protections for infants and children, and the 
estrogenic substances screening program. (Public Law 104-170, 110 Stat. 
1489 (1996)).
    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)).
    2. Safety standard for pesticide tolerances. 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

[[Page 42685]]

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(b)(2)(D) directs EPA, in making a safety determination, to:
    consider, among other relevant factors- ...
    (v) available information concerning the cumulative effects of 
such residues and other substances that have a common mechanism of 
toxicity;
    (vi) 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 
exposure from other non-occupational sources;
    (viii) such information as the Administrator may require on 
whether the pesticide chemical may have an effect in humans that is 
similar to an effect produced by a naturally occurring estrogen or 
other endocrine effects. ...

(21 U.S.C. 346a(b)(2)(D)(v), (vi) and (viii)).

    EPA must also consider, in evaluating the safety of tolerances, 
``safety factors which . . . are generally recognized as appropriate 
for the use of animal experimentation data.'' (21 U.S.C. 
346a(b)(2)(D)(ix).
    Risks to infants and children are given special consideration. 
Specifically, section 408(b)(2)(C) states that EPA:

    shall assess the risk of the pesticide chemical based on-- ...
    (II) available information concerning the special susceptibility 
of infants and children to the pesticide chemical residues, 
including neurological differences between infants and children and 
adults, and effects of in utero exposure to pesticide chemicals; and
    (III) available information concerning the cumulative effects on 
infants and children of such residues and other substances that have 
a common mechanism of toxicity. ...

(21 U.S.C. 346a(b)(2)(C)(i)(II) and (III)).

    This provision also creates a presumptive additional safety factor 
for the protection of infants and children. Specifically, it directs 
that ``[i]n the case of threshold effects, ... 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 order as the ``children's safety factor.''
    3. Procedures for establishing, amending, or revoking tolerances. 
Tolerances are established, amended, or revoked by rulemaking under the 
unique procedural framework set forth in the FFDCA. Generally, a 
tolerance rulemaking is initiated by the party seeking to establish, 
amend, or revoke a 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 and requests public comment. (21 U.S.C. 
346a(d)(3)). After reviewing the petition, and any comments received on 
it, EPA may issue a final rule establishing, amending, or revoking the 
tolerance, issue a proposed rule to do the same, or deny the petition. 
(21 U.S.C. 346a(d)(4)).
    Once EPA takes final action on the petition by either establishing, 
amending, or revoking the tolerance or denying the petition, any person 
may file objections with EPA and seek an evidentiary hearing on those 
objections. (21 U.S.C. 346a(g)(2)). Objections and hearing requests 
must be filed within 60 days. (Id.). The statute provides that EPA 
shall ``hold a public evidentiary hearing if and to the extent the 
Administrator determines that such a public hearing is necessary to 
receive factual evidence relevant to material issues of fact raised by 
the objections.'' (21 U.S.C. 346a(g)(2)(B). EPA regulations make clear 
that hearings will only be granted where it is shown that there is ``a 
genuine and substantial issue of fact,'' the requestor has identified 
evidence ``which, if established, resolve one or more of such issues in 
favor of the requestor,'' and the issue is ``determinative'' with 
regard to the relief requested. (40 CFR 178.32(b)). EPA's final order 
on the objections is subject to judicial review. (21 U.S.C. 
346a(h)(1)).
    4. Tolerance reassessment and FIFRA reregistration. The FQPA 
required that EPA reassess the safety of all pesticide tolerances 
existing at the time of its enactment. (21 U.S.C. 346a(q)). EPA was 
given 10 years to reassess the approximately 10,000 tolerances in 
existence in 1996. In this reassessment, EPA was required to review 
existing pesticide tolerances under the new ``reasonable certainty that 
no harm will result'' standard set forth in section 408(b)(2)(A)(i). 
(21 U.S.C. 346a(b)(2)(A)(i)). This reassessment was substantially 
completed by the August 3, 2006 deadline. Tolerance reassessment was 
generally handled in conjunction with a similar program involving 
reregistration of pesticides under FIFRA. (7 U.S.C. 136a-1). 
Reassessment and reregistration decisions were generally combined in a 
document labeled a Reregistration Eligibility Decision (``RED'').
    5. Estrogenic substances screening program. The FQPA also imposed 
requirements regarding creation of an estrogenic substances screening 
program. Section 408(p) gives EPA 2 years from enactment of the FQPA to 
``develop a screening program ... to determine whether [pesticide 
chemicals and certain other substances] may have an effect in humans 
that is similar to an effect produced by a naturally occurring 
estrogen, or such other endocrine effect as the Administrator may 
designate.'' (21 U.S.C. 346a(p)(1)). This screening program must use 
``appropriate validated test systems and scientifically relevant 
information.'' (Id.). Once the program is developed, EPA is required to 
take public comment and seek independent scientific review of it. 
Following the period for public comment and scientific review, and not 
later than 3 years following enactment of the FQPA, EPA is directed to 
``implement the program.'' (21 U.S.C. 346a(p)(2)).
    The scope of the estrogenic screening program was expanded by an 
amendment to the Safe Drinking Water Act (``SDWA'') passed 
contemporaneously with the FQPA. That amendment gave EPA the authority 
to provide for the testing, under the FQPA estrogenic screening 
program, ``of any other substance that may be found in sources of 
drinking water if the Administrator determines that a substantial 
population may be exposed to such substance.'' (42 U.S.C. 300j-17).

B. EPA Risk Assessment for Tolerances--Policy and Practice

    1. The safety determination - risk assessment. To assess risk of a 
pesticide tolerance, EPA combines information on pesticide toxicity 
with information regarding the route, magnitude, and duration of 
exposure to the pesticide. The risk assessment process involves four 
distinct steps: (1) Identification of the toxicological hazards posed 
by a pesticide; (2) determination of the ``level of concern'' with 
respect to human exposure to the pesticide; (3) estimation of human 
exposure to the pesticide; and (4) characterization of risk posed to 
humans by the pesticide based on comparison of human exposure to the 
level of concern.
    a. Hazard identification. In evaluating toxicity or hazard, EPA 
reviews toxicity studies, primarily in laboratory animals,

[[Page 42686]]

to identify any adverse effects on the test subjects. Animal studies 
typically involve investigating a broad range of endpoints including 
gross and microscopic effects on organs and tissues, functional effects 
on bodily organs and systems, effects on blood parameters (such as red 
blood cell count, hemoglobin concentration, hematocrit, and a measure 
of clotting potential), effects on the concentrations of normal blood 
chemicals (including glucose, total cholesterol, urea nitrogen, 
creatinine, total protein, total bilirubin, albumin, hormones, and 
enzymes such as alkaline phosphatase, alanine aminotransfersase and 
cholinesterases), and behavioral or other gross effects identified 
through clinical observation and measurement. EPA examines whether 
adverse effects are caused by either short-term (e.g., ``acute'') or 
longer-term (e.g., ``chronic'') pesticide exposure and the effects of 
pre-natal and post-natal exposure in animals.
    EPA also considers whether the adverse effect has a threshold - a 
level below which exposure has no appreciable chance of causing the 
adverse effect. For non-threshold effects, EPA assumes that any 
exposure to the substance increases the risk that the adverse effect 
may occur. At present, EPA only considers one adverse effect, the 
chronic effect of cancer, to potentially be a non-threshold effect. 
(Ref. 4 at 8-9). Not all carcinogens, however, pose a risk at any 
exposure level (i.e., ``a non-threshold effect or risk''). Advances in 
the understanding of the mode of action of carcinogenesis have 
increasingly led EPA to conclude that some pesticides that cause 
carcinogenic effects in animal studies only cause such effects above a 
certain threshold of exposure. EPA has traditionally considered non-
cancer adverse effects on the endocrine system to be threshold effects; 
that determination is being reexamined in conjunction with the 
endocrine disruptor screening program.
    b. Level of concern/dose-response analysis. Once a pesticide's 
potential hazards are identified, EPA determines a toxicological level 
of concern for evaluating the risk posed by human exposure to the 
pesticide. In this step of the risk assessment process, EPA essentially 
evaluates the levels of exposure to the pesticide at which effects 
might occur. An important aspect of this determination is assessing the 
relationship between exposure (dose) and response (often referred to as 
the dose-response analysis). EPA follows differing approaches to 
identifying a level of concern for threshold and non-threshold hazards.
    i. Threshold effects. In examining the dose-response relationship 
for a pesticide's threshold effects, EPA evaluates an array of toxicity 
studies on the pesticide. In each of these studies, EPA attempts to 
identify the lowest observed adverse effect level (``LOAEL'') and the 
next lower dose at which there are no observed adverse affect levels 
(``NOAEL''). Generally, EPA will use the lowest NOAEL from the 
available studies as a starting point (called ``the Point of 
Departure'') in estimating the level of concern for humans. (Ref. 4 at 
9 (The Point of Departure ``is simply the toxic dose that serves as the 
`starting point' in extrapolating a risk to the human population.'')). 
At times, however, EPA will use a LOAEL from a study as the Point of 
Departure when no NOAEL is identified in that study and the LOAEL is 
close to, or lower than, other relevant NOAELs. The Point of Departure 
is in turn used in choosing a level of concern. EPA will make separate 
determinations as to the Points of Departure, and correspondingly 
levels of concern, for both short and long exposure periods as well as 
for the different routes of exposure (oral, dermal, and inhalation).
    In estimating and describing the level of concern, the Point of 
Departure is at times used differently depending on whether the risk 
assessment addresses dietary or non-dietary exposures. For dietary 
risks, EPA uses the Point of Departure to calculate an acceptable level 
of exposure or reference dose (``RfD''). The RfD is calculated by 
dividing the Point of Departure by all applicable safety or uncertainty 
factors. Typically, EPA uses a baseline safety/uncertainty factor equal 
to 100. That value includes a factor of ten (``10X'') where EPA is 
using data from laboratory animals to reflect potentially greater 
sensitivity in humans than animals and a factor of 10X to account for 
potential variations in sensitivity among members of the human 
population as well as other unknowns. Additional safety factors may be 
added to address data deficiencies or concerns raised by the existing 
data. 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. This FQPA additional 
safety factor largely replaces pre-FQPA EPA practice regarding 
additional safety factors. (Ref. 5 at 4-11).
    In implementing FFDCA section 408, EPA's Office of Pesticide 
Programs, also calculates a variant of the RfD referred to as a 
Population Adjusted Dose (``PAD''). A PAD is the RfD divided by any 
portion of the FQPA safety factor that does not correspond to one of 
the traditional additional safety factors used in general Agency risk 
assessments. (Ref. 5 at 13-16). The reason for calculating PADs is so 
that other parts of the Agency, which are not governed by FFDCA section 
408, can, when evaluating the same or similar substances, easily 
identify which aspects of a pesticide risk assessment are a function of 
the particular statutory commands in FFDCA section 408. Today, RfDs and 
PADs are generally calculated for both acute and chronic dietary risks 
although traditionally a RfD or PAD was only calculated for chronic 
dietary risks. Throughout this document general references to EPA's 
calculated safe dose are denoted as a RfD/PAD.
    For non-dietary, and combined dietary and non-dietary, risk 
assessments of threshold effects, the toxicological level of concern is 
not expressed as a RfD/PAD but rather in terms of an acceptable (or 
``target'') margin of exposure (``MOE'') between human exposure and the 
Point of Departure. The ``margin'' of interest is the ratio between 
human exposure and the Point of Departure which is calculated by 
dividing human exposure into the Point of Departure. An acceptable MOE 
is generally considered to be a margin at least as high as the product 
of all applicable safety factors for a pesticide. For example, if a 
pesticide needs a 10X factor to account for inter-species differences, 
10X factor for intra-species differences, and 10X factor for the FQPA 
children's safety provision, the safe or target MOE would be a MOE of 
at least 1,000. What that means is that for the pesticide to meet the 
safety standard, human exposure to the pesticide would have to be at 
least 1,000 times smaller than the Point of Departure. Like RfD/PADs, 
specific target MOEs are selected for exposures of different durations. 
For non-dietary exposures, EPA typically examines short-term, 
intermediate-term, and long-term exposures. Additionally, target MOEs 
may be selected based on both the duration of exposure and the various 
routes of non-dietary exposure - dermal, inhalation, and oral.
    ii. Non-threshold effects. For risk assessments for non-threshold 
effects, EPA does not use the RfD/PAD or MOE approach to choose a level 
of concern if quantification of the risk is deemed appropriate. Rather, 
EPA calculates the slope of the dose-response curve for the non-
threshold effects from relevant studies using a linear, low-dose 
extrapolation model that assumes that any amount of exposure will lead 
to some degree of risk. This dose-response

[[Page 42687]]

analysis will be used in the risk characterization stage to estimate 
the risk to humans of the non-threshold effect. Linear, low-dose 
extrapolation is typically used as the default approach for estimating 
the risk to carcinogens, unless there are mode of action data 
indicating a threshold response (or nonlinearity).
    c. Estimating human exposure. Risk is a function of both hazard and 
exposure. Thus, equally important to the risk assessment process as 
determining the hazards posed by a pesticide and the toxicological 
level of concern for those hazards is estimating human exposure. Under 
FFDCA section 408, EPA is concerned not only with exposure to pesticide 
residues in food but also exposure resulting from pesticide 
contamination of drinking water supplies and from use of pesticides in 
the home or other non-occupational settings. (See 21 U.S.C. 
346a(b)(2)(D)(vi)).
    i. Exposure from food. There are two critical variables in 
estimating exposure in food: (1) The types and amount of food that is 
consumed; and (2) the residue level in that food. Consumption is 
estimated by EPA based on scientific surveys of individuals' food 
consumption in the United States conducted by the USDA. (Ref. 4 at 12). 
Information on residue values comes from a range of sources including 
crop field trials, data on pesticide reduction (or concentration) due 
to processing, cooking, and other practices, information on the extent 
of usage of the pesticide, and monitoring of the food supply. (Id. at 
17).
    In assessing exposure from pesticide residues in food, EPA, for 
efficiency's sake, follows a tiered approach in which it, in the first 
instance, assesses exposure using the worst case assumptions that 100 
percent of the crop in question is treated with the pesticide and 100 
percent of the food from that crop contains pesticide residues at the 
tolerance level. (Id. at 11). When such an assessment shows no risks of 
concern, a more complex risk assessment is unnecessary. By avoiding a 
more complex risk assessment, EPA's resources are conserved 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.''
    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. 
(70 FR 46706, 46731 (August 10, 2005)). Second, the tolerance value 
represents a high end or worst case value. Tolerance values are chosen 
only after EPA has evaluated data from experimental crop field trials 
in which the pesticide has been used in a manner, consistent with the 
draft FIFRA label, that is likely to produce the highest residue in the 
crop in question (e.g., maximum application rate, maximum number of 
applications, minimum pre-harvest interval between last pesticide 
application and harvest). (Refs. 4 and 6). These crop field trials are 
generally conducted in several fields at several geographical 
locations. (Id. at 5, 7 and Tables 1 and 5). Several samples are then 
gathered from each field and analyzed. (Id. at 53). Generally, the 
results from such field trials show that the residue levels for a given 
pesticide use will vary from as low as non-detectable to measurable 
values in the parts per million (``ppm'') range with the majority of 
the values falling at the lower part of the range. (70 FR at 46731). 
EPA uses a statistical procedure to analyze the field trial results and 
identify the upper bound of expected residue values. This upper bound 
value is used as the tolerance value. (Ref. 7). There may be some 
commodities from a treated crop that approach the tolerance value where 
the maximum label rates are followed, but most generally fall 
significantly below the tolerance value. If less than the maximum legal 
rate is applied, residues will be even lower. Third, residue values 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.
    EPA uses several techniques to refine residue value estimates. 
(Ref. 4 at 17-28). First, where appropriate, EPA will take into account 
all the residue values reported in the crop field trials, either 
through use of an average or individually. Second, EPA will consider 
data showing what portion of the crop is not treated with the 
pesticide. Third, data can be produced showing pesticide degradation 
and decline over time, and the effect of commercial and consumer food 
handling and processing practices. Finally, EPA can consult monitoring 
data gathered by the FDA, the USDA, or pesticide registrants, on 
pesticide levels in food at points in the food distribution chain 
distant from the farm, including retail food establishments.
    Another critical component of the exposure assessment is how data 
on consumption patterns are combined with data on pesticide residue 
levels in food. Traditionally, EPA has calculated exposure by simply 
multiplying average consumption by average residue values for 
estimating chronic risks and high-end consumption by maximum residue 
values for estimating acute risks. Using average residues is a 
realistic approach for chronic risk assessment due to the fact that 
variations in residue levels and consumption amounts average out over 
time. Using average values is inappropriate for acute risk assessments, 
however, because in assessing acute exposure situations it matters how 
much of each treated food a given consumer eats and what the residue 
levels are in the particular foods consumed. Yet, using maximum residue 
values for acute risk assessment tends to greatly overstate exposure 
because it is unlikely that a person would consume at a single meal 
multiple food components bearing high-end residues. To take into 
account the variations in short-term consumption patterns and food 
residue values for acute risk assessments, EPA has more recently begun 
using probabilistic modeling techniques for estimating exposure when 
more simplistic models appear to show risks of concerns.
    All of these refinements to the exposure assessment process, from 
use of food monitoring data through probabilistic modeling, can have 
dramatic effects on the level of exposure predicted, reducing worst 
case estimates by 1 or 2 orders of magnitude or more. (Ref. 8 at 16-17; 
70 FR 46706, 46732 (August 10, 2005).
    ii. Exposure from water. EPA may use either or both field 
monitoring data and mathematical water exposure models to generate 
pesticide exposure estimates in drinking water. Monitoring and modeling 
are both important tools for estimating pesticide concentrations in 
water and can provide different types of information. Monitoring data 
can provide estimates of pesticide concentrations in water that are 
representative of specific agricultural or residential pesticide 
practices and under environmental conditions associated with a sampling 
design. Although monitoring data can provide a

[[Page 42688]]

direct measure of the concentration of a pesticide in water, it does 
not always provide a reliable estimate of exposure because sampling may 
not occur in areas with the highest pesticide use, and/or the sampling 
may not occur when the pesticides are being used.
    In estimating pesticide exposure levels in drinking water, EPA most 
frequently uses mathematical water exposure models. EPA's models are 
based on extensive monitoring data and detailed information on soil 
properties, crop characteristics, and weather patterns. (69 FR 30042, 
30058-30065 (May 26, 2004)). These models calculate estimated 
environmental concentrations of pesticides using laboratory data that 
describe how fast the pesticide breaks down to other chemicals and how 
it moves in the environment. These concentrations can be estimated 
continuously over long periods of time, and for places that are of most 
interest for any particular pesticide. Modeling is a useful tool for 
characterizing vulnerable sites, and can be used to estimate peak 
concentrations from infrequent, large storms.
    iii. Residential exposures. Generally, in assessing residential 
exposure to pesticides EPA relies on its Residential Standard Operating 
Procedures (``SOPs''). (Ref. 9). The SOPs establish models for 
estimating application and post-application exposures in a residential 
setting where pesticide-specific monitoring data are not available. 
SOPs have been developed for many common exposure scenarios including 
pesticide treatment of lawns, garden plants, trees, swimming pools, 
pets, and indoor surfaces including crack and crevice treatments. The 
SOPs are based on existing monitoring and survey data including 
information on activity patterns, particularly for children. Where 
available, EPA relies on pesticide-specific data in estimating 
residential exposures.
    d. Risk characterization. The final step in the risk assessment is 
risk characterization. In this step, EPA combines information from the 
first three steps (hazard identification, level of concern/dose-
response analysis, and human exposure assessment) to quantitatively 
estimate the risks posed by a pesticide. Separate characterizations of 
risk are conducted for different durations of exposure. Additionally, 
separate and, where appropriate, aggregate characterizations or risk 
are conducted for the different routes of exposure (dietary and non-
dietary).
    For threshold risks, EPA estimates risk in one of two ways. Where 
EPA has calculated a RfD/PAD, risk is estimated by expressing human 
exposure as a percentage of the RfD/PAD. Exposures lower than 100 
percent of the RfD/PAD are generally not of concern. Alternatively, EPA 
may express risk by comparing the MOE between estimated human exposure 
and the Point of Departure with the acceptable or target MOE. As 
described above, the acceptable or target MOE is the product of all 
applicable safety factors. To calculate the actual MOE for a pesticide, 
estimated human exposure to the pesticide is divided into the Point of 
Departure. In contrast to the RfD/PAD approach, the higher the MOE, the 
safer the pesticide. Accordingly, if the target MOE for a pesticide is 
100, MOEs equal to or exceeding 100 would generally not be of concern.
    As a conceptual matter, the RfD/PAD and MOE approaches are 
fundamentally equivalent. For a given risk and given exposure of a 
pesticide, if exposure to a pesticide were found to be acceptable under 
an RfD/PAD analysis it would also pass under the MOE approach, and 
vice-versa. However, for any specific pesticide, risk assessments for 
different exposure durations or routes may yield different results. 
This is a function not of the choice of the RfD/PAD or MOE approach but 
of the fact that the levels of concern and the levels of exposure may 
differ depending on the duration and route of exposure.
    For non-threshold risks (generally, cancer risks), EPA uses the 
slope of the dose-response curve for a pesticide in conjunction with an 
estimation of human exposure to that pesticide to estimate the 
probability of occurrence of additional adverse effects. For non-
threshold cancer risks, EPA generally considers cancer risk to be 
negligible if the probability of increased cancer cases falls within 
the range of 1 in 1 million. Risks exceeding values within that range 
would raise a risk concern.
    2. EPA policy on the children's safety factor. As the above brief 
summary of EPA's risk assessment practice indicates, the use of safety 
factors plays a critical role in the process. This is true for 
traditional 10X safety factors to account for potential differences 
between animals and humans when relying on studies in animals (inter-
species safety factor) and potential differences among humans (intra-
species safety factor) as well as the FQPA's additional 10X children's 
safety factor.
    In applying the children's safety factor provision, EPA has 
interpreted it as imposing a presumption in favor of applying an 
additional 10X safety factor. (Ref. 5 at 4, 11). Thus, EPA generally 
refers to the additional 10X factor as a presumptive or default 10X 
factor. EPA has also made clear, however, that this presumption or 
default in favor of the additional 10X is only a presumption. The 
presumption can be overcome if reliable data demonstrate that a 
different factor is safe for children. (Id.). In determining whether a 
different factor is safe for children, EPA focuses on the three factors 
listed in section 408(b)(2)(C) - the completeness of the toxicity 
database, the completeness of the exposure database, and potential pre- 
and post-natal toxicity. In examining these factors, EPA strives to 
make sure that its choice of a safety factor, based on a weight-of-the-
evidence evaluation, does not understate the risk to children. (Id. at 
24-25, 35).
    3. EPA policy on cholinesterase inhibition as a regulatory 
endpoint. Cholinesterase inhibition is a disruption of the normal 
process in the body by which the nervous system chemically communicates 
with muscles and glands. Communication between nerve cells and a target 
cell (i.e., another nerve cell, a muscle fiber, or a gland) is 
facilitated by the chemical, acetylcholine. When a nerve cell is 
stimulated it releases acetylcholine into the synapse (or space) 
between the nerve cell and the target cell. The released acetylcholine 
binds to receptors in the target cell, stimulating the target cell in 
turn. As EPA has explained, ``the end result of the stimulation of 
cholinergic pathway(s) includes, for example, the contraction of smooth 
(e.g., in the gastrointestinal tract) or skeletal muscle, changes in 
heart rate or glandular secretion (e.g., sweat glands) or communication 
between nerve cells in the brain or in the autonomic ganglia of the 
peripheral nervous system.'' (Ref. 10 at 10).
    Acetylcholinesterase is an enzyme that breaks down acetylcholine 
and terminates its stimulating action in the synapse between nerve 
cells and target cells. When acetylcholinesterase is inhibited, 
acetylcholine builds up prolonging the stimulation of the target cell. 
This excessive stimulation potentially results in a broad range of 
adverse effects on many bodily functions including muscle cramping or 
paralysis, excessive glandular secretions, or effects on learning, 
memory, or other behavioral parameters. Depending on the degree of 
inhibition these effects can be serious, even fatal.
    EPA's cholinesterase inhibition policy statement explains EPA's 
approach to evaluating the risks posed by cholinesterase-inhibiting 
pesticides such as DDVP. (Ref. 10). The policy focuses on three types 
of effects associated with cholinesterase-

[[Page 42689]]

inhibiting pesticides that may be assessed in animal and human 
toxicological studies: (1) Physiological and behavioral/functional 
effects; (2) cholinesterase inhibition in the central and peripheral 
nervous system; and (3) cholinesterase inhibition in red blood cells 
and blood plasma. The policy discusses how such data should be 
integrated in deriving an acceptable dose (RfD/PAD) for a 
cholinesterase-inhibiting pesticide.
    Clinical signs or symptoms of cholinesterase inhibition in humans, 
the policy concludes, provide the most direct evidence of the adverse 
consequences of exposure to cholinesterase-inhibiting pesticides. 
Nonetheless, as the policy notes, due to strict ethical limitations, 
studies in humans are ``quite limited.'' (Id. at 19). Although animal 
studies can also provide direct evidence of cholinesterase inhibition 
effects, animal studies cannot easily measure cognitive effects of 
cholinesterase inhibition such as effects on perception, learning, and 
memory. For these reasons, the policy recommends that ``functional data 
obtained from human and animal studies should not be relied on solely, 
to the exclusion of other kinds of pertinent information, when weighing 
the evidence for selection of the critical effect(s) that will be used 
as the basis of the RfD or RfC.'' (Id. at 20).
    After clinical signs or symptoms, cholinesterase inhibition in the 
nervous system provides the next most important endpoint for evaluating 
cholinesterase-inhibiting pesticides. Although cholinesterase 
inhibition in the nervous system is not itself regarded as a direct 
adverse effect, it is ``generally accepted as a key component of the 
mechanism of toxicity leading to adverse cholinergic effects.'' (Id. at 
25). As such, the policy states that it should be treated as ``direct 
evidence of potential adverse effects'' and ``data showing this 
response provide valuable information in assessing potential hazards 
posed by anticholinesterase pesticides.'' (Id.). Unfortunately, useful 
data measuring cholinesterase inhibition in the central and peripheral 
nervous systems has only been relatively rarely captured by standard 
toxicology testing, particularly as to peripheral nervous system 
effects. For central nervous system effects, however, more recent 
neurotoxicity studies ``have sought to characterize the time course of 
inhibition in ... [the] brain, including brain regions, after acute and 
90-day exposures.'' (Id. at 27).
    Cholinesterase inhibition in the blood is one step further removed 
from the direct harmful consequences of cholinesterase-inhibiting 
pesticides. According to the policy, inhibition of blood 
cholinesterases ``is not an adverse effect, but may indicate a 
potential for adverse effects on the nervous system.'' (Id. at 28). The 
policy states that ``[a]s a matter of science policy, blood 
cholinesterase data are considered appropriate surrogate measures of 
potential effects on peripheral nervous system acetylcholinesterase 
activity in animals, for central nervous system (``CNS'') 
acetylcholinesterase activity in animals when CNS data are lacking and 
for both peripheral and central nervous system acetylcholinesterase in 
humans.'' (Id. at 29). The policy notes that ``there is often a direct 
relationship between a greater magnitude of exposure [to a 
cholinesterase-inhibiting pesticide] and an increase in incidence and 
severity of clinical signs and symptoms as well as blood cholinesterase 
inhibition.'' (Id. at 30). Thus, the policy regards blood 
cholinesterase data as ``appropriate endpoints for derivation of 
reference doses or concentrations when considered in a weight-of-the-
evidence analysis of the entire database ....'' (Id. at 29). Between 
cholinesterase inhibition measured in red blood cell (``RBC'') or blood 
plasma, the policy states a preference for reliance on RBC 
acetylcholinesterase measurements because plasma is composed of a 
mixture of acetylcholinesterase and butyrylcholinesterase, and 
inhibition of the latter is less clearly tied to inhibition of 
acetylcholinesterase in the nervous system. (Id. at 29, 32).
    If a measure of cholinesterase inhibition (e.g., RBC 
cholinesterase) is being considered as a potential adverse effect or 
surrogate for an adverse effect, the policy advises that the level of 
inhibition must be critically evaluated ``in the context of both 
statistical and biological significance.'' (Id. at 37) (emphasis in 
Original). The policy notes that ``[n]o fixed percentage of change 
(e.g., 20% for cholinesterase enzyme inhibition) is predetermined to 
separate adverse from non-adverse effects.'' (Id.). Rather, the policy 
explains that ``OPP's experience with the review of toxicity studies 
with cholinesterase-inhibiting substances shows that differences 
between pre- and post-exposure of 20% or more in enzyme levels is 
nearly always statistically significant and would generally be viewed 
as biologically significant.'' (Id. at 37-38). The policy recommends 
that ``[t]he biological significance of statistically-significant 
changes of less than 20% would have to be judged on a case-by-case 
basis, noting, in particular the pattern of changes in the enzyme 
levels and the presence or absence of accompanying clinical signs and/
or symptoms.'' (Id. at 38). The policy notes that similar or higher 
levels of cholinesterase inhibition are used ``in monitoring workers 
for occupational exposures (even in the absence of signs, symptoms, or 
other behavioral effects).'' (Id. at 31). For example, the policy 
points out that the California Department of Health Services requires 
that workers exposed to toxic chemicals such as organophosphate 
pesticides be removed from the workplace if ``red blood cell 
cholinesterase levels show 30% or greater inhibition,'' and that the 
World Health Organization ``has guidelines with the same RBC action 
levels (i.e., 30% or greater inhibition).'' (Id.).

C. Endocrine Disruptor Screening Program

    The 1996 FQPA and SWDA amendments directed EPA to develop and 
implement an endocrine screening program. To aid in the design of this 
program called for in the FQPA and SDWA amendments, EPA created the 
Endocrine Disruptor Screening and Testing Advisory Committee 
(``EDSTAC''), which was comprised of members representing the 
commercial chemical and pesticides industries, federal and state 
agencies, worker protection and labor organizations, environmental and 
public health groups, and research scientists. (63 FR 71542, 71544, 
Dec. 28, 1998). The EDSTAC presented a comprehensive report in August 
1998 addressing both the scope and elements of the endocrine screening 
program. (Ref. 11). The EDSTAC's recommendations were largely adopted 
by EPA.
    As recommended by EDSTAC, EPA expanded the scope of the program 
from focusing only on estrogenic effects to include other effects on 
the endocrine system (i.e., androgenic and thyroid effects). (63 FR at 
71545). Further, EPA, again on the EDSTAC's recommendation, chose to 
include both human and ecological effects in the program. (Id.). 
Finally, based on EDSTAC's recommendation, EPA established the universe 
of chemicals to be screened to include not just pesticides but also a 
wide range of other chemical substances. (Id.). As to the program 
elements, EPA adopted EDSTAC's recommended two-tier approach with the 
first tier involving screening ``to identify substances that have the 
potential to interact with the endocrine system'' and the second tier 
involving testing ``to determine whether the substance causes adverse 
effects,

[[Page 42690]]

identify the adverse effects caused by the substance, and establish a 
quantitative relationship between the dose and the adverse effect.'' 
(Id.). Tier 1 screening is limited to evaluating whether a substance is 
``capable of interacting with'' the endocrine system, and is ``not 
sufficient to determine whether a chemical substance may have an effect 
in humans that is similar to an effect produced by naturally occurring 
hormones.'' (Id. at 71550). Based on the results of Tier 1 screening, 
EPA will decide whether Tier 2 testing is needed. Importantly, ``[t]he 
outcome of Tier 2 is designed to be conclusive in relation to the 
outcome of Tier 1 and any other prior information. Thus, a negative 
outcome in Tier 2 will supersede a positive outcome in Tier 1.'' (Id. 
at 71554-71555).
    The EDSTAC provided detailed recommendations for Tier 1 screening 
and Tier 2 testing. The panel of the EDSTAC that devised these 
recommendations was comprised of distinguished scientists from 
academia, government, industry, and the environmental community. (Ref. 
11 at Appendix B). As suggested by the EDSTAC, EPA has proposed a 
battery of short-term in vitro and in vivo assays for the Tier 1 
screening exercise. (63 FR at 71550-71551). Validation of all but one 
of these assays is complete. As to Tier 2 testing, EPA, on the 
recommendation of the EDSTAC, has proposed using five longer-term 
reproduction studies that, with one exception, ``are routinely 
performed for pesticides with widespread outdoor exposures that are 
expected to affect reproduction.'' (Id. at 71555). EPA is examining, 
pursuant to the suggestion of the EDSTAC, modifications to these 
studies to enhance their ability to detect endocrine effects.
    EPA has published a draft list of the first group of chemicals that 
will be tested under the Agency's endocrine disruptor screening 
program. (72 FR 33486 (June 18, 2007)). The draft list was produced 
based solely on the exposure potential of the chemicals and EPA has 
emphasized that ``[n]othing in the approach for generating the initial 
list provides a basis to infer that by simply being on this list these 
chemicals are suspected to interfere with the endocrine systems of 
humans or other species, and it would be inappropriate to do so.'' 
(Id.)

D. EPA's Human Research Rule

    EPA decisions regarding the ethics of human studies are governed by 
the Protection for Subjects in Human Research final rule (``Human 
Research rule''), which significantly strengthened and expanded 
protections for subjects of human research. (71 FR 6138 (February 6, 
2006)). The framework of the Human Research rule rests on the basic 
principle that EPA will not, in its actions, rely on data derived from 
unethical research. The rule divides studies involving intentional 
dosing of human subjects into two groups: ``new'' studies - those 
initiated after April 7, 2006 (the effective date of the rule) - and 
``old'' studies - those initiated before April 7, 2006. The Human 
Research Rule forbids EPA from relying on data from any ``new'' study, 
unless EPA has adequate information to determine that the research was 
conducted in substantial compliance with the ethical requirements 
contained therein. (40 CFR. 26.1705). These ethical rules are derived 
primarily from the ``Common Rule,'' (40 CFR part 26), a rule setting 
ethical parameters for studies conducted or supported by the federal 
government. In addition to requiring informed consent and protection of 
the safety of the subjects, among other things, the rule specifies that 
``[r]isks to subjects [must be] reasonable in relation to . . . the 
importance of the knowledge that may reasonably be expected to result 
[from the study].'' (40 CFR 26.1111(a)(2)). In other words, a study 
would be judged unethical if it did not have scientific value 
outweighing any risks to the test subjects.
    As to ``old'' studies, the Human Research Rule forbids EPA from 
relying on such data if there is clear and convincing evidence that the 
conduct of the research was fundamentally unethical or significantly 
deficient with respect to the ethical standards prevailing at the time 
the research was conducted. (40 CFR 26.1704). EPA has indicated that in 
evaluating ``the ethical standards prevailing at the time the research 
was conducted'' it will consider the Nuremburg Code, various editions 
of the Declaration of Helsinki, the Belmont Report, and the Common 
Rule, as among the standards that may be applicable to any particular 
study. (71 FR at 6161). Further, reflecting the concern that 
scientifically invalid data are ``always unethical,'' (71 FR at 6160), 
the rule limits the human research that can be relied upon by EPA to 
``scientifically valid and relevant data.'' (40 CFR 26.1701).
    Whether the data are ``new'' or ``old,'' the Human Research rule 
forbids EPA from relying on data from any study involving intentional 
exposure of pregnant women, fetuses, or children subject to a very 
limited exception. (40 CFR 26.1703, 1706).
    To aid EPA in making scientific and ethical determinations under 
the Human Research rule, the rule established an independent Human 
Studies Review Board (``HSRB'') to review both proposals for new 
research (``new'' studies) and reports of completed human research 
(``old'' studies) on which EPA proposes to rely. (40 CFR 26.1603). The 
rule directs that HSRB shall be comprised of non-EPA employees ``who 
have expertise in fields appropriate for the scientific and ethical 
review of human research, including research ethics, biostatistics, and 
human toxicology.'' (40 CFR 26.1603(a)). If EPA decides to rely on the 
results from ``old'' research conducted to identify or measure a toxic 
effect, EPA must submit the results of its assessment to the HSRB for 
evaluation of the ethical and scientific merit of the research. (40 CFR 
26.1602(b)(2)).
    EPA has established the HSRB as a federal advisory committee under 
the Federal Advisory Committee Act (``FACA'') to take advantage of 
``the benefits of the transparency and opportunities for public 
participation'' that accompany a FACA committee. (71 FR at 6156). The 
HSRB, as appointed by EPA, contains approximately 16 distinguished 
experts in the fields of bioethics, biostatistics, human health risk 
assessment and human toxicology, primarily from academia. (Ref. 12).
    NRDC and other parties have challenged the legality of the Human 
Research rule. (NRDC v. U.S. EPA, No. 06-0820-ag (2d Cir.)). A decision 
on this challenge is presently pending before the United States Court 
of Appeals for the Second Circuit.

IV. Regulatory History of DDVP

A. In General

    1. DDVP use. Dichlorvos (2, 2-dichlorovinyl dimethyl phosphate), 
also known as DDVP, is an insecticide used in controlling flies, 
mosquitoes, gnats, cockroaches, fleas, and other insect pests. (Ref. 
3). DDVP is registered for use on agricultural sites; commercial, 
institutional, and industrial sites; and for domestic use in and around 
homes. Agricultural and other commercial uses include in greenhouses; 
mushroom houses; storage areas for bulk, packaged and bagged raw and 
processed agricultural commodities; food manufacturing/processing 
plants; animal premises; and non-food areas of food-handling 
establishments. It is also registered for treatment of cattle, poultry 
and swine. DDVP is not registered for direct use on any field grown 
commodities. Currently, there are 27 tolerances listed in 40 CFR 
180.235 for DDVP on agricultural (food and feed) crops and animal 
commodities. DDVP is

[[Page 42691]]

applied with aerosols, fogging equipment, and spray equipment, and 
through use of impregnated materials such as resin strips which result 
in slow release of the pesticide. The current registrant for the 
technical active ingredient, DDVP, is Amvac Chemical Corporation 
(``Amvac'').
    2. DDVP risks. The following information on the assessment of the 
risks posed by DDVP is drawn from EPA's decision on the reassessment of 
DDVP tolerances and its response to NRDC's petition.
    DDVP is a chlorinated organophosphate pesticide which inhibits 
plasma, RBC, and brain cholinesterase in a variety of species. (Ref. 3 
at 122-123). Subchronic and chronic oral DDVP exposures to rats and 
dogs as well as chronic inhalation DDVP exposure to rats resulted in 
significant decreases in plasma, RBC and/or brain cholinesterase 
activity. However, DDVP does not cause delayed neurotoxicity in the 
hen. Repeated, oral subchronic DDVP exposures in male humans were 
associated with statistically and biologically significant decreases in 
RBC cholinesterase inhibition. There was no evidence of increased 
susceptibility to young animals following in utero DDVP exposure to rat 
and rabbit fetuses as well as pre/post natal DDVP exposure to rats in 
developmental, reproduction, and comparative cholinesterase studies. 
Evidence of sensitivity in the young was seen in one parameter, 
auditory startle amplitude, in a developmental neurotoxicity study; 
however, the effects in the rat pups here was at levels well above 
levels which result in RBC cholinesterase inhibition. Cancer studies 
with DDVP provide suggestive evidence of DDVP's potential human 
carcinogenicity; however, following the advice of numerous independent 
scientific panels, EPA has determined that DDVP poses a negligible 
cancer risk to humans due to the lack of relevance to humans of the 
tumors identified in the DDVP cancer studies. (72 FR at 68671-68673).
    Inhibition of cholinesterase activity was the toxicity endpoint 
selected to assess hazards for all acute and chronic dietary exposures, 
as well as short-, intermediate-, and long-term (chronic) dermal, 
inhalation, and incidental oral residential exposures. Doses selected 
for the Point of Departure in determining the level of concern - i.e., 
RfD/PADs and acceptable MOEs - were based on both human and animal 
studies. (Ref. 3 at 130-135). Animal studies were used in choosing 
levels of concern for evaluating risk from acute and chronic dietary 
exposure; acute dermal exposure; and acute and chronic inhalation 
exposure. A human study was used evaluating risk from short-term 
incidental oral exposure; short-, intermediate-, and long-term dermal 
exposure; and short- and intermediate-term inhalation exposure.
    Safety factor determinations used in selecting the level of concern 
differed based on whether EPA relied on one of several different animal 
studies or a human study. For levels of concerns derived from a Point 
of Departure from an animal study, EPA generally applied a 100X safety 
factor (10X for inter-species variability and 10X for intra-human 
variability). EPA removed the 10X children's safety factor for risk 
assessments based on an animal study. For levels of concerns derived 
from a Point of Departure from the human study, EPA applied a 10X 
safety factor for intra-human variability and a 3X children's safety 
factor. (Id.).
    EPA based its decision to remove the children's safety factor when 
relying on animal data on its conclusions that (1) the toxicity 
database was complete; (2) most of the data indicated no sensitivity in 
the young and the only evidence of sensitivity occurred at levels well 
above the Points of Departure used for establishing the levels of 
concern; and (3) its estimate of human exposure to DDVP was not 
understated. EPA retained a portion of the children's safety factor 
when relying on the human study because that study did not determine a 
NOAEL. EPA concluded, however, that reliable data supported reduction 
of the 10X factor because the effect seen at the LOAEL in that study 
was so marginal that a lower dose would have been unlikely to detect 
any adverse effect. (72 FR 68694-68695).
    EPA has estimated exposure to DDVP taking into account the 
potential for DDVP residues in food, drinking water, and in the home as 
the result of the use of DDVP pest strips. DDVP exposure may result not 
only from use of DDVP but use of two closely-related pesticides, naled 
and trichlorfon, which metabolize or degrade to DDVP in food, water, or 
the environment. In assessing the risks of DDVP, EPA has taken into 
account exposure to DDVP resulting from use of all three of these 
pesticides. (Ref. 3 at 147-149). Additionally, DDVP, naled, and 
trichlorfon are within a family of pesticides known as the 
organophosphates. EPA has classified the organophosphate pesticides and 
their common cholinesterase-inhibiting degradates as having a common 
mechanism of toxicity. Thus, in addition to assessing the risks posed 
by exposure to organophosphate pesticides individually, EPA has 
assessed the potential cumulative effects from concurrent exposure to 
organophosphate pesticides. (Ref. 13).
    As discussed in Unit IV.B.1. below, taking all of the above 
information into account, EPA concluded that the tolerances for DDVP 
were safe.

B. FFDCA Tolerance Reassessment and FIFRA Pesticide Reregistration

    1. In general. As required by the FQPA of 1996, EPA reassessed the 
safety of the DDVP tolerances under the new safety standard established 
in the FQPA. EPA released for comment a preliminary risk assessment for 
DDVP in October, 2000. (65 FR 60430 (October 11, 2000)). Subsequently, 
after consideration of public comment, EPA, on June 30, 2006, issued an 
Interim Reregistration Eligibility Document (``IRED'') for DDVP. In 
that document, EPA determined that aggregate exposure to DDVP as a 
result of use of DDVP, naled, and trichlorfon, complied with the FQPA 
safety standard. (Ref. 3 ). Separately, on July 31, 2006, EPA 
determined that cumulative ffects from exposure to all organophosphate 
residues were safe. (Ref. 14). In combination, these findings satisfied 
EPA's obligation to review the DDVP tolerances under the new safety 
standard.
    As a result of the FIFRA reregistration and FFDCA tolerance 
reassessment process there were numerous changes made to DDVP's 
registration that affect non-occupational exposure to DDVP. 
Specifically, on May 9, 2006, EPA received from Amvac, the only 
registrant of DDVP as a product for manufacturing end-use DDVP 
products, an irrevocable request to cancel certain uses and include 
additional pest strip label restrictions on the DDVP active ingredient 
product labels. Pursuant to section 6(f) of FIFRA, on June 30, 2006, 
the Agency published a notice in the Federal Register that it had 
received the request and sought comment on EPA's intention to grant the 
request and cancel the specified uses. (71 FR 37570 (June 30, 2006)). 
On October 20, 2006, EPA issued the final cancellation order. (71 FR 
61968 (October 20, 2006)).
    The added restrictions on the use of the pest strip products were 
approved on October 11, 2006, and provided, among other things, that 
large pest strips could no longer be used in homes except for garages, 
attics, crawl spaces, and sheds that are occupied for less than 4 hours 
per day. The only pest strips permitted for use in occupied areas 
inside the home were significantly smaller strips for use in closets, 
wardrobes, or cupboards. Additionally, in early March, 2007, Amvac 
requested the voluntary cancellation of all its pet

[[Page 42692]]

collar and bait registrations and deletion of those uses from its 
technical label. Pursuant to section 6(f) of FIFRA, Amvac's requests to 
cancel the pet collar and bait registrations as well as deleting such 
uses from the technical label were published in the Federal Register on 
March 23, 2007. (72 FR 13786 (March 23, 2007)). On June 27, 2007, EPA 
issued the final cancellation notice for the pet collar and bait 
registrations. (72 FR 35235 (June 27, 2007)).
    Cancellation of uses and label restrictions imposed on Amvac's 
registration apply to all formulated DDVP end-use products because it 
is unlawful to use a pesticide in a manner inconsistent with its label. 
(7 U.S.C. 136(ee)). This bar on use inconsistent with the label applies 
to the formulation of end-use pesticide products from manufacturing use 
products. Accordingly, because Amvac holds the only registration for a 
DDVP manufacturing use product, the removal of uses and the addition of 
restrictions with respect to Amvac's manufacturing use product label 
has the effect of imposing those use cancellations and label 
restrictions on all DDVP end-use products.
    2. Review of human study. Completion of the DDVP IRED was delayed, 
in part, by questions regarding whether it was appropriate for EPA to 
rely on several human toxicity studies conducted with DDVP which were 
submitted by Amvac. The study receiving principal attention was a study 
involving repeated dosing over several days conducted in 1997 by A.J. 
Gledhill. (Refs. 3 at 133; and 15). That study is identified by the 
Master Record Identification (``MRID'') number of 44248801. Amvac also 
cited approximately a dozen other human studies, several of which were 
also conducted by Gledhill. (Ref. 16).
    Following promulgation of the Human Research rule, EPA evaluated 
whether the human data submitted by Amvac complied with the rule, and, 
pursuant to the rule's requirements, presented these data and its 
recommendations to the Human Studies Review Board (``HSRB'') for 
review. On March 9, 2006, the HSRB published a notice in the Federal 
Register announcing that a public meeting would be held to consider the 
DDVP studies as well as human studies for several other pesticides. (71 
FR 12194 (March 9, 2006)). The meeting was scheduled for April 4-6, 
2006. The notice alerted the public of the opportunity to file both 
written comments with the HSRB and to make oral comments at the April 
meeting. The members of the HSRB at the time of this meeting are listed 
in Appendix 1.
    NRDC filed written comments with the HSRB concerning DDVP, (Ref. 
17), and also presented oral testimony at the public meeting. (Ref. 
18). NRDC's comments and oral remarks specifically focused on whether 
the Gledhill study had sufficient statistical power ``to detect an 
effect when it may occur'' and the fact that the Gledhill study only 
used healthy, male test subjects. (Ref. 7 at 13). Other subjects 
discussed at the meeting included the relative strengths and weaknesses 
of the Gledhill study such as its repeat dosing regime, the failure to 
test blood plasma cholinesterase, the failure to monitor subjects after 
testing, and the study's consent form. (Id.; Ref. 18 at 18, 20-23). On 
May 23, 2006, the HSRB published a notice in the Federal Register 
alerting the public that it had released a draft report (dated May 16, 
2006) and would be holding a public teleconference meeting on June 6, 
2006 to discuss its draft report. (71 FR 29624 (May 23, 2006)). The 
notice included instructions on how members of the public could 
participate in the teleconference and explained the procedure for 
providing oral and written comments. (Ref. 19). NRDC did not file 
comments on the draft report. (Ref. 20).
    On June 26, 2006, the HSRB issued its finding that reliance on the 
Gledhill human study was appropriate given that the study had 
scientific value and there was no clear and convincing evidence that 
the study was fundamentally unethical. (Ref. 21). The HSRB concluded 
that the other DDVP human studies should not be used in the DDVP risk 
assessment. These findings were unchanged from its May 16, 2006 draft 
report.
    EPA agreed with the findings of the HSRB and relied upon the HSRB's 
reasoning in using the Gledhill study in its DDVP risk assessment. (72 
FR at 68675).

V. NRDC Petition Regarding DDVP

    On June 2, 2006, the NRDC filed a petition with EPA which, among 
other things, requested that EPA: (1) Conclude the DDVP Special Review 
by August 3, 2006, with a finding that DDVP causes unreasonable adverse 
effects on the environment; (2) conclude the DDVP FIFRA reregistration 
process by August 3, 2006, with a finding that DDVP is not eligible for 
reregistration; (3) submit draft notices of intent to cancel all DDVP 
registrations to the FIFRA Scientific Advisory Panel and USDA by August 
3, 2006, and issue those notices 60 days thereafter; (4) conclude the 
DDVP tolerance reassessment process by August 3, 2006, with a finding 
that the DDVP tolerances do not meet the FFDCA safety standard; and (5) 
issue a final rule by August 3, 2006, revoking all DDVP tolerances. 
(Ref. 2). Shortly after the petition was filed, on June 30, 2006, EPA 
released the IRED for DDVP which addressed DDVP's eligibility for 
reregistration under FIFRA and assessed, in part, whether DDVP's 
tolerances met the new safety standard enacted by the FQPA. NRDC 
submitted comments on the IRED and some of these comments bore on 
issues in its petition. (Ref. 3).
    NRDC's petition contained dozens of claims as to why DDVP's 
registration under FIFRA should be canceled and its FFDCA tolerances 
revoked. These issues are not presented in detail here because many 
raised solely FIFRA concerns and NRDC has not pursued most of its 
tolerance-related claims in its objections and hearing requests.
    EPA published notice of the petition for comment on October 11, 
2006. (71 FR 59784 (October 11, 2006)). EPA received roughly 1,500 
brief comments in support of the petition. These comments added no new 
information pertaining to whether the tolerances were in compliance 
with the FFDCA. Detailed comments in opposition to the petition were 
submitted by Amvac. (Ref. 22).
    EPA responded to the petition in three separate documents: (1) It 
issued an order closing out the DDVP Special Review; (72 FR 72709 
(December 21, 2007)); (2) it issued an order denying the request to 
cancel DDVP's FIFRA registration (72 FR 68581(December 5, 2007)); and 
(3) it issued an order pursuant to FFDCA section 408(d)(4)(iii) denying 
the request to revoke DDVP's FFDCA tolerances (78 FR 68662 (December 5, 
2007). Today's final order only concerns the objections filed to the 
section 408(d)(4)(iii) order denying the request to revoke tolerances.

VI. EPA Response to the Petition to Revoke DDVP Tolerances

    EPA issued a section 408(d)(4)(iii) order responding to the 
petition's request to revoke DDVP tolerances on December 5, 2007 
(hereinafter referred to as EPA's ``petition response'' or ``petition 
denial order''). (72 FR 68662 (December 5, 2005). That order denied the 
petition finding that none of the grounds asserted by NRDC demonstrated 
that the DDVP tolerances should be revoked. Nonetheless, EPA did 
conclude that NRDC raised several pertinent concerns with EPA's 
assessment of the risks posed by DDVP.
    To respond to NRDC's concerns, EPA completely revamped both its 
dietary

[[Page 42693]]

and residential risk assessments. In its new risk assessments, EPA 
included updated information on residue levels of DDVP in food, the 
amount of usage of DDVP and related pesticides in agriculture, and food 
consumption patterns of infants and children. EPA also adopted modified 
and more conservative assumptions regarding exposure patterns to DDVP 
in residential settings and exposure to DDVP from naled's use to 
control mosquitoes. Because, however, EPA concluded that the revised 
risk assessments still showed that the DDVP tolerances are safe, EPA 
denied NRDC's petition.
    EPA's specific responses to the claims in the petition that are 
relevant to NRDC's objections are summarized in the portion of this 
order responding to the objections and hearing requests.

VII. NRDC's Objections and Requests for Hearing

    On February 1, 2008, NRDC filed, pursuant to FFDCA section 
408(g)(2), objections to EPA's denial of its tolerance revocation 
petition and requested a hearing on those objections. As indicated 
above, NRDC's objections and requests for hearing raise two main 
claims: (1) that EPA has unlawfully failed to retain the full 10X 
safety factor for the protection of infants and children; and (2) that 
it was unlawful for EPA to rely on a toxicity study for DDVP that was 
conducted with humans.
    NRDC cites three grounds for its assertion that EPA unlawfully 
lowered the 10X children's safety factor: (1) that EPA lacked adequate 
data on DDVP's potential effects on the endocrine system; (2) that EPA 
lacked adequate data on several matters related to assessing dietary 
exposure to DDVP residues in food; and (3) that EPA has inadequate data 
on exposure to DDVP from its use in residential pest strips. As to the 
DDVP human study, NRDC claimed that EPA's regulation concerning use of 
human studies is unlawful and that the study is scientifically flawed 
and ethically compromised. In analyzing NRDC's claims, EPA has broken 
NRDC's two main claims down into 19 separate sub-issues. Each sub-issue 
is described in detail and responded to separately in Unit VIII.
    In support of its request for hearing, NRDC proffered the following 
documents as evidence that a hearing would be appropriate:
    (1) the Interim Reregistration Eligibility Determination for 
DDVP; (2) the entire record for the IRED and the documents 
referenced and cited therein; (3) NRDC's comments on the IRED; (4) 
EPA's petition denial and the references cited in that denial; (5) 
NRDC's petition and all references cited in the petition; and (6) 
the arguments, citations, and attachments contained in these 
objections.

(Ref. 1 at 3) (citations and references to attachments omitted).

VIII. Response to Objections and Requests for Hearing

A. Overview

    EPA denies each of NRDC's objections as well as its hearing 
requests. NRDC's hearing requests fail to meet the statutory and 
regulatory requirements for holding a hearing. NRDC has failed to 
proffer evidence on its hearing requests which would, if established, 
resolve one or more issues in its favor. Rather, NRDC relies on mere 
allegations and general denials and contentions. Further, many of 
NRDC's claims do not present genuine and substantial issues of fact 
and/or are immaterial to the relief requested. On the merits, NRDC's 
objections are denied for substantially the same reasons given in EPA's 
petition denial order. NRDC's objections largely restate the claims in 
its petition. Significantly, NRDC does not acknowledge or respond to 
the substantial revisions to the DDVP dietary and residential risk 
assessments made in response to the NRDC petition. Similarly, NRDC does 
not acknowledge or respond to EPA's detailed summary of why it adopted 
the conclusion by the independent HSRB that the Gledhill human study 
complied with EPA's Human Research rule.
    The remainder of this Unit is organized in the following manner. 
Unit VIII.B. describes in greater detail the requirements pertaining to 
when it is appropriate to grant a hearing request. Unit VIII.C. 
examines the evidence proffered by NRDC in support of its hearing 
requests. Units VIII.D. and E. provide EPA's response to the NRDC's 
objections and hearing requests. Unit VIII.D. addresses NRDC's claims 
regarding the children's safety factor and subunit E addresses NRDC's 
arguments concerning reliance on the Gledhill human study. EPA's 
conclusions on the hearing requests and objections are summarized in 
Units VIII.F. and G., respectively.
    EPA has adopted a 4-part format in Units VIII.D. and E. for 
explaining its ruling on each of the 19 sub-issues EPA identified in 
the objections. First, NRDC's claim and any arguments or evidence 
tendered to support that claim are described. Second, background 
information on the claim is provided including whether and how the 
claim was presented in NRDC's petition and, if it was presented, EPA's 
reasons for denying the claim in its earlier petition denial order. 
Third, EPA explains its reasons for denying a hearing on that claim. 
Finally, EPA explains its reasons for denying the claim on the merits.

B. The Standard for Granting an Evidentiary Hearing

    EPA has established regulations governing objections to tolerance 
rulemakings and tolerance petition denials and requests for hearings on 
those objections. (40 CFR Part 178; 55 FR 50291 (December 5, 1990)). 
Those regulations prescribe both the form and content of hearing 
requests and the standard under which EPA is to evaluate requests for 
an evidentiary hearing.
    As to the form and content of a hearing request, the regulations 
specify that a hearing request must include: (1) a statement of the 
factual issues on which a hearing is requested and the requestor's 
contentions on those issues; (2) a copy of any report, article, or 
other written document ``upon which the objector relies to justify an 
evidentiary hearing;'' and (3) a summary of any other evidence relied 
upon to justify a hearing. (40 CFR 178.27).
    The standard for granting a hearing request is set forth in section 
178.32. That section provides that a hearing will be granted if EPA 
determines that the ``material submitted'' shows all of the following:

(1) There is a genuine and substantial issue of fact for resolution 
at a hearing. An evidentiary hearing will not be granted on issues 
of policy or law.
(2) There is a reasonable possibility that available evidence 
identified by the requestor would, if established, resolve one or 
more of such issues in favor of the requestor, taking into account 
uncontested claims or facts to the contrary. An evidentiary hearing 
will not be granted on the basis of mere allegations, denials, or 
general descriptions of positions and contentions, nor if the 
Administrator concludes that the data and information submitted, 
even if accurate, would be insufficient to justify the factual 
determination urged.
 (3) Resolution of the factual issue(s) in the manner sought by the 
person requesting the hearing would be adequate to justify the 
action requested. An evidentiary hearing will not be granted on 
factual issues that are not determinative with respect to the action 
requested. For example, a hearing will not be granted if the 
Administrator concludes that the action would be the same even if 
the factual issue were resolved in the manner sought.


(40 CFR 178.32(b)).
    This provision essentially imposes four requirements upon a hearing 
requestor. First, the requestor must show it is raising a question of 
fact, not

[[Page 42694]]

one of law or policy. Hearings are for resolving factual issues not for 
debating law or policy questions. Second, the requestor must 
demonstrate that there is a genuine dispute as to the issue of fact. If 
the facts are undisputed or the record is clear that no genuine dispute 
exists, there is no need for a hearing. Third, the requestor must show 
that the disputed factual question is material - i.e., that it is 
outcome determinative with regard to the relief requested in the 
objections. Finally, the requestor must make a sufficient evidentiary 
proffer to demonstrate that there is a reasonable possibility that the 
issue could be resolved in favor of the requestor. Hearings are for the 
purpose of providing objectors with an opportunity to present evidence 
supporting their objections; as the regulation states, hearings will 
not be granted on the basis of ``mere allegations, denials, or general 
descriptions of positions or contentions.'' (40 CFR 178.32(b)(2)).
    EPA's hearing request requirements are based heavily on FDA 
regulations establishing similar requirements for hearing requests 
filed under other provisions of the FFDCA. (53 FR 41126, 41129 (October 
19, 1988)). FDA pioneered the use of summary judgment-type procedures 
to limit hearings to disputed material factual issues and thereby 
conserve agency resources. FDA's use of such procedures was upheld by 
the Supreme Court in 1972, (Weinberger v. Hynson, Westcott & Dunning, 
Inc., 412 U.S. 609 (1973)), and, in 1975, FDA promulgated generic 
regulations establishing the standard for evaluating hearing requests. 
(40 FR 22950 (May 27, 1975)). It is these regulations upon which EPA 
relied in promulgating its hearing regulations in 1990.
    Unlike EPA, FDA has had numerous occasions to apply its regulations 
on hearing requests. FDA's summary of the thrust of its regulations, 
which has been repeatedly published in the Federal Register in orders 
ruling on hearing requests over the last 24 years, is instructive on 
the proper interpretation of the regulatory requirements. That summary 
states:
    A party seeking a hearing is required to meet a `threshold 
burden of tendering evidence suggesting the need for a hearing.' [] 
An allegation that a hearing is necessary to `sharpen the issues' or 
`fully develop the facts' does not meet this test. If a hearing 
request fails to identify any evidence that would be the subject of 
a hearing, there is no point in holding one.
    A hearing request must not only contain evidence, but that 
evidence should raise a material issue of fact concerning which a 
meaningful hearing might be held. [] FDA need not grant a hearing in 
each case where an objection submits additional information or 
posits a novel interpretation of existing information. [] Stated 
another way, a hearing is justified only if the objections are made 
in good faith and if they ``draw in question in a material way the 
underpinnings of the regulation at issue.'' Finally, courts have 
uniformly recognized that a hearing need not be held to resolve 
questions of law or policy.

(49 FR 6672, 6673 (February 22, 1984); 72 FR 39557, 39558 (July 19, 
2007) (citations omitted)). EPA has been guided by FDA's application of 
its regulations in this proceeding.

    Congress confirmed EPA's authority to use summary judgment-type 
procedures with hearing requests when it amended FFDCA section 408 in 
1996. Although the statute had been silent on this issue previously, 
the FQPA added language specifying that when a hearing is requested, 
EPA ``shall . . . hold a public evidentiary hearing if and to the 
extent the Administrator determines that such a public hearing is 
necessary to receive factual evidence relevant to material issues of 
fact raised by the objections.'' (21 U.S.C. 346a(g)(2)(B)). This 
language grants EPA broad discretion to determine whether a hearing is 
``necessary to receive factual evidence'' to objections.

C. Evidentiary Proffer by NRDC

    As noted above, the purpose for holding hearings is ``to receive 
factual evidence.'' (U.S.C. 346a(g)(2)(B); 53 FR 41126, 41129 
(``Hearings are for the purpose of gathering evidence on disputed 
factual issues . . . .'')). A requestor must identify evidence relied 
upon to justify a hearing and either submit copies of that evidence or 
summarize it. (40 CFR 178.27). After reviewing the proffer, EPA must 
find that there is a reasonable possibility that the proffered 
evidence, if established, would resolve one or more genuinely-disputed, 
material factual issues in a requestor's favor. (40 CFR 178.32(b)). 
Because a substantial portion of NRDC's evidentiary proffer is 
deficient on its face, EPA finds it most efficient to preliminarily 
review the proffer before turning to the individual issues raised by 
NRDC.
    As previously mentioned, NRDC proffered the following items as 
evidence supporting its requests for hearing:
    (1) the Interim Reregistration Eligibility Determination for 
DDVP; (2) the entire record for the IRED and the documents 
referenced and cited therein; (3) NRDC's comments on the IRED; (4) 
EPA's petition denial and the references cited in that denial; (5) 
NRDC's petition and all references cited in the petition; and (6) 
the arguments, citations, and attachments contained in these 
objections.

(Ref. 1 at 3). These items can be divided into two groups: (1) items 
produced or assembled by EPA (the IRED; the IRED record; and EPA's 
petition denial); and (2) items produced by NRDC (NRDC's comments on 
the IRED; NRDC's petition; and NRDC's objections).
    The items in the first group - the EPA documents - clearly do not 
constitute a proper proffer. Essentially, this is a non-specific 
identification of every document and piece of data EPA has considered 
and relied upon in the multi-year process of conducting the FIFRA 
reregistration and FFDCA tolerance reassessment for DDVP and in 
responding to NRDC's DDVP petition. This could easily encompass 
hundreds, if not thousands of documents, and tens of thousands of pages 
of analysis and data. EPA's petition response alone cited 82 documents 
and those documents generally were EPA analytical papers and not the 
underlying data. EPA concludes that NRDC's citation to the thousands of 
pages in the IRED, the IRED record, and the petition denial is so vague 
a proffer as to not constitute a proffer at all. It would be as if a 
lawyer, in responding to a court's request for case law authority for a 
principle he or she was defending, cited the court to West's Federal 
Reporter, 3rd Series. While somewhere in those hundreds of volumes a 
case may exist that supports the asserted principle, the lawyer cannot 
be said to have identified it by a vague wave at a substantial portion 
of the law library. Further, given that the purpose of a hearing is to 
gather or receive evidence, proffering evidence already considered and 
relied upon by EPA would not seem to be grounds for holding a hearing. 
Finally, as a matter of law, EPA does not understand how it can be 
argued that a proffer consisting of a general reference to a record of 
decision which EPA has found supported one result could constitute 
evidence that if established, would justify the opposite conclusion. At 
bottom, the proffer of the items in the first group fails to 
``identify'' evidence which would, if established, resolve an issue in 
NRDC's favor.
    NRDC's second group of documents consists of NRDC's comments on the 
IRED; NRDC's petition; and NRDC's objections. In analyzing this 
proffer, EPA has focused on NRDC's objections because the objections 
appear to contain, almost word-for-word, the arguments and claims put 
forward in its petition and IRED comments with regard to the children's 
safety factor and reliance on human studies. The objections reference 
16 documents. For the reasons explained below, 10 of these documents 
can be rejected on their face

[[Page 42695]]

as not justifying a hearing. Four of the documents, however, 
potentially include factual evidence supporting a hearing and are 
analyzed more thoroughly in connection with the specific issue in the 
hearing request to which they are tied. The other two documents that 
are referenced are NRDC's DDVP petition and NRDC's comments on the DDVP 
IRED. As described above, these documents do not add anything beyond 
what is in the objections.
    1. Documents that clearly do not proffer evidence of a genuinely-
disputed, material issue of fact. (10 items)
     Five Newspaper Stories. NRDC cites to an Associated Press 
story from 2002 and four Los Angeles Times stories from 2007. These 
news stories contain basic background information about DDVP; general 
contentions from Amvac, NRDC, and EPA regarding the safety of DDVP; and 
no more than a cursory, passing reference to any of the issues raised 
in the petition. There can be no serious contention that these articles 
present evidence justifying a hearing.
     NRDC comments to HSRB. NRDC references the comments it 
submitted to the HSRB with regard to the HSRB's review of the human 
studies conducted with DDVP. The comments - three pages of bulleted 
talking points and one graph - are a summary of the slightly more 
detailed arguments contained in NRDC's objections. This document adds 
no justification for a hearing not otherwise included in NRDC's 
objections.
    2. Legal Briefs in NRDC v. EPA, No. 06-0820-ag (2d Cir.). NRDC 
cites to its opening and reply briefs in NRDC v. EPA, the case 
adjudicating NRDC's challenge to EPA's Human Research rule. These 
briefs contain legal arguments regarding the lawfulness of the Human 
Research rule. They contain no factual evidence justifying NRDC's DDVP 
hearing requests.
     Three Law Review Articles. NRDC references: (1) a short 
article by a NRDC attorney summarizing his legal objections to EPA's 
Human Research rule; (2) an article concerning EPA's implementation of 
the FQPA; and (3) an article focusing on how tort law might be used to 
supplement the FQPA to protect children. None of these articles mention 
DDVP and no serious contention can be made that they provide factual 
evidence justifying a hearing.
    3. Documents which may present evidence of a genuinely-disputed, 
material issue of fact. (4 items)
     Lockwood Articles. NRDC cites two articles by Dr. Alan 
Lockwood which discuss science and ethical issues with regard to 
several human intentional dosing studies involving pesticides. Several 
of the human studies addressed were DDVP studies, one of which is the 
Gledhill human study that is the focus of this proceeding. Whether the 
information presented in these articles supports NRDC's hearing 
requests is examined in Unit VIII.E.3.a.
     Sass Letters. NRDC cites two letters published in the 
journal Environmental Health Perspectives co-authored by Dr. Jennifer 
Sass of NRDC. These letters discuss science and ethical issues with 
regard to two human studies, including the DDVP human study in question 
in this proceeding. Whether the information presented in these letters 
supports NRDC's hearing requests is examined in Unit VIII.E.3.a.

D. Response to Specific Issues Raised in Objections and Hearing 
Requests - Children's Safety Factor

    1. Failure to support children's safety factor decision with DDVP-
specific data-- a. Objection/hearing request sub-issue. NRDC asserts 
that EPA, in choosing a 3X children's safety factor for DDVP, did not 
rely on reliable data showing that such a factor was safe for infants 
and children because EPA's choice of 3X ``is not based on any data 
specific to DDVP.'' (Ref. 1 at 5). NRDC's argument is that EPA erred by 
not deriving a precise safety factor for DDVP but instead used a value 
that EPA considered to be half of the 10X safety factor. NRDC claims 
that ``EPA could not have determined that `such margin' [i.e., 3X] will 
be safe, when the replacement safety factor is simply a generic stand-
in for EPA's conclusion that `something less than 10X' is enough.'' 
(Id.). According to NRDC, EPA should have explained ``what reliable 
data supports a 3X safety factor in particular, as opposed to 4X or 
some other number, for DDVP specifically.'' (Id.).
    b. Background. Similar assertions were made in NRDC's petition and 
its IRED comments. For example, the petition claimed that ``[t]he 
Agency did not explain why it chose 3X as opposed to 4X or any other 
factor,'' (Ref. 2 at 14), and the IRED comments asserted that there was 
a ``complete lack of explanation'' for EPA's safety factor decisions. 
(Ref. 23 at 5). Both documents also alleged there were inadequacies in 
the toxicity and exposure databases. (Refs. 2 at 15, and 38-41; and 23 
at 8-9).
    In response to these claims by NRDC, EPA, in the petition response, 
comprehensively restated its reasoning for its decisions on the 
children's safety factor for DDVP in the IRED. (72 FR at 68694-68695). 
EPA noted that it had a complete toxicity database for DDVP and it 
carefully reviewed the evidence regarding the sensitivity of the young 
to DDVP and explained why an additional safety factor was not needed to 
protect infants and children. Further, EPA detailed why it had 
concluded that its exposure assessments would not understate human 
exposure to DDVP.
    For some DDVP risk assessments EPA chose to remove the children's 
safety factor entirely, and for others EPA reduced the safety factor to 
3X. EPA explained that it retained a 3X children's safety for certain 
assessments because the toxicity study which was relied upon in 
conducting those risk assessments had not identified a ``no adverse 
effect level'' (``NOAEL'') in its subjects but rather only a ``lowest 
adverse effect level'' (``LOAEL''). Despite the failure to identify a 
NOAEL in the study, EPA concluded that ``a 3X factor'' would be more 
than adequate to identify a NOAEL based upon the slight adverse effect 
(marginal RBC cholinesterase inhibition in a human study) observed at 
the LOAEL.'' (72 FR at 68695). EPA noted that an independent science 
review board had confirmed that lower doses were unlikely to produce a 
measurable effect. Finally, EPA explained why it chose 3X instead of 4X 
or some other value. (Id.). The petition response noted that ``where 
the data does not warrant a full 10X, EPA generally does not attempt to 
mathematically derive a precise replacement safety factor because 
regulatory agencies' traditional use of 10X safety factors (upon which 
the FQPA safety factor was modeled) was based on rough estimates rather 
than detailed calculations. Instead, where a 10X factor would clearly 
overstate the uncertainty, EPA simply applies a factor valued at half 
of 10X.'' (Id.). EPA explained that it considers 3X to be half of 10X 
assuming a lognormal distribution of effects. (Id.).
    c. Denial of hearing request. In analyzing whether a hearing would 
be appropriate on this sub-issue, it is helpful to break the sub-issue 
down into three separate, but related, questions: (1) Whether EPA, in 
selecting a children's safety factor lower than 10X, is required to 
justify with precision why it chose one factor over another; (2) 
whether EPA offered a justification for the children's safety factor it 
chose; and (3) whether EPA relied upon DDVP specific information in 
choosing a safety factor or instead relied upon ``generic assertions.'' 
When broken down in this way, it is clear that none of these questions 
meets the standard for a hearing.

[[Page 42696]]

    The first question is a pure question of law - does FFDCA section 
408(c) require EPA to offer a reasoned explanation for its choice of a 
children's safety factor, including an explanation as to why a 
different factor is not needed. A question of fact, not of law, is 
required to justify a hearing. (40 CFR 178.32(b)(1)).The second and 
third questions fail to present a matter of genuinely-disputed facts 
because it is plain on the record that EPA did offer a reasoned 
justification for its decision and, in that justification, relied upon 
DDVP-specific facts. EPA's petition response to NRDC's 10X arguments 
laid out in careful detail information regarding the extent of the 
toxicity and exposure database on DDVP and the data bearing on DDVP's 
effects on young animals. (72 FR at 68694-68695 (discussing the 
completeness of the DDVP toxicity database, DDVP studies bearing on 
pre- and post-natal toxicity, and the basis for DDVP exposure 
estimates)). Further, NRDC proffers no evidence - because there is none 
to proffer - suggesting that EPA did not consider DDVP-specific 
information in making its children's safety factor decision. Therefore, 
this question does not meet the standard for a hearing both because 
there are no genuinely-disputed facts and NRDC has proffered no 
evidence which, if established, could resolve this issue in its favor. 
57 FR 6667, 6672 (February 27, 1992) (``A hearing must be based on 
reliable evidence, not on mere allegations or on information that is 
inaccurate and contradicted by the record.'')
    d. Denial of objection. EPA agrees with NRDC that general 
principles of administrative law require it to provide a reasoned 
explanation for its decision on selection of a children's safety 
factor. (Baltimore Gas & Electric Co. v. NRDC, 462 U.S. 87, 103 
(1983)). EPA disagrees with NRDC, however, to the extent it is 
suggesting that as part of this reasoned explanation for its selection 
of a children's safety factor, EPA must show why it did not choose some 
other mathematical value. Rather, the statute imposes upon EPA, if it 
decides to vary from the presumptive 10X children's safety factor, the 
burden to show that any ``different'' safety factor is safe. Once EPA 
has made that showing, its obligation to offer a reasoned explanation 
is complete. Because EPA offered a reasoned explanation as to why the 
children's safety factors it chose protect the safety of infants and 
children, (72 FR 68694-68695), EPA denies NRDC's objection on this 
point.
    As to the substance of EPA's explanation of why it chose a 3X 
safety factor for certain DDVP risk assessments, NRDC claims that EPA 
erred because its choice of 3X is based on ``a generic assertion not [] 
on any data specific to DDVP.'' (Ref. 1 at 5). NRDC is wrong. The 
generic assertion NRDC mentions is EPA's explanation of why 3X is half 
of 10X. EPA's choice of 3X, however, is not based on its conclusion 
that 3X is half of 10X but on the data in the DDVP human study at 
issue. As noted above, the petition response explained in detail that a 
full 10X safety factor was not needed to address the uncertainty raised 
by the failure of the DDVP human study to identify a NOAEL. The effects 
seen in that study at the LOAEL were only marginally adverse at best, 
and therefore, EPA concluded that applying the full 10X safety factor 
(i.e., dividing the LOAEL by another factor of 10X in addition to the 
10X factor for intra-human variability) was more than was needed to 
address the lack of a NOAEL. The HSRB confirmed as much when it wrote: 
``because the decreased activity in RBC cholinesterase activity 
observed in this study was at or near the limit of what could be 
distinguished from baseline values, it was unlikely that a lower dose 
would produce a measurable effect in RBC cholinesterase activity.'' 
(Ref. 21 at 41).
    EPA chose a safety factor of 3X for DDVP based on its conclusion 
that not only was 10X overprotective but that 3X would be protective 
given the results seen in the relevant DDVP study. (72 FR at 68695). As 
EPA concluded in the petition denial order: ``a 3X safety factor would 
be more than adequate to identify a NOAEL based upon the slight adverse 
effect (marginal RBC cholinesterase inhibition in a human study) 
observed at the LOAEL.'' (Id.). Generally, EPA uses a 3X safety factor 
as the default value when reducing a 10X safety factor. (Refs. 5 at 9-
10, 26; and 24 at 4-40 - 4-41; ). A safety factor of 3X is deemed to be 
approximately half the value of a safety factor of an order of 
magnitude (10X). As EPA explained in the petition denial order:
    In choosing a safety factor in circumstances where the data does 
not warrant a full 10X, EPA generally does not attempt to 
mathematically derive a precise replacement safety factor because 
regulatory agencies' traditional use of 10X safety factors (upon 
which the FQPA safety factor was modeled) was based on rough 
estimates rather than detailed calculations. Instead, where a 10X 
factor would clearly overstate the uncertainty, EPA simply applies a 
factor valued at half of 10X. In determining half of a 10X factor, 
EPA assumes that the distribution of effects within the range of a 
safety factor is distributed lognormally (which is generally the 
case for biological effects), and reduction of a lognormal 
distribution by half is equal to half a log (10-5) or 
approximately 3X. A lognormal distribution is a distribution which 
if plotted based on the logarithm of each of its values would yield 
a bell-shaped (normal) distribution but if plotted according to 
actual values would be skewed having a clumping of values along the 
vertical axis of the plot.

(72 FR at 68695) (citations omitted).

    NRDC does not challenge EPA's reasoning regarding whether the 
choice of 3X is justified based on the results of a DDVP-specific study 
and thus, the merits of EPA's DDVP-specific reasoning is not here at 
issue. Rather, NRDC denies that EPA engaged in DDVP-specific reasoning 
in choosing 3X. Because NRDC's argument is contradicted on the face of 
the petition response, it is denied.
    2. Endocrine effects. As described below, NRDC claims that EPA 
cannot remove the children's safety factor because it has not completed 
the endocrine screening program for DDVP under section 408(p) and 
because EPA has inadequate endocrine data for DDVP. Although NRDC did 
argue in its petition that EPA cannot make a safety finding without 
completing the endocrine screening program, it did not assert claims 
regarding endocrine data and the children's safety factor. EPA has 
previously ruled that a petitioner may not raise new issues in filing 
objections to EPA's denial of its Original petition. (72 FR 39318, 
39324 (July 18, 2007) (``The FFDCA's tolerance revocation procedures 
are not some sort of `game,' whereby a party may petition to revoke a 
tolerance on one ground, and then, after the petition is denied, file 
objections to the denial based on an entirely new ground not relied 
upon by EPA in denying the petition.'')). Accordingly, NRDC's 
objections and hearing requests as to the children's safety factor and 
endocrine data are denied.
    Even if these claims were properly presented in these objections, 
for the reasons set forth below they neither entitle NRDC to a hearing 
nor justify the relief sought.
    a. Endocrine disruptor screening program--i. Objection/hearing 
request sub-issue. NRDC argues that EPA must retain the 10X children's 
safety factor because EPA has not fulfilled its obligations under FFDCA 
section 408(p) to screen pesticides, including DDVP, for endocrine 
disruption potential. (Ref. 1 at 5). Essentially, NRDC argues that EPA 
must retain the children's safety factor for any pesticide until 
testing under the endocrine screening program is completed for that 
pesticide.
    ii. Background. In its petition, NRDC claimed that failure to 
conduct the

[[Page 42697]]

endocrine screening program for DDVP under section 408(p) made it 
impossible for EPA to conclude that the DDVP tolerances are safe. (Ref. 
2 at 49). EPA responded to this argument by citing its denial of a 
petition to revoke various pesticide tolerances in which the claim was 
made that EPA could not remove the children's safety factor if 
endocrine screening under section 408(p) had not been conducted. (72 FR 
at 68676). There, EPA concluded that the statute did not impose a 
mandatory bar upon removal of the children's safety factor until 
completion of the endocrine screening program. (71 FR 43906, 43920 
(August 2, 2006)). EPA also found in responding to the prior petition 
that it had sufficient data on endocrine screening for the pesticide in 
question to make a safety finding. (71 FR at 43920-43921). After 
analyzing the endocrine data for DDVP, EPA concluded that it had 
sufficient data to make a safety finding as to DDVP. (72 FR at 68676 - 
68677).
    iii. Denial of hearing request. The question of whether completion 
of the endocrine screening program under FFDCA section 408(p) is a 
mandatory prerequisite to removal of the children's safety factor is a 
legal issue. A question of fact, not of law, is required to justify a 
hearing. (40 CFR 178.32(b)(1)).
    iv. Denial of objection. In response to a prior pesticide tolerance 
revocation petition, and objections filed as to EPA's denial of that 
petition, EPA has already rejected the legal claim presented in this 
objection. (71 FR at 43920; 72 FR 39318, 39327-39328 (July 18, 2007). 
After analyzing the statutory language, structure, and legislative 
history, EPA concluded that section 408(p) does not override the 
``clear and unmistakable language[] [in section 408(b)(2)(C)] 
grant[ing] EPA discretion to make a fact-based determination of whether 
a safety factor different than the 10X default value is safe for 
children.'' (71 FR at 43920). EPA summarized its reasoning as follows:
under section 408(b)(2)(C) EPA clearly has the discretion to 
determine, in any given case, whether it has reliable data to choose 
a factor different than the 10X default value. Not only is there no 
statutory language supporting the [petitioners'] argument in favor 
of automatic retention of the 10X until completion of the endocrine 
screening program but the legislative history is in no way 
supportive of construing the enactment of the program as intended to 
have such a dramatic impact. Further, since the enactment of the 
FQPA, EPA's contemporaneous and consistent approach to the endocrine 
screening program has been to treat that information-gathering 
exercise as not imposing some type of statutorily-prescribed, 
automatic injunction barring removal of the children's safety factor 
until completion of information-gathering under the program.

(Id.). EPA also catalogued the extensive data requirements already in 
place for pesticides that produced information on a pesticide's 
potential endocrine effects. (71 FR at 43920-43921). EPA concluded that 
``in many instances the totality of the information gleaned from 
current data required for pesticides used on food will make it possible 
to develop a meaningful weight-of-the-evidence determination on the 
potential of the pesticide to adversely affect the endocrine system.'' 
(Id.).
    NRDC has done nothing more than state in a conclusory fashion that 
completion of endocrine screening under section 408(p) is necessary to 
a decision to remove the children's safety factor. Accordingly, EPA 
denies this objection for the reasons stated in its previous two orders 
addressing this claim. (71 FR at 43920 - 43921; 72 FR at 39327-39328).
    b. DDVP endocrine data--i. Objection/hearing request sub-issue. In 
its objections, NRDC argues that EPA has inadequate data on endocrine 
effects to remove the children's safety factor. As support for this 
argument NRDC asserts: (1) that the studies relied upon by EPA ``were 
not designed to detect endocrine disruption . . . ;'' and (2) that the 
two-generation rat reproduction study does not meet EPA's 1998 
guideline for such studies and, given that the reproduction study did 
show endocrine effects, a ``[p]roper histopathology in the two 
generation rat reproduction study could have revealed adverse effects 
at lower levels than'' the levels at which cholinesterase inhibition 
was seen in DDVP studies. (Ref. 1 at 6).
    ii. Background. As noted above, NRDC's petition argued that EPA 
could not make a safety finding for DDVP in the absence of data 
collected under the section 408(p) screening program. EPA responded to 
this claim by examining the data on DDVP bearing on its potential 
endocrine effects. EPA concluded that it could make a safety finding 
for DDVP in absence of further endocrine data given that: ``(1) data 
bearing on potential endocrine effects from a two-generation 
reproduction study as well as other chronic data in which effects on 
reproductive organs were examined; (2) EPA well understands DDVP's most 
sensitive mechanism of toxicity (cholinesterase inhibition); and (3) 
the potential endocrine-related effects seen for DDVP appeared in the 
presence of significant cholinesterase inhibition and at levels nearly 
two orders of magnitude above the most sensitive cholinesterase 
effects. . . .'' (72 FR at 68677).
    iii. Denial of hearing request. A hearing on this sub-issue is not 
appropriate because NRDC's request is based on mere allegations, 
general contentions, and speculation. NRDC claims that the studies EPA 
relied upon were not ``designed'' to investigate endocrine effects; 
however, NRDC proffers no evidence to support such an allegation. 
Further, such a claim has little, if any, materiality, given that the 
important question is not whether the studies were ``designed'' to 
measure endocrine effects but whether they actually measure such 
effects. Notably, NRDC does not, and cannot upon this record, make the 
latter contention. (See 72 FR at 68676 (discussing the numerous 
endocrine-related endpoints assessed in the DDVP database)). Further, 
NRDC's claim that if the DDVP two-generation rat reproduction study had 
been conducted pursuant to the 1998 guidelines it might have shown 
endocrine effects at lower doses than the doses at which DDVP's 
cholinesterase effects were seen is nothing more than speculation. In 
applying its hearing regulations, FDA has routinely denied hearings on 
speculation about what redoing a study might show. For example, in a 
proceeding establishing a food additive regulation for acesulfame 
potassium, FDA denied a hearing to an objector who challenged FDA's 
rejection of a study for only containing partial histopathological 
data. (57 FR 6667 (February 27, 1992)). The objector had argued that 
full histopathological data might have altered FDA's conclusion. FDA 
found such an argument unconvincing: ``Because complete 
histopathological examination of tissues from all animals in the first 
rat study was not done and cannot be done now, any prediction of the 
results of such an examination is simply speculation. Speculation 
regarding data that do not exist cannot serve as the basis for a 
hearing.'' (Id. at 6671). For all of the above reasons, the hearing 
request on this sub-issue is denied.
    iv. Denial of objection. EPA denies NRDC's objection that EPA does 
not have adequate endocrine data on DDVP to remove the children's 
safety factor. First, NRDC is wrong to imply that existing, required 
toxicity studies do not provide valuable information on potential 
endocrine effects. EPA discussed this issue in detail in an earlier 
order involving similar claims concerning a different pesticide. There, 
EPA pointed out that:
    The primary proposed Tier 2 study [for the Endocrine Disruptor 
Screening Program]

[[Page 42698]]

relevant to endocrine effects on humans is the 2-generation 
reproductive toxicity study in rats. This is one of the core studies 
required for all food-use pesticides since 1984. In this 
reproduction study, potential hormonal effects can be detected 
through behavioral changes, ability to become pregnant, duration of 
gestation, signs of difficult or prolonged parturition, apparent sex 
ratio (as ascertained by anogenital distances) of the offspring, 
feminization or masculinization of offspring, number of pups, 
stillbirths, gross pathology and histopathology of the vagina, 
uterus, ovaries, testis, epididymis, seminal vesicles, prostate, and 
any other identified target organs. In fact, EPA, in 1998, in 
discussing this study's use in Tier 2, identified 39 endpoints 
examined in this study relevant to estrogenic, androgenic, or 
thyroid effects. At that time, EPA noted that it was evaluating 
whether to add another 10 endocrine-related endpoints to the study 
protocol to enhance the utility of the study to detect endocrine 
effects. Despite the ongoing evaluation of additional endpoints, EPA 
has concluded that the existing 2-generation mammalian assay is 
valid for the identification and characterization of reproductive 
and developmental effects, including those due to endocrine 
disruption, based on the long history of its use, the endorsement of 
the 1998 test guideline by the FIFRA Scientific Advisory Panel, and 
acceptance by member countries of the Organizations for Economic 
Cooperation and Development (OECD).

(71 FR 43906, 43921 (August 2, 2006) (citations omitted)). That order 
also catalogued the numerous endocrine-related endpoints in other 
chronic toxicities routinely-required for pesticides used on 
agricultural commodities. (Id.).
    Specifically as to DDVP, in its response to NRDC's petition, EPA 
detailed four long-term DDVP toxicity studies, submitted under EPA data 
requirements that provided data on numerous effects that are relevant 
to potential endocrine disruption. EPA wrote:
    EPA has adequate data on DDVP's potential endocrine effects to 
evaluate DDVP's safety. In the 1989 NTP cancer studies with rats and 
mice, male and female reproductive organs (prostate, testes, 
epididymis, ovaries, uterus) were examined and no changes 
attributable to DDVP were found. The 52-week dog study with DDVP 
also was without effect in the reproductive organs (testes, 
prostate, epididymides, cervix, ovaries, uterus, vagina). EPA also 
has a 1992 two-generation rat reproduction study with DDVP (via 
drinking water) that is similar to the most recent guidelines (1998) 
for conduct of such a study with respect to endocrine-related 
endpoints. Although that study did not include certain evaluations 
that the 1998 guidelines recommended related to endocrine-related 
effects (age of vaginal opening and preputial separation), it did 
incorporate other aspects of the 1998 guidelines such as an 
examination of esterous cycling in females and sperm number, 
motility, and morphology in males. The study did identify an adverse 
effect on esterous cycling in females but only at the high dose (8.3 
mg/kg/day). All doses in the study showed significant cholinesterase 
inhibition. Further, the NOAEL and LOAEL from the esterous cycling 
endpoint in the reproduction study are nearly two orders of 
magnitude higher than the NOAEL and LOAEL used as a Point of 
Departure in setting the chronic RfD/PAD for DDVP.

(72 FR at 68676 (citations omitted). Further, the petition response 
additionally discussed a DDVP study from the scientific literature 
examining endocrine-related effects. (Id.).
    NRDC's speculation - that further testing of DDVP might reveal 
endocrine effects at levels below those at which cholinesterase 
inhibition has been measured - does not convince EPA that there is not 
a reliable basis for removing the children's safety factor as regards 
endocrine effects. As EPA indicated in its denial of the NRDC petition, 
it has several studies addressing numerous endpoints bearing on DDVP's 
potential endocrine effects, DDVP's cholinesterase inhibition effects 
are well-defined by existing data, and the only endocrine effect seen 
in the DDVP data occurred in the presence of significant cholinesterase 
inhibition and at a level two orders of magnitude (i.e., 100X) greater 
than the level at which the most sensitive cholinesterase effects were 
seen. As a pesticide, DDVP is subject to testing under the endocrine 
disruptor screening program; however, EPA expects that that data will 
confirm its conclusion regarding DDVP's potential endocrine effects. 
NRDC's objection on this point is denied.
    3. Dietary exposure--a. Objection/hearing request sub-issue. NRDC 
claims that there are numerous uncertainties in EPA's estimate of 
dietary exposure to DDVP from food and that these uncertainties 
preclude EPA from departing from the 10X children's safety factor. 
(Ref. 1 at 6). Specifically, NRDC cites to a list of uncertainties 
noted by EPA in a preliminary risk assessment for DDVP released in 
2000. Those uncertainties involve the number of infants surveyed for 
the food consumption database; foods consumed from farm stands; use of 
data on residue decline from cooking studies; reliance on the residue 
sampling from the FDA Total Diet Study; and lack of monitoring data, 
and extensive use of data translation, for fumigated commodities. With 
the exception of the infant consumption issue, NRDC makes no claim 
other than to allege that ``[e]ach of these shortcomings poses a 
serious risk of understating the risks posed by DDVP contamination of 
food.'' (Id.). As to the infant consumption data, NRDC offers various 
challenges to the size and representativeness of the group of infants 
sampled in conjunction to the 2000 preliminary risk assessment. NRDC 
acknowledges that EPA, in its response to the NRDC petition, states 
that it used updated infant consumption data but NRDC objects that 
``EPA does not assert that these data represent a statistically 
adequate or representative sample.'' (Id.). Finally, NRDC implies that 
EPA thinks the data are not reliable by citing an EPA statement 
regarding the reliability of monitoring data.
    b. Background. NRDC made almost identical claims in its petition to 
revoke DDVP tolerances. EPA responded with a detailed examination of 
each of the factors cited by NRDC as well as several additional 
factors. (72 FR at 68684-68686). Where EPA identified weaknesses in the 
exposure database it either incorporated new, updated data in its risk 
assessment (for example, replacing data from the FDA Total Diet Study 
with data from USDA's Pesticide Data Program) or explained how that 
weakness had been addressed by conservative assumptions. (72 FR at 
68684). This led to an entirely revised dietary exposure and risk 
assessment for DDVP. As to this revised assessment, EPA concluded that 
``its assessment of exposure to DDVP from food will not under-estimate 
but rather over-estimate, and in all likelihood substantially over-
estimate, DDVP exposure.'' (72 FR at 68686). EPA also noted that the 
largest ``driver'' or contributor to dietary exposure of DDVP was DDVP 
in drinking water and not DDVP in food. (Id.). Specifically, as to food 
consumption data for infants, EPA stated that it had incorporated the 
most recent consumption data for infants that is used in all EPA 
pesticide risk assessments currently in its revised risk assessment for 
DDVP. This most recent data was collected at the direction of Congress 
in the FQPA. (Public Law 104-170, sec. 301; 110 Stat. 1489, 1511).
    c. Denial of hearing request. NRDC's objection and request for a 
hearing on this sub-issue suffers from several infirmities. First, NRDC 
has objected to an outdated document, EPA's preliminary risk assessment 
for DDVP. With the exception of the issue concerning food consumption 
data for infants, NRDC has made no effort to object to EPA's current 
assessment of the reliability of various factors cited by NRDC in EPA's 
petition response issued under FFDCA section 408(d)(4)(iii). When an 
objector does not challenge EPA conclusions in the section 
408(d)(4)(iii) order but rather challenges some prior conclusion that 
was

[[Page 42699]]

superseded by the section 408(d)(4)(iii) order, the objector has not 
raised a live controversy as to an issue material to the section 
408(d)(4)(iii) order. (See 53 FR 53176, 53191 (December 30, 1988) 
(where FDA responds to a comment in the final rule, repetition of the 
comment in objections does not present a live controversy unless the 
objector proffers some evidence calling FDA's conclusion into 
question)). In fact, in these circumstances, it is questionable whether 
EPA has jurisdiction to consider the objection and hearing request 
because objections may only be filed as to a section 408(d)(4)(iii) 
order or other statutorily-specified action. (21 U.S.C. 346a(g)(2)(A)).
    Second, NRDC has made no proffer of evidence supporting its claim 
that each of the factors cited from EPA's preliminary risk assessment 
``poses a serious risk of understating the risks posed by DDVP 
contamination of food.'' (Ref. 1 at 6). NRDC's entire argument 
concerning the effect these factors (other than the infant food 
consumption data issue) would have on the DDVP exposure assessment is a 
single conclusory sentence. A hearing will not be granted on ``mere 
allegations'' or ``general contentions.'' (40 CFR 178.32(b)(2)). 
Although NRDC discusses the infant food consumption data issue at 
greater length, this discussion provides no support for granting a 
hearing. NRDC's discussion is limited to: (1) a presentation of a short 
analysis of the adequacy of the superseded consumption data as opposed 
to the data upon which EPA relied in denying NRDC's objection; and (2) 
a claim that EPA has not made a finding that the more recent infant 
food consumption data ``represent a statistically adequate or 
representative sample.'' (Ref. 1 at 6-7). However, the superseded data 
is irrelevant to the present proceeding and the allegation about an 
absent finding is framed as a procedural/legal challenge, not an 
identification of evidence supporting factual contentions. (See 53 FR 
53176, 53199 (December 30, 1998) (``Rather than presenting evidence, 
[the objector] asserts that FDA did not adequately justify its 
conclusions. Such an assertion will not justify a hearing.'').
    Third, ignoring for a moment the other serious flaws identified 
above, a hearing is inappropriate on this issue because NRDC has not 
shown a disputed factual issue. Rather, NRDC is essentially arguing 
about the correct conclusion that should be drawn from the factual 
findings made by EPA in its preliminary risk assessment. (47 FR 55471, 
55474 (December 10, 1982) (``[Objectors] assertion about this evidence 
is, at best, an argument that a different inference (i.e., that the 
pieces are not `reasonably uniform' and `cube shaped') should be drawn 
from established fact (the dimensions of the pieces) than the agency 
has drawn. No hearing is required in such circumstances.'').
    Finally, this entire issue suffers a materiality problem because 
dietary exposure to DDVP in food is so small relative to other DDVP 
exposures. As EPA noted in its petition denial, the ``latest dietary 
assessment shows that, by a large margin, the biggest driver in the 
DDVP dietary risk assessment are DDVP residues in water not food.'' (72 
FR at 68686). Moreover, in evaluating aggregate exposure to DDVP from 
all sources EPA found that dietary exposure from food and water was 
``insignificant'' compared to exposures from pest strips. NRDC has made 
no showing that its concerns regarding dietary exposure to DDVP in food 
are material to the overall exposure assessment. (See 53 FR 53176, 
53202 (December 30, 1998) (The objector claims that radiation causes 
nutrient loss but ``to justify a hearing on this point, it is not 
enough for [the objector] to simply assert that some nutrient loss can 
occur. [The objector] must present evidence that suggests that nutrient 
losses in food irradiated at doses permitted by the regulation are 
sufficiently large and would so affect the diet that such food would be 
nutritionally unwholesome or unsafe.'').
    For all of the above reasons, NRDC's hearing request on the 
adequacy of the DDVP dietary exposure assessment are denied.
    d. Denial of objections. EPA questions whether NRDC's repetition of 
EPA's statements from a preliminary risk assessment constitute an 
objection to a superseding risk assessment in a section 408(d) petition 
denial. In any event, EPA has already explained in great detail in its 
petition denial why the factors cited in its preliminary risk 
assessment do not raise a concern that EPA in its latest assessment has 
understated DDVP dietary exposure. To the contrary, EPA concluded that 
its dietary assessment will ``over-estimate, and in all likelihood 
substantially over-estimate, DDVP exposure.'' (72 FR at 68686). 
Accordingly, NRDC's objections, to the extent they merely repeat the 
claims in the petition, are denied for the same reasons stated in the 
petition denial. (72 FR at 68684-68686).
    EPA also denies NRDC's apparent objection that the updated infant 
food consumption data is unreliable and thus EPA may not depart from 
the 10X children's safety factor. The only two grounds NRDC cited for 
this objection were: (1) EPA's alleged failure to confirm that these 
data are ``statistically adequate or [a] representative sample;'' and 
(2) a reference EPA made to monitoring data. NRDC's arguments here are 
without merit.
    EPA has traditionally relied upon large scale surveys of food 
consumption conducted by the USDA in assessing dietary exposure and 
risk from pesticides. USDA generally conducts these surveys roughly 
every 10 years. EPA currently relies primarily on the Continuing Survey 
of Food Intakes by Individuals (``CSFII'') which was conducted in 1994-
96. Prior surveys were performed by USDA in 1977-78 and 1989-91. The 
1994-96 CSFII was supplemented in 1998 to expand the number of data 
points for infants and children. As EPA has explained: ``These surveys 
were designed to monitor food use and food consumption patterns in the 
U.S. population. The data were collected as a multistage, stratified, 
probability sample that was representative of the U.S. population. [] 
The most recent survey (CSFII 1994-1996/1998) was designed to obtain a 
sample that would provide equal precision over all sex-age domains. The 
data are used by a number of federal and state agencies to improve 
understanding of factors that affect food intake and the nutritional 
status of the U.S. population. [EPA's Office of Pesticide Programs] 
considers the CSFII data adequate to model the daily variability in the 
U.S. diet.'' (Ref. 5 at 39).
    The 1998 supplemental survey was collected in response to the 
mandate in the FQPA specifying that USDA, in consultation with EPA, was 
to ``coordinate the development and implementation of survey procedures 
to ensure that adequate data on food consumption patterns of infants 
and children are collected.'' (Public Law 104-170, sec. 301; 110 Stat. 
1489, 1511). Congress specified that ``[t]o the extent practicable, 
[these] procedures [] shall include the collection of data on food 
consumption patterns of a statistically valid sample of infants and 
children.'' (Id.). Working together, EPA and USDA adopted a survey plan 
designed to be statistically reliable and representative. (Refs. 25 and 
26). The 1998 survey involved sampling of 5,559 infants and children. 
When combined with the 4,253 infants and children from the 1994-96 
survey, the total sample size for infants and children in the two 
surveys is near 10,000. EPA and USDA concluded that that ``the sample 
sizes for each sex-age group [from the combined surveys] provide a 
sufficient level of precision to ensure statistical reliability of the 
estimates'' except as to

[[Page 42700]]

certain low consumption items for individual age groups (e.g., infant 
consumption of lettuce). (Ref. 25 at 1). Comparison of the 1994-96 and 
1998 surveys indicated few statistical differences in nutrient 
consumption for the different age groups with the exception of 3-5 year 
olds. Even so, ``[t]he differences seen, although statistically 
significant, were relatively small and likely to be of little practical 
or biological significance.'' (Ref. 26 at 2-3).
    Because EPA, in conjunction with USDA, has taken care to insure 
that its surveys of food consumption constitute a statistically valid 
and representative sample of infants and children, NRDC's unsupported 
objection suggesting that this data is somehow inadequate is rejected.
    NRDC's reference to an EPA statement about monitoring data does not 
in any way undermine this conclusion. EPA began a section of the 
petition denial which discusses, among other things, monitoring data of 
residues in food, infant food consumption data, and fumigant monitoring 
data, with the broad statement that ``[i]n general, EPA disagrees that 
the monitoring data are unreliable.'' (72 FR at 68684). While NRDC 
highlights the qualifying language ``in general,'' it ignores the 
critical following sentence that provides: ``To the contrary, EPA 
believes that the monitoring data provide for an appropriately 
conservative risk assessment.'' (Id.). The first sentence was qualified 
by the phrase ``[i]n general,'' because in two instances the EPA's 
residue monitoring data were less than optimal; however, as noted in 
the second sentence, EPA concluded that the risk assessment was 
appropriately conservative because either the data in question were 
insignificant or other factors compensated for any uncertainty in the 
data. The first instance involved residue monitoring data for one minor 
commodity (berries not including strawberries) out of dozens of 
commodities where EPA relied on FDA enforcement monitoring data rather 
than its preferred source, data from USDA's Pesticide Data Program. EPA 
prefers using the USDA data because it is collected using a sampling 
plan designed to capture a representative sample of food in the United 
States, whereas sampling for FDA enforcement data is targeted at food 
where violations are more likely to occur. Such targeted enforcement 
data generally overstates, in comparison to a more representative 
sample, both the frequency of finding pesticide residues in commodities 
and the level of the residues detected. In the second instance, 
fumigant monitoring data was not available for all bagged and packaged 
commodities so EPA translated data across commodities. Although noting 
that this translation introduced some uncertainty, EPA concluded that 
``this uncertainty was more than offset by other factors,'' including a 
testing procedure that utilized maximum application rates and sampling 
within six hours of treatment and the assumption that all bagged and 
packaged commodities would be treated. Finally, the mention of 
``monitoring data'' is a reference to studies that ``monitor'' residues 
in food not surveys of people's food consumption patterns. The latter 
topic was inadvertently included in a section of the order devoted to 
``[f]ood monitoring data.'' (72 FR at 68683). Thus, the sentence cited 
by NRDC does not even refer to food consumption survey data.
    4. Pest strip exposure. NRDC claims that EPA's assessment of 
exposure to DDVP from residential pest strips ``is based on unsupported 
assumptions and inadequate data.'' (Ref. 1 at 8). Accordingly, NRDC 
concludes the EPA lacks reliable data on DDVP exposure from pest strips 
and cannot reduce or remove the 10X children's safety factor. EPA has 
identified seven separate allegations made by NRDC and they are 
analyzed individually below.
    a. Representativeness of Collins and DeVries study--i. Objection/
hearing request sub-issue. NRDC argues that the Collins and DeVries 
study which EPA used to estimate DDVP exposure from pest strips had an 
inadequate sample size (15 houses). According to NRDC, 15 houses is not 
adequate to represent the diversity of housing in the United States 
given the variations in housing design and ventilation characteristics. 
(Ref. 1 at 7). Additionally, NRDC claims that, because the study was 
conducted in a single geographic area and for a period no longer than 
91 days, it does not account for the varying weather conditions which 
can have differential effects on the movement and degradation of 
airborne residues.
    ii. Background. NRDC made the identical claim in its petition. 
EPA's response in its petition denial order was two-fold. First, EPA 
pointed out that the Collins and DeVries study was not the only study 
considered by EPA in assessing DDVP exposure from pest strips. EPA 
reviewed several other studies involving over 100 homes in the United 
States and Europe. The results in the Collins and DeVries study were 
consistent with the results in the other studies and, thus, EPA 
concluded that it was reasonable to use the data from the Collins and 
DeVries study in assessing DDVP risk. (72 FR at 68692). Second, in 
response to this claim (as well as several of NRDC's other claims), EPA 
substantially revised the DDVP exposure and risk assessment. (72 FR at 
68687-68691). Additional conservative assumptions were adopted and 
these conservative assumptions further offset any theoretical 
unrepresentativeness of the Collins and DeVries study. These 
assumptions were that exposed individuals spent 24 hours per day in a 
treated home, that a person spent all of the 24 hours per day in a room 
in the house with a pest strip, and that inclusion of a pest strip in a 
closet resulted in the same exposure as hanging the strip in the room 
itself. Further, EPA no longer averaged the exposure results from the 
houses in the study but evaluated each house individually.
    iii. Denial of hearing request. NRDC's request for hearing on this 
issue is flawed for two reasons. First, as in its petition, NRDC 
proffers no evidence to support its claim that the Collins and DeVries 
study is inadequate due to the diversity of housing stock and 
geographic conditions in the United States. NRDC merely asserts that to 
be the case. However, hearings will not be granted on the basis of mere 
allegations or general contentions. (40 CFR 178.32(b)(2); see also 68 
FR 46403, 46406-46407 (8/5/2003) (FDA denied a hearing involving a 
challenge to FDA's reliance on consumption pattern data because the 
objector ``did not present any specific information to dispute P & G's 
consumption pattern data; instead, [objector] simply asserted that 
other consumption patterns were likely.''); accord Community Nutrition 
Institute v. Novitch, 773 F.2d 1356, 1363 (D.C. Cir. 1985) (``Mere 
differences in the weight or credence given to particular scientific 
studies . . . are insufficient [to show a material issue of fact for a 
hearing].'')).
    Second, NRDC's hearing request is inadequate because NRDC does not 
object to the basis EPA asserted in its petition denial for concluding 
that the Collins and DeVries study does provide a sufficient basis for 
estimating residential exposure. Specifically, NRDC does not challenge 
EPA's conclusion that the Collins and DeVries study is consistent with 
several other pest strip studies and proffer evidence in support of 
that challenge. Neither does NRDC challenge and proffer evidence 
regarding EPA's conservative use of the Collins and DeVries study in 
assessing exposure. Rather, NRDC just repeats its assertions regarding 
the unrepresentativeness of the Collins and DeVries study from its 
petition. This

[[Page 42701]]

failure to challenge the basis of EPA's petition denial affects the 
materiality of the objection and hearing request. Even if NRDC could 
demonstrate in a hearing that the ventilation design of a house, for 
example, can affect the rate at which airborne contaminants are 
dissipated, that evidence would not contradict the fact that the 
Collins and DeVries study is consistent with DDVP pest strip studies in 
over 100 other homes in varying locations.
    Prior FDA decisions under its regulations are instructive here. 
Objections and hearing requests were filed in response to a food 
additive regulation covering the irradiation of poultry. (62 FR 64102 
(December 3, 1997). The objector argued that the addition of an anti-
oxidant (ethoxyquin) to irradiated chicken prior to the chicken's use 
in animal feeding studies compromised the studies because the 
ethoxyquin would have decreased the level of lipid peroxides in the 
chicken to levels found in chicken that had not been irradiated. The 
FDA noted, however, that it had considered the question of ethoxyquin's 
effect on lipid peroxide levels in the final rule and determined that 
while ethoxyquin can retard the normal oxidation of chicken fat to 
peroxides, ethoxyquin cannot reverse oxidation that has already 
occurred. FDA denied the hearing request reasoning that because the 
objector did ``not dispute FDA's explanation in the final rule as to 
why addition of ethoxyquin did not compromise the CIVO studies, and 
provided no information that would have altered the agency's conclusion 
on this issue . . . there is no factual issue that can be resolved by 
available and specifically identified reliable evidence.'' (62 FR at 
64105; see also 53 FR 53176, 53191 (December 30, 1988) (FDA denied a 
hearing request noting that given FDA's prior conclusion that the 
studies relied upon by the objector were unreliable, the ``burden 
shifted to [the objector] to maintain the viability of its objection by 
proffering some information that called into question the agency's 
conclusion on this matter.'')). Similarly, here, NRDC has not 
challenged the basis EPA asserted for rejecting NRDC's challenge to 
EPA's reliance on the Collins and DeVries study and NRDC has not 
proffered any information calling into question EPA's conclusion.
    iv. Denial of objection. Because NRDC offers no basis for its 
objection to EPA's denial of the challenge in its petition to EPA's 
reliance on the Collins and DeVries study--other than the claims made 
in its petition, itself--EPA denies the objections for the reasons in 
the petition denial order (i.e., the consistency of the Collins and 
DeVries study with other DDVP pest strip studies and the 
conservativeness of the DDVP pest strip exposure assessment).
    b. Sampling location in the Collins and DeVries study--i. 
Objection/hearing request sub-issue. NRDC argues that the Collins and 
DeVries study is flawed because air concentration levels of DDVP were 
sampled in only one location in the house. According to NRDC, this 
sampling regime was inadequate because it ``provides no information 
about the movement of residues from room-to-room and therefore exposure 
in other rooms in the homes.'' (Ref. 1 at 7).
    ii. Background. NRDC repeats this claim verbatim from its petition. 
The petition denial order rejected this challenge to the Collins and 
DeVries study and the manner of EPA's use of the study in its exposure 
assessment noting that ``the sample location in each instance was in a 
room with a pest strip, pest strips were used in other rooms of the 
house, and EPA assumed, for its calculation of the MOE, that the air 
concentration for all areas of a house is the same as at the sampled 
location.'' (72 FR at 68692).
    iii. Denial of hearing request. This objection and hearing request 
does not involve a genuine and substantial issue of disputed fact. 
There is no dispute concerning how or where sampling was done in the 
Collins and DeVries study or how EPA used that data in estimating DDVP 
exposure from pest strips. NRDC's objection attacks EPA's conclusion 
that it is reasonable to assess residential DDVP exposure from pest 
strips using air concentrations of DDVP from rooms which contained a 
pest strip. A challenge to an EPA inference drawn from undisputed facts 
does not qualify as a disputed factual question. (47 FR 55471, 55474 
(December 10, 1982) (``[Objectors] assertion about this evidence is, at 
best, an argument that a different inference (i.e., that the pieces are 
not `reasonably uniform' and `cube shaped') should be drawn from 
established fact (the dimensions of the pieces) than the agency has 
drawn. No hearing is required in such circumstances.'')). Moreover, 
NRDC does not explain why knowledge of the amount of room-to-room DDVP 
movement is relevant given that EPA based its exposure assumption on 
the level of DDVP found in a room with a pest strip, much less proffer 
any evidence to suggest why this issue is material and should be 
resolved in its favor. For all of these reasons, NRDC's hearing request 
on this issue is denied.
    iv. Denial of objection. This objection is denied for the same 
reason stated in the petition denial order: knowledge of the amount of 
room-to-room movement of DDVP is irrelevant if EPA bases its exposure 
assessment on a room that contains a pest strip. In both its petition 
and its objections, NRDC cites the following statement from EPA's 
preliminary risk assessment as supporting its conclusion regarding the 
inadequacy of use of a single air monitor in the Collins and DeVries 
study: ``A more accurate exposure would be possible if air measurements 
were available from different rooms in the house.'' (Ref. 1 at 7). 
NRDC, however, misunderstands the thrust of this sentence. EPA was 
simply pointing out that monitoring in rooms without pest strips would 
have provided a more accurate and realistic - i.e., lower - estimate of 
exposure than using values from a room containing a pest strip. The 
sentences immediately following the language quoted by NRDC make this 
clear. EPA stated: ``Limited data suggest that the level of Dichlorvos 
in the air declines with distance from the resin pest strip. There are 
data from the Dichlorvos Flea Collar Study that show Dichlorvos levels 
are lower some distance away from the pet flea collar.'' (Ref. 27 at 
53).
    c. Averaging DDVP concentrations over 120 days--i. Objection/
hearing request sub-issue. NRDC objects to EPA's assessment of exposure 
to pest strips challenging EPA's alleged use of a 120-day average of 
DDVP concentration levels. NRDC argues that ``[r]ather than using 
averages, the Agency should have presented the range of risks displayed 
over time, peak measurements, and the daily monitoring data so that 
trends over time could be determined.'' (Ref. 1 at 7).
    ii. Background. NRDC repeats this claim verbatim from its petition. 
In its petition denial order, EPA agreed with NRDC and revised its 
residential exposure assessment to examine exposure and risk based on 
the first day of exposure after hanging the pest strip, the first 2 
weeks of exposure, and exposure over a 91 day period. (72 FR at 68687).
    iii. Denial of hearing A hearing can only be based on a genuine 
issue of disputed fact. Where a party's factual allegations are 
contradicted by the record, there is no genuine dispute. (57 FR 6667, 
6672 (February 27, 1992) (``A hearing must be based on reliable 
evidence, not on mere allegations or on information that is inaccurate 
and contradicted by the record.'').
    iv. Denial of objection. NRDC's objection is directed at a prior,

[[Page 42702]]

superseded risk assessment, not the risk assessment relied upon in the 
petition denial order. Thus, this objection is not material to this 
proceeding and is denied. (See Unit VIII.D.3.c.).
    d. Replacement cycle for pest strips--i. Objection/hearing request 
sub-issue. NRDC objects to EPA's assumption that pest strips are 
replaced no more frequently than 120 days even though the pest strip 
label does not prohibit more frequent replacement. (Ref.1 at 8). NRDC 
argues that EPA has no data to substantiate this assumption and claims 
that homeowners may decide ``to replace strips sooner `for good 
measure.''' (Id.). Recognizing that EPA decreased its assumption 
concerning the replacement cycle to 91 days in the revised risk 
assessment in the petition denial order, NRDC asserts that this value 
is equally arbitrary.
    ii. Background. The challenge to the 120-day replacement assumption 
was included in NRDC's petition. EPA responded to NRDC's argument in 
the petition denial order by decreasing its assumption as on the 
replacement cycle of pest strips to 91 days. (72 FR at 68692).
    iii. Denial of hearing. This sub-issue does not meet the standard 
for a hearing. NRDC disputes the reasonableness of EPA's choice of a 
replacement cycle for pest strips in the absence of a restriction on 
the pesticide label or data documenting consumer usage. NRDC proffers 
no evidence challenging EPA's use of a 91-day replacement cycle. 
Rather, NRDC asserts a legal argument that in the absence of specific 
data on consumer usage, EPA may not make an assumption about consumer 
practices. Hearings are not appropriate on legal questions. (40 CFR 
178.32(b)(1)). Similarly, NRDC's speculation about how often homeowners 
may replace pest strips does not constitute an evidentiary proffer 
justifying a hearing. (See 57 FR 33244, 33248 (July 27, 1992) (NRDC 
claimed that the removal of premix batch analysis would lead to 
misformulation of selenium in feeds. A hearing was denied because NRDC 
``provided no factual information to support its claim . . . . [A] 
hearing will not be granted on the basis of mere allegations.'')).
    iv. Denial of objection. In its preliminary risk assessment and in 
the IRED, EPA assumed that pest strips would be replaced no more 
frequently than 120 days because the pest strip label specifies: 
``Drafts, weather, and other conditions may affect the performance, but 
treatment usually last for 4 months. Record the date of installation 
and replace with a new, fresh, full-strength strip at the end of 4 
months or when effectiveness diminishes.'' (Ref. 28). Given that the 
manufacturer was essentially designating 120 days as the likely 
effective period and that consumers might leave the pest strips up for 
either longer or shorter periods, EPA assumed that 120 days was a 
reasonable estimate of the average replacement cycle for pest strips. 
EPA generally uses average values for chronic exposure scenarios 
because over time high and low values tend to average out. (Ref. 5 at 
42). Nonetheless, in recognition of NRDC's contention that homeowners 
might replace strips more frequently, EPA amended its pest strip 
exposure to assume a 91-day replacement cycle (the length of the 
Collins and DeVries study) rather than extrapolate the data from the 
Collins and DeVries study over 120 days as was done previously. EPA 
believes 91 days is a reasonable estimate of the replacement cycle 
especially given the label language and the numerous conservative 
assumptions in the risk assessment such as, for example, the assumption 
of 24 hours per day exposure in a room containing a pest strip. 
Accordingly, NRDC's objection on this sub-issue is denied.
    e. Number of pest strips--i. Objection/hearing request sub-issue. 
NRDC claims that EPA's assessment of DDVP exposure from pest strips is 
not based on adequate data because EPA does not have any data on how 
many strips people use in their homes. EPA assessed residential DDVP 
exposure based on the Collins and DeVries study which used 3-4 strips 
per house in each of the studied houses. NRDC argues that some 
homeowners may use more than 3-4 strips because there is no limitation 
on the label as to the number of strips per house.
    ii. Background. NRDC repeats this claim verbatim from its petition. 
EPA rejected NRDC's concern in the petition denial order reasoning that 
its assessment was based on data on the air concentration of DDVP in a 
room containing a pest strip. (72 FR at 68692). EPA also noted that the 
only strips allowed in occupied areas of the home under the current 
registration are for closets, wardrobes, or cupboards and given that 
they treat a relatively small space, compared to the bigger strips used 
in the Collins and DeVries study, they are unlikely to result in 
significant DDVP air concentrations in rooms other than in the room 
containing the treated area. (Id.).
    iii. Denial of hearing. NRDC has not alleged and proffered evidence 
on a genuine and substantial issue of disputed fact. NRDC speculates 
that use of pest strips in every, or almost every, room in a house may 
lead to higher residues in a room containing a pest strip than a room 
containing a pest strip in a house which has a pest strip in 3-4 rooms. 
Based on this speculation, NRDC claims that EPA's exposure assessment 
is inadequate because EPA has not documented how many strips people use 
in their houses. A hearing will not be granted on the basis of mere 
allegations or speculation about what other studies might show. (See 57 
FR 33244, 33248 (July 27, 1992) (NRDC claimed that the removal of 
premix batch analysis would lead to misformulation of selenimum in 
feeds. A hearing was denied because NRDC ``provided no factual 
information to support its claim . . . . [A] hearing will not be 
granted on the basis of mere allegations.'')).
    iv. Denial of objection. For several reasons, NRDC's speculation 
that a house containing strips in nearly every room might lead to 
greater DDVP exposures than estimated by EPA must be rejected. First, 
EPA based its DDVP pest strip exposure assessment on a study (Collins 
and DeVries) which measured DDVP concentrations in a room containing a 
pest strip. Second, the Collins and DeVries study did not involve a 
house with a single strip but used pest strips in 3-4 rooms of the 
studied houses. Third, the results of the Collins and DeVries study 
were consistent with the results of several other pest strip studies. 
Fourth, although corrected for the smaller size of current pest strips 
compared to the pest strips used in the Collins and DeVries study, EPA 
did not adjust its assessment for the fact that current strips may not 
be used for general space treatment but must be put in closets, 
wardrobes, or cupboards. Taking into account these factors, EPA's 
assessment of exposure from DDVP pest strips was reasonable and based 
upon adequate, reliable data to reduce or remove the children's safety 
factor.
    f. Exposure time per day--i. Objection/hearing request sub-issue. 
NRDC objects that it was unreasonable for EPA to assume that the high 
end exposure period in the home is 16 hours and that a low end exposure 
period is 2 hours. NRDC argues that some groups of people may spend 
significantly greater amounts of time in their homes. NRDC asserts that 
EPA does not adequately justify these assumptions in its petition 
denial order.
    ii. Background. NRDC repeats this claim verbatim from its petition. 
In response to NRDC's petition, EPA substantially revised its pest 
strip exposure assessment. As to exposure

[[Page 42703]]

periods, EPA completely dropped its prior approach and assessed 
exposure assuming a person spent 24 hours per day in their home in a 
room containing a pest strip. (72 FR at 68687).
    iii. Denial of hearing. A hearing can only be based on a genuine 
issue of disputed fact. Where a party's factual allegations are 
contradicted by the record, there is no genuine dispute. (57 FR 6667, 
6672 (February 27, 1992) (``A hearing must be based on reliable 
evidence, not on mere allegations or on information that is inaccurate 
and contradicted by the record.'').
    iv. Denial of objection. NRDC's objection is directed at a prior, 
superseded risk assessment, not the risk assessment relied upon in the 
petition denial order. Thus, this objection is not material to this 
proceeding and is denied. (See Unit VIII.D.3.c.).
    g. Movement of DDVP from unoccupied areas of the home to occupied 
areas--i. Objection/hearing request sub-issue. NRDC claims that EPA 
does not have a sufficient basis for its conclusion that pest strips 
used in unoccupied places in a house (garages, attics, crawl spaces, 
sheds) will not migrate to occupied portions of the house. Thus, NRDC 
argues EPA does not have reliable data to reduce or remove the 
children's safety factor.
    ii. Background. NRDC made the same argument in its petition. 
Additionally, in the petition, NRDC cited a study with another 
pesticide which NRDC claimed showed that pesticides could migrate into 
the house. EPA disagreed with NRDC's assertion, pointing out that 
migration was unlikely unless the unoccupied portion was connected to 
the air exchange system for the house. EPA also explained in detail why 
the study cited by NRDC was not relevant to DDVP. NRDC did not renew 
its arguments based on this study.
    iii. Denial of hearing. NRDC has not alleged and proffered evidence 
on a genuine and substantial issue of disputed fact. NRDC speculates 
that use of pest strips in unoccupied areas of a house may lead to 
migration of DDVP residues to occupied portions of the house. Based on 
this speculation, NRDC claims that EPA's exposure assessment is 
inadequate because EPA has not documented that such migration does not 
occur. A hearing will not be granted on the basis of mere allegations 
or speculation about what other studies might show. (See 57 FR 33244, 
33248 (July 27, 1992) (NRDC claimed that the removal of premix batch 
analysis would lead to misformulation of selenium in feeds. A hearing 
was denied because NRDC ``provided no factual information to support 
its claim . . . . [A] hearing will not be granted on the basis of mere 
allegations.'')).
    iv. Denial of objection. NRDC's objection is denied. Given EPA's 
knowledge of the chemical properties of DDVP, it was reasonable to 
assume that DDVP would not migrate from unoccupied portions of the home 
to occupied portions absent some type of air exchange connection 
between the two areas. DDVP is a highly volatile chemical that quickly 
degrades once released to the environment. EPA reasonably concluded 
that the low concentration of airborne DDVP produced from a DDVP pest 
strip would not penetrate the walls of a home in meaningful amounts.

E. Response to Specific Issues Raised in Objections and Hearing 
Requests - Reliance on Human Study

    1. Background. In making its FFDCA tolerance reassessment decision 
and FIFRA reregistration decision for DDVP, EPA relied upon one human 
toxicity study in deriving an acceptable level of exposure for several 
exposure scenarios. The study in question was conducted in 1997 by A.J. 
Gledhill. In this study, six male volunteers were administered 7 mg of 
DDVP in corn oil (equivalent to approximately 0.1 mg/kg/day) via 
capsule daily for 21 days. Three control subjects received corn oil as 
a placebo. Baseline values for RBC cholinesterase activity for each 
study participant were determined based upon repeated measurements 
prior to the administration of DDVP. After dosing started, RBC 
cholinesterase activity was monitored on days 2, 4, 7, 9, 11, 14, 16, 
and 18, and then on day 25 or 28 post-dosing. Although no toxicity 
attributable to administration of DDVP was reported by the test 
subjects, mean RBC cholinesterase activity was statistically 
significantly reduced in treated subjects on days 7, 11, 14, 16, and 
18. These values were 8, 10, 14, 14, and 16 percent below the pre-dose 
mean. (Refs. 15 and 16).
    EPA's decision to rely on the Gledhill study was made pursuant to 
its Human Research rule. As explained in Unit III.D, that rule 
establishes different ethical standards for the review of completed 
human studies depending on whether they were initiated before or after 
the effective date of the rule on April 7, 2006. For an intentional 
human exposure study such as the Gledhill study, that was initiated 
prior to April 7, 2006, EPA is barred, subject to a very limited 
exception, from relying on it if there is clear and convincing evidence 
that the conduct of the research was fundamentally unethical or 
significantly deficient with respect to the ethical standards 
prevailing at the time the research was conducted. (40 CFR 26.1704, 
1706). Further, the rule limits the human research that can be relied 
upon by EPA to ``scientifically valid and relevant data.'' (40 CFR 
26.1701). Finally, because the Gledhill study was conducted with the 
purpose of identifying or measuring a toxic effect, EPA is required by 
the rule to submit its determination regarding these issues to an 
independent expert advisory body known as the Human Studies Review 
Board (``HSRB'') for review. These procedures were followed with regard 
to the Gledhill study.
    Previously, NRDC has challenged the lawfulness of the Human 
Research rule. Following promulgation of the Human Research Rule, NRDC 
filed a petition for judicial review of the rule in the United States 
Court of Appeals for the Second Circuit. (NRDC v. U.S. EPA, No. 06-
0820-ag (2d Cir.)). That case has been briefed and argued and is 
awaiting decision.
    NRDC also previously challenged the scientific merit and ethics of 
the Gledhill study in comments to EPA and to the HSRB. Specifically as 
to the HSRB, NRDC filed written comments prior to the HSRB's review of 
EPA's determination regarding the appropriateness of relying on the 
Gledhill study and also presented oral testimony at the public hearing 
the HSRB held with regard to that study. Subsequently, the HSRB, after 
taking into account the comments of NRDC and others, advised EPA that 
reliance on the Gledhill study was consistent with the Human Research 
rule. EPA relied heavily on the analysis of the HSRB in denying NRDC's 
petition to revoke DDVP tolerances. (72 FR at 68675).
    In its petition to revoke DDVP tolerances, NRDC repeated its 
arguments made to the HSRB as to why the Gledhill study does not comply 
with the Human Research rule. As support, NRDC cited to a draft HSRB 
report on the Gledhill study, released shortly before NRDC filed its 
petition, which noted scientific and ethical deficiencies in the study. 
(Ref. 2 at 26). NRDC did not acknowledge, however, that despite 
identifying deficiencies in the Gledhill study, the HSRB, in its draft 
report, stated its agreement with EPA's determination that it would be 
acceptable to rely on the Gledhill study.
    In its objections, NRDC once again makes the same arguments on the 
Gledhill study it made to the HSRB and in its petition to EPA 
(including the misleading reference to a portion of the draft report of 
the HSRB). Similar to the approach taken in the petition, NRDC does not 
even acknowledge the

[[Page 42704]]

recommendations made by the HSRB in its draft and final decisions 
despite EPA's explicit reliance on the HSRB's reasoning in EPA's 
petition denial order.
    NRDC's objections also include a challenge to the legality of the 
Human Research rule paralleling the case pending in the Second Circuit.
    2. Challenge to the human research rule--a. Objection/hearing 
request sub-issue. NRDC argues that ``to the extent [its] facial 
challenge to the [Human Research] rule is not proper,'' it is renewing 
its arguments regarding the legality of the rule in its objections. 
(Ref. 1 at 9-10). The objections incorporate by reference NRDC's legal 
briefs filed in the Second Circuit and its comments filed on the Human 
Research rule as support for this objection. In its legal briefs, NRDC 
argues that EPA's rule is inconsistent with a congressional funding 
moratorium in an Appropriations Act. (Ref. 29). That Act prohibited EPA 
from ``accept[ing], consider[ing] or rely[ing] on third-party 
intentional dosing human toxicity studies for pesticides . . . until 
[EPA] issues a final rulemaking on this subject.'' (Public Law 109-54, 
sec. 201, 119 Stat. 499, 531 (August 2, 2005)). According to NRDC, EPA 
did not comply with this legislation's requirement that the EPA human 
testing rule bar testing on pregnant women, infants and children and be 
consistent with the principles in a 2004 National Academy of Sciences 
Report and the Nuremburg Code on human experimentation. (Ref. 29 at 
23). NRDC did not specifically lay out the arguments in its legal 
briefs in its objections other than to include a summary of some of the 
principles of the Nuremberg Code. (Ref. 1 at 11-12). Similar arguments 
are made in NRDC's comments on EPA's proposed Human Research rule. 
(Ref. 30).
    b. Background. Arguments concerning the legality of the Human 
Research Rule were not contained in the petition.
    c. Denial of hearing request. In this sub-issue, NRDC presents, by 
reference, various arguments that the Human Research rule is not 
consistent with congressional legislation bearing on the rule. These 
arguments raise questions regarding the proper interpretation of 
statutory language and hearings are not appropriate on such issues. (40 
CFR 178.32(b)(1)).
    d. Denial of objection. To the extent this matter is not resolved 
by the Second Circuit and NRDC has standing to challenge a rule whose 
``primary concern'' is the ``[p]rotection of the health and safety of 
human test subjects,'' (Ref. 1 at 15), EPA denies NRDC's objections to 
the legality of the Human Research rule. EPA believes the Human 
Research rule is fully consistent with the Appropriations Act and EPA 
has fully explained the basis for this conclusion in the rulemaking 
record (EPA-HQ-OPP-2003-0132) and its legal brief filed in the Second 
Circuit proceeding. (Ref. 31).
    3. Challenge to reliance on the Gledhill Study--a. Statistical 
power - too few subjects to detect an effect--i. Objection/hearing 
request sub-issue. NRDC objects that the number of test subjects in the 
Gledhill study was low and thus there are statistical issues with 
extrapolating from the results of the Gledhill study to the general 
human population. (Ref. 1 at 13). In part, NRDC frames this argument as 
the Gledhill study lacks ``statistical power'' and NRDC references four 
published letters or articles in support of this claim. (Ref. 1 at 15). 
Further, NRDC claims that the statistical power issue is particularly 
important for studies such as the Gledhill study which measure 
cholinesterase inhibition because of the variability among individuals 
of cholinesterase inhibition over time. According to NRDC, the ``range 
of variability both between and for the individual test subjects means 
that even greater than the customary number of test subjects would be 
required to permit adequate statistical power to detect effects caused 
by the test substance above background variations.'' (Ref. 1 at 13). As 
evidence of this cholinesterase inhibition variability in humans, NRDC 
cites to another human study by Gledhill (MRID  4428802 rather 
than MRID  44248801).
    NRDC's objection here appears to be confusing two separate issues: 
(1) did the Gledhill study have sufficient statistical power to detect 
an effect caused by DDVP; and (2) does the Gledhill study contain 
sufficient data to reliably estimate a safe dose for humans. The first 
issue is addressed in this Unit and the second in Unit VIII.E.3.b.
    ii. Background. NRDC's objection repeats assertions made in its 
petition to revoke DDVP tolerances and its comments on the DDVP IRED. 
(Ref. 2 at 26-27; Ref. 23 at 14-17). EPA rejected NRDC's claims about 
statistical power, explaining that ``[a]lthough as a general matter 
more subjects would provide greater `statistical power,' in this case 
the use of 6 to 9 subjects with the appropriate statistical methodology 
is acceptable to EPA because a positive response was seen.'' (72 FR at 
68675). EPA also noted that the variability within the cholinesterase 
inhibition of the tested subjects ``is not large, particularly since 
the percentage inhibition in all instances was at the marginal end of 
the range.'' (Id.).
    iii. Denial of hearing. A hearing is not required on NRDC's 
statistical power claim because the concept of statistical power is 
simply not applicable to the conclusions EPA drew with regard to the 
Gledhill study and thus this issue is not material to NRDC's requested 
relief. Further, the evidence proffered by NRDC would not, if 
established, resolve this issue in NRDC's favor.
    To understand EPA's ruling here, some basic definitional 
information on the concept of ``statistical power'' and how it applies 
in the context of toxicity studies may be helpful. Toxicity testing is 
designed to test the veracity of the hypothesis that there will be no 
differences in health outcomes between treated and untreated (control) 
subjects. Statisticians refer to this hypothesis as the ``null 
hypothesis.'' The ``alternative hypothesis'' is that there will be a 
difference between treated and control subjects. In general terms, 
statistical power measures the probability that a toxicological study 
will find a treatment-related adverse health outcome when there is a 
treatment-related adverse effect to be found. (Ref. 32 at 125 and 
n.144). In the language of a statistician, statistical power measures 
the ``probability of rejecting the null hypothesis when the alternative 
hypothesis is right.'' (Id.). A study with a statistical power value of 
near one (1) would have a very high chance of (properly) rejecting the 
null hypothesis if the alternative hypothesis is true, whereas a power 
value close to zero (0) would indicate that there is little chance that 
the study will identify any true adverse health outcomes occurring as a 
result of treatment.
    Statistical power can also be used to calculate the probability 
that the study will falsely find that there is no difference in the 
health outcomes between treated and control subjects, that is, whether 
the study will falsely affirm the null hypothesis. The probability of 
such a false negative, is determined by subtracting the statistical 
power of a study from one (1). (Id.). Thus, the chance that a study 
will result in a false negative is directly related to the chance that 
the study will identify any effects present. For example, if a study 
has low statistical power, there will be a low probability that the 
study will find an effect if there is one and a high probability that 
the study will falsely affirm that there is no effect. Statistical 
power, therefore, is a important tool in designing studies to ensure 
that effects from treatment are not missed and may play a role in

[[Page 42705]]

evaluating completed studies that confirm the null hypothesis to 
determine the probability that the null hypothesis was not falsely 
affirmed (i.e., a false negative).
    If analysis of a toxicological study shows that there are 
treatment-related effects (i.e., the null hypothesis of no treatment-
related effect is rejected), then the question of the statistical power 
of the study becomes largely irrelevant. Put another way, if a study 
shows a positive outcome, the probability that the study might have 
produced a false negative becomes a moot point. Importantly, with the 
Gledhill study, the null hypothesis of no treatment-related effect was 
rejected: that is, the HSRB and EPA concluded that there was a 
significant difference in cholinesterase inhibition both between 
controls and DDVP-treated subjects and between the inhibition levels 
pre- and post-treatment of the DDVP-treated subjects.
    With that background, the scientific papers cited by NRDC can be 
more easily followed. First, NRDC cites a one-page letter to the 
Environmental Health Perspectives journal which was co-authored by 
Jennifer Sass, a NRDC senior scientist, and a subsequent letter, again 
co-authored by Sass, that responded to various letters expressing a 
different viewpoint. (Ref. 1 at 15, and Refs. 33 and 34). The topic of 
both Sass letters is nicely captured by the title attached to the first 
letter: ``Industry Testing of Toxic Pesticide on Human Subjects 
Concluded `No Effect,' Despite the Evidence.'' (Ref. 33 ).
    The first letter discusses the DDVP Gledhill study and a second 
human study involving a different pesticide. With regard to the DDVP 
Gledhill study, Sass criticizes Amvac's analysis of that study. Amvac 
had concluded that the Gledhill study demonstrated a NOAEL arguing that 
the cholinesterase inhibition effects seen at the single dose in that 
study were not biologically significant. Sass counters that ``the only 
biological end point measured in the study was cholinesterase 
inhibition, and this was significantly inhibited.'' (Ref. 33 at A150). 
As to statistical power, Sass claims that studies involving only a few 
human subjects ``often lack enough subjects to provide adequate 
statistical power to detect an effect if it is present.'' (Id.).
    The second letter repeats this latter assertion and claims that the 
statistical power of human studies then available have such low 
statistical power that they ``practically guarantee[d] a finding of no 
effect.'' (Ref. 34 at A340). Sass then returns to the Gledhill study 
and notes with approval EPA's conclusion that that study demonstrated a 
LOAEL: ``the U.S. Environmental Protection Agency (EPA) rejected 
AMVAC's interpretation of the results, instead concluding that `the 
reduction in RBC cholinesterase activity was considered by the Hazard 
ID [identification] Committee to be biologically significant, and the 
dose tested was considered to be a lowest observed effect level 
(LOEL).''' (Id.). EPA's reversal of the Amvac conclusion is cited by 
the letter as illustrative of bias by chemical manufacturers in the 
design and interpretation of studies.
    For at least two reasons, these letters neither demonstrate the 
materiality of NRDC's statistical power claims nor constitute a 
sufficient evidentiary proffer. First, although they do contain 
allegations about low statistical power of human studies with low 
numbers of subjects, they only address the question of whether such 
studies can detect an effect even if an effect is present (i.e., are 
they likely to falsely affirm the null hypothesis that there are no 
treatment-related adverse effects). In the DDVP Gledhill study, 
however, EPA and the HSRB concluded that the study did identify an 
adverse effect. Accordingly, the letters have little relevance to EPA's 
ultimate finding with regard to the Gledhill study. Second, these 
letters do not challenge EPA's analysis of the Gledhill study - rather, 
they ratify it. Thus, the letters do not proffer evidence, which would, 
if established, resolve a material issue in NRDC's favor. (See 57 FR 
33244, 33246 (July 7, 1992) (Studies cited by NRDC do not provide a 
basis for the hearing because they ``support the [FDA] conclusion in 
question.'')).
    NRDC also cites two articles by Alan Lockwood. One is an article in 
the American Journal of Public Health discussing ethical and scientific 
considerations with regard to six human toxicology studies, including 
the Gledhill study at issue in this proceeding. (Refs. 1 at 15; and 
35). The second is a one-page summary of the earlier article that was 
published in The Environmental Forum. (Ref. 36). The first article 
contains the following paragraph discussing statistical power:
    A power analysis to define the proper size of study group(s) is 
an essential part of the design. If too many participants are 
enrolled, the excess will be subjected to unnecessary risk. If too 
few are enrolled, the investigator risks erroneous acceptance of the 
null hypothesis. Underpowered studies are inconclusive, and all 
participants in an underpowered study will have been exposed to risk 
unnecessarily. All of these studies were underpowered.

(Ref. 35 at 1912). There is little to no explanation provided in the 
article for the ``underpowered'' conclusion other than the notation 
that the six studies involved young healthy adults. There is little, if 
any, discussion of the Gledhill DDVP study at issue in this proceeding. 
The summary article adds nothing new to the longer article.
    Like the Sass letters, therefore, the Lockwood articles do not 
constitute a proffer of evidence that if established would resolve a 
material issue in favor of NRDC. Not only do they not proffer any 
evidence, they focus on an issue not involved here - do human studies, 
such as the Gledhill study, have sufficient statistical power to avoid 
``erroneous acceptance of the null hypothesis.'' Both EPA and the HSRB 
rejected the null hypothesis as to the Gledhill study (i.e., an adverse 
effect on the treated subjects was identified). Additionally, these 
articles do not advance specific evidence, or even arguments, 
concerning the Gledhill study itself. (See 53 FR 53176, 53179-53180 
(December 30, 1998) (a general assertion in a letter to Science 
magazine is not basis for a hearing); 68 FR 46403, 46405-46406 (August 
5, 2003) (a hearing was denied because the cited studies only contained 
equivocal statements supporting the objector's position)).
    NRDC also cites the variable level of cholinesterase inhibition 
within individuals as supporting its statistical power argument. NRDC 
references a different DDVP human study by Gledhill (MRID  
44248802) to show variability in cholinesterase inhibition. This 
argument and these data also do not justify a hearing.
    Initially, it must be noted that EPA cannot consider this other 
Gledhill study because both EPA and the HSRB concluded it was without 
scientific merit and therefore does not qualify for EPA consideration 
under the Human Research rule. (Ref. 21 at 42-43). Whether or not the 
aspect of the study cited by NRDC is implicated by this conclusion has 
not been evaluated; nonetheless, EPA does not disagree with NRDC's 
assertion that individual humans have variable levels of cholinesterase 
inhibition and thus this is not a disputed issue of fact. Neither does 
EPA dispute that variability of cholinesterase inhibition should be 
taken into account in considering statistical power and in analyzing 
the results of a human study.
    However, as discussed above, statistical power is no longer a 
relevant concept once EPA has concluded that a toxicity study shows 
that the pesticide has an adverse effect on treated subjects. 
Statistical power is a tool used to evaluate the possibility of 
accepting false negatives. Moreover, the variability

[[Page 42706]]

of cholinesterase inhibition in subjects is also a factor relating to a 
concern with false negatives. Normal variation in the responses of 
individual test subjects may mask treatment-related effects leading to 
a false conclusion that there were no treatment-related effects. 
Finally, NRDC's claims on variability amount to no more than a mere 
allegation that the existence of variable rates of cholinesterase 
inhibition indicate a flaw in the Gledhill study and EPA's reliance on 
it. Without an evidentiary proffer, however, a hearing is not 
appropriate.
    iv. Denial of objection. NRDC has misconstrued the concept of 
statistical power. It has little relevance in circumstances where a 
positive effect is found in a toxicological study. NRDC's objection 
that EPA should not have relied upon the Gledhill study because it 
lacked statistical power is denied.
    b. Too few test subjects to establish a NOAEL--i. Objection/hearing 
request. NRDC objects to reliance on the Gledhill study claiming that 
because it only involved six treated test subjects it cannot ``support 
the establishment of a reliable NOAEL or dose response curve . . . .'' 
(Ref. 1 at 13).
    ii. Background. NRDC's claim was contained in both its petition and 
its comments on the IRED. (Refs. 1 at 26; and 23 at 15). In its 
petition denial order, EPA responded to these claims by concurring with 
the HSRB's conclusion that the Gledhill study was ``sufficiently robust 
for developing a Point of Departure for estimating dermal, incidental 
oral, and inhalation risk from exposure to DDVP in a single chemical 
assessment.'' (72 FR at 68675 (quoting HSRB Report)). The HSRB found 
the study to be ``robust'' based on the following attributes: ``the 
repeated dose approach which allowed examination of the sustained 
nature of RBC cholinesterase inhibition; robust analysis of RBC 
cholinesterase inhibition both in terms of identifying pre-treatment 
levels and consistency of response within and between subjects; and the 
observation of a low, but statistically significant RBC cholinesterase 
inhibition response.'' (Id.; Ref. 21 at 39-41).
    iii. Denial of hearing. NRDC has not met the requirements for a 
hearing on this sub-issue. First, NRDC has proffered no evidence that 
the six treated subjects in the Gledhill subject were too few for EPA 
to use data from that study as a Point of Departure. Rather, NRDC does 
no more than state ``[w]e are aware of no statistical test'' which 
would support EPA's use of the Gledhill data. (Ref. 1 at 13). As EPA's 
regulations make clear, a mere ``denial'' of an EPA position is not 
sufficient to satisfy the standard for granting a hearing. (40 CFR 
178.32(b)(2)). Second, NRDC does not confront the reasoning of the 
HSRB, which was adopted by EPA, for why the data from the Gledhill 
study are sufficiently robust to justify their use as a Point of 
Departure. This failure to challenge the basis of EPA's petition denial 
affects the materiality of the objection and hearing request. Even if 
NRDC could demonstrate in a hearing that generally more test subjects 
are needed to derive a Point of Departure for a RfD/PAD, that evidence 
would not address the specific factors in the Gledhill study that EPA 
and the HSRB found convincing on this question. (See Unit 
VIII.D.4.a.iii).
    iv. Denial of objections. EPA does not agree with NRDC's 
undocumented assertion that the Gledhill study does not provide an 
appropriate Point of Departure for assessing DDVP risk. EPA, and the 
HSRB, found that there were several features of the study and the 
statistical analysis of the study that made it ``sufficiently robust 
for developing a Point of Departure . . . .'' (72 FR at 68675). 
Important factors cited by the HSRB, and adopted by EPA, included: (1) 
the study design which involved repeated dosing and repeated 
measurement of cholinesterase effects in individuals; (2) extensive 
pre-dosing measurement of the test subjects' cholinesterase inhibition 
levels which showed consistency both within and between individual test 
subjects; and (3) the clear study results which showed a statistically 
significant effect on cholinesterase inhibition was found (both between 
controls and treated subjects and between the tested subjects' pre- and 
post-dosing levels) that was at or near the lowest level that could be 
distinguished from baseline values. (72 FR at 68675). Further, as EPA 
noted in its petition denial order, a similar number of test subjects 
(four per sex) are recommended for a toxicology study in non-rodents 
(usually the dog) routinely required for pesticide risk assessment. (72 
FR at 68675).
    In response to EPA's and the HSRB's conclusions as to the Gledhill 
study, NRDC does little more than repeat its allegation that the 
Gledhill study was underpowered. NRDC does respond to EPA's reference 
to the chronic dog study, alleging without providing any basis that 
that study is underpowered, and claiming that ``EPA rarely relies upon 
that study.'' (Ref. 1 at 13). NRDC is incorrect. The chronic dog study 
was added to EPA's testing requirement regulations in 1984 and was 
included in the revised regulations re-promulgated just last year, 
although the length of the study was shortened from 1 year to 13 weeks. 
(72 FR 60934, 60940-60941 (October 26, 2007); 49 FR 42881 (October 24, 
1984)). As a standard study required in evaluating pesticides used on 
food, the chronic dog study would have been considered and relied upon 
in virtually every one of the roughly 10,000 FFDCA tolerance 
reassessments conducted in the 10 years following enactment of the 
FQPA. (Ref. 37). If, by ``rarely relied upon,'' NRDC means the results 
from chronic dog are rarely used as a Point of Departure, NRDC is still 
incorrect. For example, a cursory review of rules establishing new 
tolerances in 2005 showed at least eight instances in which the Point 
of Departure for assessment of a pesticide's risk was based on the 
chronic dog study. (70 FR 77363, 77366 (December 30, 2005) 
(hexythiazox); 70 FR 74688, 74690 (December 16, 2005) (bifenazate); 70 
FR 55740, 55743 (September 23, 2005) (fenpropathrin); 70 FR 55752, 
55757 (September 23, 2005) (amicarbazone); 70 FR 55761, 55764 
(September 23, 2005) (pyridaben); 70 FR 54640, 54644 (September 16, 
2005) (fluoxastrobin); 70 FR 53944, 53946 (September 13, 2005); 70 FR 
51615, 51617 (August 31, 2005) (halosulfuron-methyl). A retrospective 
analysis performed by EPA in 2005 also showed that 116 out of 304 
chronic RfDs for pesticides was based on the chronic dog study. (Ref. 
38). Finally, another example somewhat closer to home would be DDVP, 
where the NOAEL from the chronic dog study is used as the Point of 
Departure in assessing chronic dietary risk. (Ref. 3 at 132).
    Further, EPA's recommendation for four test subjects per sex per 
dose in the sub-chronic and chronic non-rodent (dog) study is widely 
followed. The FDA has a similar recommendation for conducting non-
rodent studies of sub-chronic and chronic duration as does the 
Organisation for Economic Co-operation and Development (``OECD''), 
Canada which has accepted the OECD guideline on the sub-chronic and 
chronic non-rodent (dog) study, and the European Commission's Joint 
Research Centre of the European Union. (Refs. 39, 40, 41, 42, and 43).
    c. Adult males only--i. Objection/hearing request sub-issue. NRDC 
objects to the Gledhill study because it included as test subjects only 
adult males. (Ref. 1 at 14). NRDC claims that adult males are 
``biologically unrepresentative'' of the human population.
    ii. Background. NRDC's objection is drawn verbatim from its 
comments on the DDVP IRED. EPA responded to this argument by pointing 
out that ``no sex differences were observed in the

[[Page 42707]]

comparative cholinesterase studies.'' (72 FR at 68675). EPA also found 
no age-related differences in cholinesterase inhibition. (72 FR at 
68694).
    iii. Denial of hearing. A hearing is denied on this sub-issue 
because there is no disputed factual matter for resolution at a 
hearing. There is no dispute concerning the subjects in the Gledhill 
study - they were adult males. Thus, the only question is whether a 
human study using only adult males meets the regulatory requirement of 
``scientifically valid and relevant data.'' (40 CFR 26.1701). Because 
NRDC has proffered no evidence regarding the representativeness of 
adult males to the general population, this question requires the 
application of a legal standard to undisputed facts. Hearings are not 
appropriate on questions of law or policy. (40 CFR 178.32(b)(1)). FDA 
has repeatedly confirmed that the application of a legal standard to 
undisputed facts is a question of law for which a hearing is not 
required. (See, e.g., 68 FR 46403, 46406 n.18, 46408, 46409 (August 5, 
2003) (whether facts in the record show there is a reasonable certainty 
of no harm is a question of law; whether a particular effect is a 
``harm'' is a question of law)).
    NRDC's hearing request is also flawed because NRDC does not object 
to the basis EPA asserted in its petition denial for concluding that 
the Gledhill study provided scientifically valid data despite its use 
of only adult male subjects. As noted above, EPA thought 
representativeness concerns were addressed by the fact that animal 
studies with DDVP showed no differences in sensitivities between males 
and females and adults and the young. NRDC, however, has not challenged 
and proffered evidence to rebut this conclusion nor has NRDC challenged 
or proffered evidence to rebut EPA's analysis of the underlying data. 
Rather, NRDC just repeats its assertions regarding the 
unrepresentativeness of adult males generally. This failure to 
challenge the basis of EPA's petition denial affects the materiality of 
the objection and hearing request. Even if NRDC offers evidence to show 
sex- and age-related sensitivities in the population to some toxicants, 
such evidence would not rebut the DDVP-specific data on sensitivity. 
(53 FR 53176, 53191 (December 30, 1988) (FDA denied a hearing request 
noting that given FDA's prior conclusion that the studies relied upon 
by the objector were unreliable, the ``burden shifted to [the objector] 
to maintain the viability of its objection by proffering some 
information that called into question the agency's conclusion on this 
matter.'')).
    iv. Denial of objection. EPA concludes that it was reasonable to 
use the Gledhill study despite that fact that it only examined adult 
males given that the animal toxicology data on DDVP's cholinesterase 
effects consistently showed no differences between males and females 
and adults and the young. Multiple studies involving adult animals 
yielded consistent cholinesterase inhibition results in males and 
females. (Ref. 3 at 124-126). Similarly, Benchmark Dose Method analysis 
of the developmental neurotoxicity data ``did not demonstrate any 
substantial numerical differences in [Benchmark Dose Method Level] 
values for either RBC or brain cholinesterase between young and adult 
animals.'' (72 FR at 68694).
    d. Plasma--i. Objection/hearing request. NRDC objects that the 
Gledhill study is unreliable because it measured only RBC 
cholinesterase inhibition and not plasma cholinesterase inhibition. 
NRDC claims that measuring plasma cholinesterase might have reduced the 
variability measured in RBC cholinesterase.
    ii. Background. In its petition, NRDC argued that plasma 
cholinesterase should have been measured because it might be a more 
sensitive indicator of DDVP's cholinesterase effects. EPA responded to 
the petition by noting that RBC cholinesterase is the Agency's 
preferred cholinesterase inhibition endpoint as compared to plasma 
cholinesterase. (72 FR at 68676). EPA explained that ``[s]ince the red 
blood cell contains only acetylcholinesterase, the potential for 
exerting effects on neural or neuroeffector acetylcholinesterase may be 
better reflected by changes in red blood cell acetylcholinesterase than 
by changes in plasma cholinesterases which contain both 
butyrylcholinesterase and acetylcholinesterase in varying ratios 
depending upon the species.'' (Id.). EPA concluded that information on 
a less preferred endpoint ``adds little meaningful information.'' 
(Id.).
    iii. Denial of hearing. NRDC proffers no evidence in support of its 
allegation that collection of plasma cholinesterase inhibition data 
would be useful in limiting the variability seen in the RBC 
cholinesterase inhibition data. Hearings will not be granted on mere 
allegations. (40 CFR 178.32(b)(2)). Further, given EPA's conclusion 
that the variability in RBC cholinesterase inhibition in the test 
subjects was accounted for by pre- and post-treatment measurement, this 
issue is not material to resolution of NRDC's claim. Finally, to the 
extent NRDC is advocating reliance on plasma cholinesterase inhibition 
data over RBC cholinesterase inhibition data that is a policy issue and 
hearings will not be held as to policy issues. (40 CFR 178.32(b)(1)).
    iv. Denial of objection. EPA's well-established policy when 
evaluating blood cholinesterase inhibition is to use RBC cholinesterase 
data in preference to plasma cholinesterase. (Ref. 10 at 32). EPA's 
reasoning here is straightforward. Blood cholinesterase data is used as 
an indicator of possible effects on acetylcholinesterase in the 
peripheral nervous system. RBC cholinesterase is composed entirely of 
acetylcholinesterase, whereas plasma cholinesterase is a mixture of 
acetylcholinesterase and butyrylcholinesterase, a compound somewhat 
similar to acetylcholinesterase in structure that nonetheless is 
``different in important ways which often result in it having binding 
affinities to anticholinesterase agents as well as other 
characteristics that are quite different from those of 
acetylcholinesterase.'' (Id. at 32). The ratio of acetylcholinesterase 
to butyrylcholinesterase in plasma differs by species; in humans, 
plasma ``is overwhelmingly butyrylcholinesterase with a ratio of 
butyrylcholinesterase to acetyl cholinesterase of 1,000:1.'' (Id.)
    It is preferable to have both RBC and plasma cholinesterase data 
from a study because effects in the RBC may be non-existent, equivocal, 
or fail to establish a clear-dose response pattern. In those 
circumstances, plasma cholinesterase inhibition data may serve as a 
Point of Departure or may aid in the interpretation of the RBC data, 
particularly when extrapolating animal data to humans. In the Gledhill 
study, however, the robust RBC cholinesterase sampling approach in 
humans (multiple pre- and post-dosing samples and sampling after repeat 
dosing) as well as the clear pattern on RBC cholinesterase inhibition 
means the absence of plasma cholinesterase inhibition data is of little 
to no consequence.
    In its objections NRDC claims that plasma cholinesterase inhibition 
data ``might have reduced somewhat'' the variability in the RBC 
cholinesterase data. EPA disagrees both because plasma cholinesterase 
in humans is overwhelmingly composed of butyrylcholinesterase not 
acetylcholinesterase, and because the robust sampling plan in the 
Gledhill study well-characterized the RBC cholinesterase variability. 
For all of these reasons, NRDC's objection on this issue are denied.
    e. Controls over environment--i. Objection/hearing request sub-
issue. NRDC argues that because there were

[[Page 42708]]

not controls over the Gledhill test subjects' exposure to environmental 
factors which might affect cholinesterase inhibition (e.g., ingestion 
of pharmaceuticals), the results of Gledhill study might be caused 
environmental factors and are thus invalid.
    ii. Background. This claim is contained in NRDC's petition and was 
not specifically addressed by EPA in the petition denial order other 
than through its acceptance of the HSRB's analysis.
    iii. Denial of hearing request. The control measures used in the 
Gledhill study are set forth in the study report and are not in 
dispute. The only question is whether these control measures make the 
Gledhill study scientifically invalid and thus not in compliance with 
EPA regulations. Legal questions such as this are not appropriate for a 
hearing. (40 CFR 178.32(b)(1); see, e.g., 68 FR 46403, 46406 n.18, 
46408, 46409 (August 5, 2003) (whether facts in the record show there 
is a reasonable certainty of no harm is a question of law and thus is 
not a hearing issue; whether a particular effect is a ``harm'' is a 
question of law not of fact and a hearing will not be held on issues of 
law)). Additionally, NRDC proffers no evidence regarding the effect of 
the study's control measures other than speculation about how 
environmental factors might have affected the study. A hearing will not 
be granted on the basis of mere allegations or speculation. (40 CFR 
178.32(b)(2); (57 FR 6667, 6671 (February 27, 1992)). Finally, NRDC's 
argument here is immaterial to its claim. As EPA explains below in 
denying this objection, the lack of control measures would only be an 
issue if NRDC is arguing that EPA has wrongfully concluded that the 
Gledhill study has not shown a measurable effect in the treated 
subjects.
    iv. Denial of objection. NRDC's objection here might warrant some 
consideration if the study results had shown no pattern and EPA had 
concluded that the study established a NOAEL for DDVP. In those 
circumstances, it could be argued that any effects from DDVP exposure 
may have been masked by other factors. However, the study results here 
showed a clear and consistent pattern of marginal effects on RBC 
cholinesterase inhibition in connection with DDVP dosing. Given these 
results and the fact that the test subjects were pre-screened for 
environmental factors that might affect study results (e.g., regular 
use of pharmaceuticals; excessive alcohol consumption; exposure to 
organophosphurus compounds), NRDC's speculation that environmental 
factors might have affected the study results is without merit.
    f. Consent--i. Objection/hearing request sub-issue. NRDC asserts 
that informed consent was not obtained from the Gledhill test subjects 
because the consent form for the experiment identified DDVP as a 
``drug.'' (Ref. 1 at 14). NRDC claims that EPA has ignored this issue. 
NRDC cites an EPA memorandum dated March 16, 2006, examining the ethics 
of the Gledhill study and asserts that it ``fails to mention [the 
informed consent] issue when it concludes that the study was not 
fundamentally unethical.'' (Id. at 15). NRDC argues that describing 
DDVP as a drug ``constitute[s] `fundamentally unethical' actions by any 
reasonable understanding of that term.'' (Id.).
    ii. Background. This objection comes verbatim from NRDC's comments 
on the DDVP IRED. EPA responded to this issue in its denial of NRDC's 
petition by adopting the HSRB's conclusion that informed consent was 
obtained. EPA explained that ``[t]he HSRB reasoned that references to 
DDVP as a drug did not vitiate informed consent because `the consent 
materials clearly advised subjects that this was a study involving 
consuming an insecticide.''' (72 FR at 68675).
    iii. Denial of hearing. It is not clear from NRDC's objections 
whether NRDC is challenging EPA's conclusion on the ethics of consent 
issue based on (1) an alleged failure of EPA to address this question; 
or (2) the legal proposition that identification of a pesticide as a 
drug ``constitute[s] `fundamentally unethical' actions by any 
reasonable understanding of that term.'' In either case, a hearing is 
not appropriate on NRDC's objection.
    First, NRDC's allegation that EPA did not address the consent issue 
does not present a genuinely-disputed issue of fact. It is plain on the 
face of EPA's petition denial order, that EPA adopted the reasoning of 
the HSRB on why references on the consent form to DDVP as a drug do not 
constitute clear and convincing evidence that the Gledhill study is 
fundamentally unethical. (72 FR at 68675). After summarizing the 
decision of the HSRB on the consent issue (see quoted language in Unit 
VIII.E.3.f.ii. above), EPA stated: ``EPA adopts the HSRB's reasoning 
and finds it persuasive in rejecting NRDC's arguments concerning why 
the Gledhill study should not be relied upon.'' (Id.). NRDC's argument 
that EPA offered no explanation is based on a memorandum that predates 
and is superseded by EPA's denial of NRDC's petition. The March 16, 
2006 memorandum was finalized more than 20 months before issuance of 
the DDVP petition denial order and the order contains EPA's rationale 
on the consent issue. As noted earlier in Unit VIII.D.3.c., when an 
objector to a section 408(d)(4)(iii) order challenges an EPA conclusion 
that has been superseded by the section 408(d)(4)(iii) order, the 
objector has not raised a live controversy as to a material issue. (See 
53 FR 53176, 53191 (December 30, 1988) (where FDA responds to a comment 
in the final rule, repetition of the comment in objections does not 
present a live controversy unless the objector proffers some evidence 
calling FDA's conclusion into question)). Moreover, objections, and 
hearing requests on objections, may only be filed as to a section 
408(d)(4)(iii) order or other statutorily-specified action. (21 U.S.C. 
346a(g)(2)(A)).
    Second, the informed consent question as to the Gledhill study is a 
legal/policy issue not a factual one. There are no disputed facts 
regarding the consent form. The consent form used in the Gledhill study 
is set forth in the study report and NRDC has not proffered any other 
evidence bearing on consent. Accordingly, the only question is the 
legal/policy one of whether use of the Gledhill study consent form is 
``clear and convincing evidence'' that the Gledhill study was 
``fundamentally unethical'' and thus not in compliance with EPA 
regulations. (40 CFR 26.1704). In fact, NRDC has framed the consent 
issue as a legal question, arguing that the undisputed reference to 
DDVP as a drug in the consent form for the Gledhill study 
``constitute[s] [a] `fundamentally unethical' action[] by any 
reasonable understanding of that [regulatory] term.'' (Ref. 1 at 15). 
Further, to support this legal argument, NRDC turns to other legal 
authorities arguing that ``[t]he requirement for obtaining informed 
consent is at the core of the [40 CFR] Part 26 regulations and FIFRA 
section 12(a)(2)(P),'' and ``[v]iolation of these regulations, laws and 
international standards in the design and conduct of human studies is 
fundamentally unethical.'' (Id.). Hearings are not appropriate on 
questions of law or policy. (40 CFR 178.32(b)(1)).
    Finally, a hearing is not appropriate on this sub-issue because 
NRDC's objection does not respond to EPA's conclusion, based on the 
HSRB's reasoning, as to why there was not a problem with consent in the 
Gledhill study. As such, NRDC's objection on this point is nothing more 
than a general denial of EPA's conclusion and a hearing cannot be 
justified on this basis. (40 CFR 178.32(b)(2)).
    iv. Denial of objection. NRDC has offered no response to EPA's 
petition

[[Page 42709]]

denial order which incorporated the HSRB's reasoning as to why the 
references to DDVP as a drug did not constitute clear and convincing 
evidence that the Gledhill study was fundamentally unethical. 
Specifically, NRDC does not address the HSRB's conclusion, adopted by 
EPA, that the test subjects' consent was informed because ``the consent 
materials clearly advised subjects that this was a study involving 
consuming an insecticide.'' (Ref. 21 at 46). Thus, EPA denies the 
objection.
    g. Protection of health of the test subjects--i. Objection/hearing 
request sub-issue. NRDC differs with EPA's conclusion that there was 
not clear and convincing evidence that the Gledhill study was rendered 
fundamentally unethical by the failure of the test conductors to retest 
the subjects until their cholinesterase inhibition levels returned to 
baseline levels. (Ref. 1 at 14-15). According to NRDC, EPA 
acknowledged, in a March 16, 2006, memorandum, that the failure to 
retest was inconsistent with the standards in the Declaration of 
Helskinki by showing a lack of concern for the safety of the test 
subjects. (Id.). NRDC claims that EPA has offered no explanation for 
why it concluded that the Gledhill study was not fundamentally 
unethical despite this inconsistency with the Declaration of Helsinki. 
(Id. at 15).
    ii. Background. This objection is adopted verbatim from the 
comments that NRDC filed on the IRED. (Ref. 23 at 16-17). In responding 
to this claim, EPA adopted the reasoning of the HSRB that 
``[d]eficiencies in monitoring of subjects were found not to provide 
clear and convincing evidence that the study was ethically deficient by 
subjecting the test subjects to the threat of serious harm because 
prior studies by this researcher involving higher doses had only 
invoked minimal responses.'' (72 FR at 68675).
    iii. Denial of hearing. As with the consent issue, it is not clear 
from NRDC's objections whether NRDC is challenging EPA's conclusion on 
the ethics of not retesting based on (1) an alleged failure of EPA to 
offer an explanation for its conclusion; or (2) the legal proposition 
that a study that is inconsistent with the Declaration of Helsinki is 
necessarily ``fundamentally unethical'' under the Human Research rule. 
In either case, a hearing is not appropriate on NRDC's objections.
    If NRDC is challenging EPA's alleged lack of an explanation, then 
NRDC has failed to identify a genuinely-disputed issue of fact. As with 
the consent issue, EPA, in its petition denial order, summarized and 
then adopted the reasoning of the HSRB on why the failure to retest 
does not constitute clear and convincing evidence that the Gledhill 
study is fundamentally unethical. (72 FR at 68675) (see quoted language 
in Unit VIII.E.3.g.ii. above). NRDC's argument that EPA offered no 
explanation is based on a memorandum that predates and is superseded by 
EPA's denial of NRDC's petition. For the reasons set forth in Unit 
VIII.D.3.c and Unit VIII.E.3.f.iii., an objection and hearing request 
as to a section 408(d)(4)(iii) order based on a memorandum superseded 
by the section 408(d)(4)(iii) order does not constitute a live 
controversy on an issue material to the section 408(d)(4)(iii) order 
and, arguably, not even a valid objection under section 408(g)(2)(A). 
(21 U.S.C. 346a(g)(2)(A); see 53 FR 53176, 53191 (December 30, 1988) 
(where FDA responds to a comment in the final rule, repetition of the 
comment in objections does not present a live controversy unless the 
objector proffers some evidence calling FDA's conclusion into 
question)).
    If NRDC is challenging the substance of EPA's conclusion on the 
ethics of the Gledhill study, this objection also does not warrant a 
hearing because NRDC is making no more than a legal or policy argument. 
There is no dispute with regard to what post-testing was performed as 
to the Gledhill subjects. NRDC admits as much. (Ref. 1 at 15 (``There 
is nothing in the [EPA] memo that suggests that there is any 
uncertainty or controversy about what the various study documents said 
or what was done in the study in relation to this ethical 
`inconsistency' with the Helsinki Declaration. . . . Notwithstanding 
the clear facts of the case [regarding retesting] . . . .''). The only 
question is whether the failure to test subjects until cholinesterase 
inhibition levels returned to baseline is ``clear and convincing 
evidence'' that the Gledhill study was ``fundamentally unethical.'' (40 
CFR 26.1704). Like the consent issue, NRDC, itself, has framed the 
issue as involving a legal question as to which there is only one 
answer. According to NRDC, ``these failings [as to retesting subjects 
and consent] both constitute `fundamentally unethical' actions by any 
reasonable understanding of that term.'' (Ref. 1 at 15). Further, NRDC 
argues categorically that ``[v]iolation of . . . international 
standards in the design and conduct of human studies is fundamentally 
unethical.'' (Id.). This is a legal/policy determination regarding 
application of an EPA regulatory standard and the standards of the 
Declaration of Helsinki to undisputed facts. Certainly, NRDC has 
proffered no genuine factual issue to be resolved at a hearing. 
Hearings are not appropriate on questions of law or policy. (40 CFR 
178.32(b)(1)).
    Finally, a hearing is not appropriate on this sub-issue because 
NRDC's objection does not respond to EPA's conclusion, based on the 
HSRB's reasoning, as to why the failures in monitoring of subjects 
following the conclusion of dosing did not amount to clear and 
convincing evidence that the study was fundamentally unethical. As 
such, NRDC's objection on this point is nothing more than a general 
denial of EPA's conclusion and a hearing cannot be justified on this 
basis. (40 CFR 178.32(b)(2)).
    iv. Denial of objection. NRDC has offered no response to EPA's 
petition denial order which incorporated the HSRB's reasoning as to why 
the failure to retest subjects did not constitute clear and convincing 
evidence that the Gledhill study was fundamentally unethical. 
Specifically, NRDC does not address the HSRB's conclusion, adopted by 
EPA, that the lack of retesting was not fundamentally unethical because 
``prior studies by this researcher involving higher doses had only 
invoked minimal responses.'' (72 FR at 68675). Thus, NRDC's objection 
on this point is denied.

F. Summary of Reasons for Denial of NRDC's Hearing Requests

    EPA denies NRDC's request for a hearing on whether reliable data 
support EPA's reduction of the children's safety factor and on whether 
EPA properly relied on the Gledhill human study. EPA's close 
examination of each of the 19 sub-issues involved in these two hearing 
requests demonstrates that none of the issues satisfies the standard 
for granting a hearing in 40 CFR 178.32. Most fail for multiple 
reasons.
    Several sub-issues do not present an issue of genuinely-disputed 
fact. Instead, NRDC raises issues presenting purely legal or policy 
questions or questions involving the application of legal standards to 
undisputed facts. For example, with regard to its children's safety 
factor objection, NRDC makes the legal argument that failure to 
complete the mandatory endocrine screening program compels EPA to 
retain the children's safety factor for DDVP and all other pesticides. 
(See Unit VIII.D.2.a.). In other cases, NRDC's description of a factual 
dispute is clearly contradicted by the record. An example here is 
NRDC's assertion that EPA failed to consider acute residential exposure 
even though EPA, in response to

[[Page 42710]]

NRDC's petition, amended its risk assessment to include examination of 
exposure for 1-day and 14-day periods. (See Unit VIII.D.4.c.)
    Many of NRDC's sub-issues lack materiality. In some instances that 
is due to NRDC's misunderstanding of a scientific concept - as when 
NRDC raises questions about the statistical power of the Gledhill study 
or seeks to invalidate the Gledhill study based on a alleged inadequacy 
to control for environmental factors. Both of these concepts have 
little relevance given the positive results found in that study. (See 
Units VIII.E.3.a. and VIII.E.3.e.). In other instances, the sub-issues 
presented by NRDC lack materiality either because (1) NRDC objects to 
aspects of EPA's risk assessments that were changed in response to the 
petition; (2) NRDC fails to address the reasons given by EPA for 
denying NRDC's petition; or (3) NRDC objects to prior conclusions of 
EPA that were superseded by the petition denial order. (See Units 
VIII.D.3., VIII.E.3.b., and VIII.E.3.g.)
    Most importantly, as to all of the sub-issues, NRDC fails to 
identify and proffer evidence which, if established, would resolve one 
or more questions in NRDC's favor. As EPA's analysis shows, NRDC 
essentially proffered no evidence in support of its hearing requests 
and objections and instead relies upon legal and policy arguments and 
unsupported or speculative factual assertions. NRDC's attempted 
evidentiary proffers are either: (1) so broad as to be meaningless 
(e.g., the complete EPA docket for DDVP); (2) too general to define a 
factual issue as to DDVP (e.g., newspaper and law review articles); (3) 
supportive of scientifically irrelevant claims (e.g., Sass and Lockwood 
articles); or (4) mere allegations or general denials (e.g., NRDC's 
claim that dietary risk assessment ``poses a serious risk of 
understating risks posed by DDVP;'' NRDC's speculation about how many 
DDVP pest strips a homeowner may use). (See Units VIII.C., VIII.D.3., 
and VIII.D.4.e.).
    NRDC's failure to offer evidence in support of its contentions is a 
consistent pattern in this proceeding. NRDC offered no greater support 
for its arguments in its petition, in its comments on the IRED, or, for 
that matter, in its written or oral comments to the HSRB. In these 
circumstances, EPA questions whether granting a hearing would have been 
appropriate even if NRDC had, at this last stage of the administrative 
process, suddenly produced factual evidence in support of its claims. 
Presumably, Congress created a multi-stage administrative process for 
resolution of tolerance petitions to give EPA the opportunity in the 
first stage of the proceeding to resolve factual issues, where 
possible, through a notice-and-comment process, prior to requiring EPA 
to hold a full evidentiary hearing - which can involve a substantial 
investment of resources by all parties taking part. While EPA has not 
held any pesticide tolerance hearings under the FFDCA, its experience 
with pesticide hearings under FIFRA in the 1970s indicates the process 
can be quite lengthy. (See were e.g., Environmental Defense Fund v. 
EPA, 548 F.2d 998, 1002 (D.C. Cir. 1976) (4 months were needed for 
testimony in an expedited FIFRA suspension proceeding); Environmental 
Defense Fund, Inc. v. EPA, 510 F.2d 1292, 1297 (D.C. Cir. 1975) (13 
months of testimony in a FIFRA cancellation proceeding); Environmental 
Defense Fund v. Ruckelshaus, 489 F.2d 1247, 1251 n. 24 (D.C. Cir. 1973) 
(``During seven months of hearings [in the DDT cancellation 
proceeding], 125 witnesses appeared to testify and 365 exhibits were 
placed in evidence. The transcript of the hearings was over 9,000 pages 
long.''); Ref. 44 at 246 (referring to FIFRA cancellation proceedings 
in the 1970s as the ```100-years' pesticide wars''). Given that in the 
ensuing 30 years the pesticide risk assessment process has become 
exponentially more complex, FFDCA pesticide hearings have the potential 
for being even more resource intensive. Accordingly, if a party were to 
withhold evidence from the first stage of a tolerance petition 
proceeding and only produce it as part of a request for a hearing on an 
objection, EPA might very likely determine that such an untimely 
submission of supporting evidence constituted an amendment to the 
Original petition requiring a return to the first stage of the 
administrative process (if, consideration of information that was 
previously available is appropriate at all).
    Finally, EPA notes that it is denying NRDC's hearing requests under 
40 CFR 178.32 and does not here rely on the even broader discretionary 
authority to deny hearing requests in FFDCA section 408(g)(2)(B). As 
recounted previously, 40 CFR 178.32 predates the explicit addition to 
the statute by the FQPA of the grant of authority to EPA to deny 
hearings. That language provides that EPA shall ``hold a public 
evidentiary hearing if and to the extent the Administrator determines 
that such a public hearing is necessary to receive factual evidence 
relevant to material issues of fact raised by the objections.'' (21 
U.S.C. 346a(g)(2)(B)). EPA does not interpret this language as 
requiring it to hold a hearing in any instance where factual evidence 
relevant to a material issue of fact is proffered (essentially the 
standard set forth in 40 CFR 178.32); rather, EPA construes the 
statutory language as requiring it to hold a hearing only where it 
determines a hearing is necessary to receive such proffered evidence. 
In other words, a party wishing to obtain a hearing must not only 
satisfy the requirements of 40 CFR 178.32, it must also show that an 
evidentiary hearing is necessary to presentation of proffered evidence 
to the Agency. Because, however, NRDC has not satisfied the standard 
set forth in 40 CFR 178.32, EPA does not need to address whether a 
hearing is necessary to receive NRDC's ``evidentiary'' proffer.

G. Summary of Reasons for Denial of NRDC's Objections

    EPA denies NRDC's objections to EPA's petition denial that EPA 
lacked sufficient data to reduce the children's safety factor for DDVP, 
and EPA unlawfully relied on the Gledhill intentional human dosing 
study in assessing the risk of DDVP exposure.
    1. Children's safety factor objection. In support of its children's 
safety factor objection, NRDC claims that EPA has inadequate data on 
endocrine effects, dietary exposure to DDVP residues in food, and 
exposure from residential pest strips. On endocrine effects, NRDC 
argues that EPA lacks adequate data, as a legal matter, because it has 
not completed the section 408(p) endocrine screening program, and, as a 
factual matter, because DDVP has not been tested under the most recent 
two-generation rat reproduction study. EPA has previously rejected 
NRDC's legal argument as not consistent with the statutory language, 
structure, or history, and NRDC has offered no arguments as to why 
EPA's previous conclusion was incorrect. On the factual question of 
whether EPA has adequate endocrine data on DDVP, EPA concluded in the 
petition denial that, given the existing data bearing on DDVP's 
potential to cause endocrine effects and large difference in 
sensitivity between DDVP's cholinesterase inhibition effects and 
potential endocrine effects, EPA had sufficient reliable data on DDVP's 
potential endocrine effects to vary from the default children's safety 
factor. In its objections, NRDC offers nothing other than speculation 
about what another two-generation rat reproduction study might show. 
NRDC's speculation does not convince EPA that its analysis was 
incorrect.
    As to dietary exposure to DDVP residues in food, NRDC argues that 
EPA's dietary exposure assessment has

[[Page 42711]]

many shortcomings that may lead to underestimation of dietary exposure 
to DDVP. In support of this claim, NRDC relies on statements EPA made 
in 2000 in a preliminary risk assessment of DDVP. NRDC places 
particular emphasis on its claim that EPA's database on food 
consumption by infants is inadequate. These allegations by NRDC lack 
merit because NRDC has ignored the many revisions to the DDVP risk 
assessment since the 2000 preliminary risk assessment. First, EPA 
completely revised the dietary exposure and risk assessment in response 
to NRDC's petition. One of the specific reasons for revising the risk 
assessment was so that EPA's latest information on infant food 
consumption could be incorporated. Second, also in response to NRDC's 
petition, EPA comprehensively analyzed its dietary exposure assessment 
to evaluate whether that assessment potentially underestimated dietary 
exposure to DDVP. EPA concluded that ``its assessment of exposure to 
DDVP from food will not under-estimate but rather over-estimate, and in 
all likelihood substantially over-estimate, DDVP exposure.'' (72 FR at 
68686). NRDC neither acknowledges nor challenges the revised dietary 
exposure assessment or EPA's detailed analysis of whether that 
assessment under- or over-estimates DDVP exposure. Finally, EPA 
questions the materiality of NRDC's argument with regard to DDVP 
exposure from food given that DDVP exposure from this source is trivial 
compared with other sources. For all of these reasons, EPA rejects 
NRDC's arguments on the alleged inadequacy of EPA's assessment of human 
dietary exposure to DDVP in food.
    With regard to DDVP exposure from residential pest strips, NRDC 
claims that the data relied upon by EPA (the Collins and DeVries study) 
was inadequate and EPA's risk assessment based on that study was based 
on inadequately-supported assumptions. These arguments, however, are 
without merit because not only does NRDC offer nothing other than 
general, undocumented contentions in support but once again NRDC has 
ignored clear evidence and analysis in the record that contradict its 
allegations. First, NRDC ignores the other DDVP pest strip exposure 
studies relied upon by EPA to support the findings in the Collins and 
DeVries study. EPA concluded that these studies confirmed that the 
findings in Collins and DeVries were representative of DDVP 
concentration levels from pest strips that could be expected in houses 
in other locations. Second, NRDC ignores EPA's complete revision to the 
DDVP residential exposure assessment that was conducted in response to 
its petition. That revision modified numerous assumptions in the 
assessment to ensure that the data from the Collins and DeVries study 
were analyzed in a conservative fashion. NRDC does not acknowledge the 
new assessment much less offer a rebuttal to EPA's revised analysis. 
Most surprisingly, NRDC repeats challenges to several assumptions (only 
examining DDVP exposure as averaged over a 120-day period; considering 
16 hours per day a maximum exposure in a home) that were explicitly 
modified (adding consideration of 1-day and 14-day exposure periods; 
assuming 24 hours exposure per day) in the revised risk assessment in 
response to NRDC's petition. Accordingly, EPA disagrees with NRDC's 
allegations concerning the inadequacy of the data and assumptions 
underlying its residential pest strip risk assessment.
    2. Human study objection. NRDC challenged EPA's reliance on the 
Gledhill human study arguing that EPA's Human Research rule is unlawful 
and the study was both scientifically flawed and unethically conducted.
    NRDC relies on its legal briefs filed in a separate challenge to 
the Human Research rule and its comments on that rule in support of its 
legal attack on the rule. Similarly, to the extent NRDC has standing to 
challenge a rule whose ``primary concern'' is the ``[p]rotection of the 
health and safety of human test subjects,'' (Ref. 1 at 15), EPA relies 
on its legal brief in the 2nd Circuit proceeding and the administrative 
record for the rule, in denying NRDC's challenge to Human Research 
Rule.
    As to the Gledhill study, itself, NRDC makes various claims 
regarding its scientific validity and ethicality. NRDC has previously 
presented these claims in writing and orally to EPA's HSRB. The HSRB is 
an independent scientific panel, consisting of experts in bioethics, 
biostatistics, human health risk assessment, and human toxicology, 
created specifically for the purpose of advising EPA on whether human 
studies have scientific value and conform to ethical standards. 
Although NRDC's concerns as to the Gledhill study were presented to the 
HSRB, the HSRB concluded that the Gledhill study complied with the 
Human Research rule and could be considered by EPA in assessing the 
risk of DDVP. EPA relied heavily on the advice by the HSRB in denying 
NRDC's petition. Remarkably, NRDC, in its objections, proceeds as if 
the HSRB review never occurred. NRDC neither acknowledges the existence 
of the HSRB report nor attempts to refute its reasoning. In Unit 
VIII.E. above, EPA repeats the findings of the HSRB and EPA's reasons 
for accepting the HSRB's conclusions with regard to the specific 
contentions of NRDC. Based on both the findings of the HSRB and EPA in 
its petition denial, as described above, as well as NRDC's failure to 
meaningfully dispute those findings, EPA rejects NRDC's challenge to 
EPA's reliance on the Gledhill study.

H. Conclusion

    For all of the reasons set forth above, EPA denies NRDC's 
objections and its requests for a hearing on those objections.

IX. References

    1. Natural Resources Defense Council, ``Objection to the Order 
Denying NRDC's Petition to Revoke All Tolerances for Dichlorvos (DDVP), 
and Request for Public Evidentiary Hearing'' (February 1, 2008).
    2. Natural Resources Defense Council, Petition of Natural Resources 
Defense Council To Conclude Special Review, Reregistration and 
Tolerance Reassessment Processes and To Revoke All Tolerances and 
Cancel All Registrations for the Pesticide DDVP (June 2, 2006).
    3. Office of Prevention, Pesticides and Toxic Substances, EPA, 
``Interim Reregistration Eligibility Decision for Dichlorvos (DDVP)'' 
(June 2006).
    4. U.S. EPA, ``A User's Guide to Available EPA Information on 
Assessing Exposure to Pesticides in Food'' (June 21, 2000).
    5. Office of Pesticide Programs, US EPA, ``Office of Pesticide 
Programs' Policy on the Determination of the Appropriate FQPA Safety 
Factor(s) For Use in the Tolerance Setting Process'' (February 28, 
2002).
    6. U.S. EPA, ``Residue Chemistry Test Guidelines: OPPTS 860.1500 
Crop Field Trials'' (August 1996).
    7. Office of Pesticide Programs, U.S. EPA and Pest Regulatory 
Management Agency, ``Health Canada, NAFTA Guidance Document for 
Guidance for Setting Pesticide Tolerances Based on Field Trial Data'' 
(September 28, 2005).
    8. Office of Pesticide Programs, U.S. EPA, ``Choosing a Percentile 
of Acute Dietary Exposure as a Threshold of Regulatory Concern'' March 
16, 2000).
    9. Office of Pesticide Programs, U.S. EPA,``Standard Operating 
Procedures (SOPs) for Residential Exposure Assessments'' (Draft 
December 19, 1997).
    10. Office of Pesticide Programs, U.S. EPA, ``The Use of Data on

[[Page 42712]]

Cholinesterase Inhibition for Risk Assessments of Organophosphorous and 
Carbamate Pesticides'' (August 18, 2000).
    11. U.S. EPA, ``Endocrine Disruptor Screening and Testing Advisory 
Committee Final Report'' (August 1998).
    12. U.S. EPA, U.S. EPA Charter: Human Studies Review Board (2008) 
(available at http://www.epa.gov/osa/hsrb/files/dated-hsrb-renewal-
charter-effect-030408.pdf).
    13. Office of Pesticide Programs, U.S. EPA, ``Organophosphorus 
Cumulative Risk Assessment - 2006 Update'' (August 2006).
    14. Office of Prevention, Pesticides and Toxic Substances, EPA, 
Memorandum from Debra Edwards to Jim Jones, ``Finalization of Interim 
Reregistration Eligibility Decisions (IREDs) and Interim Tolerance 
Reassessment and Risk Management Decisions (TREDs) for the 
Organophosphate Pesticides, and Completion of the Tolerance 
Reassessment and Reregistration Eligibility Process for the 
Organophosphate Pesticides'' (July 31, 2006).
    15. Office of Pesticide Programs, U.S. EPA, ``Data Evaluation 
Report: Dichlorvos: A Single Blind, Placebo Controlled, Randomized 
Study to Investigate the Effects of Multiple Oral Dosing on Erythrocyte 
Cholinesterase Inhibition in Healthy Male Volunteers'' (March 24, 
1998).
    16. Office of Prevention, Pesticides and Toxic Substances, EPA, 
Memorandum from Ray Kent/William Dykstra to Tina Levine, ``Human 
Studies Review Board: Final Weight of Evidence Comparison of Human and 
Animal Toxicology Studies and Endpoints for DDVP Human Health Risk 
Assessment and Discussion of Interspecies Extrapolation in the 
Organophosphate Cumulative Risk Assessment'' (March 20, 2006).
    17. Sass, J., Natural Resources Defense Council, ``NRDC comments 
for the HSRB meeting April 4-6, 2006'' (undated).
    18. EPA Human Studies Review Board, Minutes of the United States 
Environmental Protection Agency (EPA) Human Studies Review Board (HSRB) 
April 4-6, 2006 Public Meeting Docket Number: EPA-HQ-ORD-2006-0187 (May 
15, 2006).
    19. EPA Human Studies Review Board, Letter from Celia Fisher to 
George Gray, April 4-6, 2006 Meeting EPA Human Studies Review Board 
Report -- Proposed Final Draft V. 1 (May 16, 2006).
    20. EPA Human Studies Review Board, Minutes of the United States 
Environmental Protection Agency (EPA) Human Studies Review Board (HSRB) 
June 8, 2006 Public Teleconference Docket Number: EPA-HQ-ORD-2006-0187 
(June 19, 2006).
    21. EPA Human Studies Review Board, Letter from Celia Fisher to 
George Gray, April 4-6, 2006 Meeting EPA Human Studies Review Board 
Report (June 26, 2006).
    22. Amvac Chemical Corporation, Comments of Amvac Chemical 
Corporation in Reponse to EPA's Notice of a Petition to Revoke 
Tolerances Established for Dichlorvos (November 13, 2006).
    23. Natural Resources Defense Council, Letter submitting comments 
Re: Dichlorvos Interim Reregistration Eligibility Decision, 71 FR 37568 
(June 30, 2006) (August 28, 2006).
    24. Reference Dose/Reference Concentration (RfD/RfC) Technical 
Panel, Risk Assessment Forum, U.S. EPA, ``A Review of the Reference 
Dose and Reference Concentration Processes'' (December 2002).
    25. USDA, ``Food and Nutrient Intakes by Children 1994-96, 1998, 
Table Set 17'' (December 1999).
    26. USDA, ``Documentation: Supplemental Children's Survey (CSFII 
1998) to the 1994-96 Continuing Survey of Food Intakes by Individuals'' 
(2000).
    27. Office of Prevention, Pesticides and Toxic Substances, EPA, 
Memorandum from Susan V. Hummel to Kimberly Lowe/Robert McNally, 
``Revised Preliminary HED Risk Assessment for Dichlorvos'' (August 9, 
2000).
    28. U.S. EPA, Letter from George T. LaRocca, Product Manager (13), 
Insecticide Branch, Registration Division, to Jon C. Wood, ``Amvac 
Chemical Corp., Dichlorvos (DDVP) Label Amendments'' (October 11, 
2006).
    29. Petitioners' Brief, NRDC v. EPA, (2nd Cir. 06-0820-ag) (October 
4, 2006).
    30. Natural Resources Defense Council, ``Protections for Subjects 
in Human Research; Proposed Rule, 70 FR 53838'' (Sept. 12, 2005) 
(December 12, 2005).
    31. Respondent's Brief, NRDC v. EPA, (2nd Cir. 06-0820-ag) 
(November 16, 2006).
    32. Federal Judicial Center, ``Reference Manual on Scientific 
Evidence'' (2d ed. 2000).
    33. Sass, J.B., Needleman, H.L., ``Industry Testing of Toxic 
Pesticides on Human Subjects Concluded No Effect, Despite the 
Evidence,'' Environmental Health Perspectives. 2004 Mar; 112(3) A150-
151.
    34. Sass, J.B., Needleman, H.L., ``Human Testing: Sass and 
Needleman Respond to Industry,'' Environmental Health Perspectives. 
2004 Ma; 112(6) A340-341.
    35. Lockwood, A.H., ``Human Testing of Pesticides: Ethical and 
Scientific Considerations,'' American Journal of Public Health 2004 
Nov; 94(11) 1908-1916.
    36. Lockwood, A.H., ``The Ethical Bar Drops to Unacceptable,'' 
Environmental Forum. 2005 Nov/Dec; 48.
    37. U.S. EPA, Tolerance Reassessment (March 6, 2008) (published at 
http://www.epa.gov/pesticides/tolerance/reassessment.htm).
    38. Baetcke, K.P., Phang, W., and Dellarco, V., Health Effects 
Division, Office of Pesticide Programs, U.S. EPA, ``A Comparison of the 
Results of Studies on Pesticides from 12- or 24-Month Dog Studies with 
Dog Studies of Shorter Duration'' (April 7, 2005).
    39. U.S. Food and Drug Administration, ``Toxicological Principles 
for the Safety Assessment of Food Ingredients: Redbook 2000,'' secs. 
IV.C.4b and IV.C.5. (November 2003).
    40. OECD, ``OECD Guideline For The Testing Of Chemicals: Repeated 
Dose 90-day Oral Toxicity Study in Non-Rodents -- 409'' (September 
1998).
    41. OECD, ``OECD Guideline For The Testing Of Chemicals: Chronic 
Toxicity Studies -- 452'' (May 1981).
    42. OECD Test Guideline No. 452, ``Chronic Toxicity Studies'' dated 
May 12, 1981; (CPR 52(a)(iii), 52(b)(ii), 52(c)(ii), 59(a)(iii), 
59(b)(ii), 59(c)(ii) and 63) (Can).
    43. Council Directive No. 2001/59/EC, O.J. L 225 (2001) (Annex V of 
Dir 67/548/EEC on the Classification, Packaging and Labeling of 
Dangerous Substances (http://ecb.jrc.it/testing-methods/annex5)).
    44. William Rodgers, Environmental Law: Pesticides and Toxic 
Substances (1988).

X. 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.

XI. 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).

[[Page 42713]]

Appendix 1--United States Environmental Protection Agency Human Studies 
Review Board

Chair

Celia B. Fisher, Ph.D. Marie Ward Doty Professor of Psychology, 
Director, Center for Ethics Education, Fordham University, 
Department of Psychology, Bronx, NY

Vice Chair

William S. Brimijoin, Ph.D., Chair and Professor, Molecular 
Pharmacology and Experimental Therapeutics, Mayo Foundation, 
Rochester, MN


Members

David C. Bellinger, Ph.D., Professor of Neurology, Harvard Medical 
School Professor in the Department of Environmental Health, Harvard 
School of Public Health Children's Hospital, Boston, MA

Alicia Carriquiry, Ph.D., Professor, Department of Statistics, Iowa 
State University Snedecor Hall, Ames, IA

Gary L. Chadwick, PharmD, MPH, CIP, Associate Provost, Director, 
Office for Human Subjects Protection, University of Rochester, 
Rochester, NY

Janice Chambers, Ph.D., D.A.B.T., William L. Giles Distinguished 
Professor, Director, Center for Environmental Health Sciences, 
College of Veterinary Medicine, Mississippi State University, Wise 
Center, Mississippi State, MS

Richard Fenske, Ph.D., MPH, Professor, Department of Environmental 
and Occupational Health Sciences, University of Washington, Seattle, 
WA

Susan S. Fish, PharmD, MPH, Professor, Biostatistics and 
Epidemiology, Boston University School of Public Health, Co-
Director, MA in Clinical Investigation Boston University School of 
Medicine, Boston, MA

Suzanne C. Fitzpatrick, Ph.D., DABT, Senior Science Policy Analyst, 
Office of the Commissioner, Office of Science and Health 
Coordination, U.S. Food and Drug Administration, Rockville, MD

Kannan Krishnan, Ph.D., Professor, D[eacute]partement de 
sant[eacute] environnementale et sant[eacute] au travail, 
Facult[eacute] de medicine, Universit[eacute] de Montr[eacute]al, 
Montr[eacute]al, Canada

KyungMann Kim, Ph.D., CCRP, Professor and Associate Chair, 
Department of Biostatistics and Medical Informatics, School of 
Medicine and Public Health, University of Wisconsin-Madison, 
Madison, WI

Michael D. Lebowitz, Ph.D., FCCP, Professor of Public Health and 
Medicine. University of Arizona, Tucson, AZ

Lois D. Lehman-Mckeeman, Ph.D., Distinguished Research Fellow, 
Discovery Toxicology, Bristol-Myers Squibb Company, Princeton, NJ

Jerry A. Menikoff, M.D., Associate Professor of Law, Ethics and 
Medicine, Director of the Institute for Bioethics, Law and Public 
Policy, University of Kansas Medical Center, Kansas City, KS

Robert Nelson, M.D., Ph.D., Associate Professor of Anesthesiology 
and Critical Care, Department of Anesthesiology and Critical Care, 
University of Pennsylvania School of Medicine, The Children's 
Hospital of Philadelphia, Philadelphia, PA

Sean M. Philpott, Ph.D., Research Scientist, David Axelrod 
Institute, Wadsworth Center for Laboratories and Research, New York 
State Department of Health, Albany, NY


List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.


    Dated: July 11, 2008.
Debra Edwards,
Director, Office of Pesticide Programs.
[FR Doc. E8-16617 Filed 7-22-08; 8:45 am]

BILLING CODE 6560-50-S