Dichlorvos (DDVP); Order Denying NRDC's Petition to Revoke All Tolerances, 68662-68698 [E7-23571]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 72, Number 233 (Wednesday, December 5, 2007)]
[Rules and Regulations]
[Pages 68662-68698]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-23571]



[[Page 68661]]

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Part IV





Environmental Protection Agency





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40 CFR Part 180



Dichlorvos (DDVP); Order Denying NRDC's Petition to Revoke All 
Tolerances; Final Rule

Federal Register / Vol. 72, No. 233 / Wednesday, December 5, 2007 / 
Rules and Regulations

[[Page 68662]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2002-0302; FRL-8341-9]


Dichlorvos (DDVP); Order Denying NRDC's Petition to Revoke All 
Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Order.

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SUMMARY: In this Order, EPA denies a petition requesting that EPA 
revoke all pesticide tolerances for dichlorvos (DDVP) under section 
408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA). The 
petition was filed on June 2, 2006, by the Natural Resources Defense 
Council (NRDC).

DATES: This order is effective December 5, 2007. Objections and 
requests for hearings must be received on or before February 4, 2008, 
and must be filed in accordance with the instructions provided in 40 
CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).

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 https://www.regulations.gov, select ``Advanced 
Search,'' then ``Docket Search.'' Insert the docket ID number where 
indicated and select the ``Submit'' button. 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 https://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 a petition by the Natural Resources 
Defense Council (``NRDC'') 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 https://
www.regulations.gov, you may access this Federal Register document 
electronically through the EPA Internet under the ``Federal Register'' 
listings at https://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 https://www.gpoaccess.gov/ecfr.

C. Can I File an Objection or Hearing Request?

    Under section 408(g) of FFDCA, any person may file an objection to 
any aspect of this order and may also request a hearing on those 
objections. You must file your objection or request a hearing on this 
order in accordance with the instructions provided in 40 CFR part 178. 
To ensure proper receipt by EPA, you must identify docket ID number 
EPA-HQ-OPP-2002-0302 in the subject line on the first page of your 
submission. All requests must be in writing, and must be mailed or 
delivered to the Hearing Clerk as required by 40 CFR part 178 on or 
before February 4, 2008.
    In addition to filing an objection or hearing request with the 
Hearing Clerk as described in 40 CFR part 178, please submit a copy of 
the filing that does not contain any CBI for inclusion in the public 
docket that is described in ADDRESSES. Information not marked 
confidential pursuant to 40 CFR part 2 may be disclosed publicly by EPA 
without prior notice. Submit this copy, identified by docket ID number 
EPA-HQ-OPP-2002-0302, by one of the following methods:
     Federal eRulemaking Portal: https://www.regulations.gov. 
Follow the on-line instructions for submitting comments.
     Mail: Office of Pesticide Programs (OPP) Regulatory Public 
Docket (7502P), Environmental Protection Agency, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460-0001.
     Delivery: OPP Regulatory Public Docket (7502P), 
Environmental Protection Agency, Rm. S-4400, One Potomac Yard (South 
Bldg.), 2777 S. Crystal Dr., Arlington, VA. Deliveries are only 
accepted during the Docket's normal hours of operation (8:30 a.m. to 4 
p.m., Monday through Friday, excluding legal holidays). Special 
arrangements should be made for deliveries of boxed information. The 
Docket Facility telephone number is (703) 305-5805.

II. Introduction

A. What Action Is the Agency Taking?

    On June 2, 2006, the Natural Resources Defense Council (NRDC) filed 
a petition with EPA which, among other things, requested that EPA 
revoke all tolerances for the pesticide dichlorvos (DDVP) established 
under section 408 of the Federal Food, Drug, and Cosmetic Act 
(``FFDCA''), 21 U.S.C. 346a. (Ref. 1). NRDC's petition asserts that the 
DDVP tolerances are unsafe and should be revoked for numerous reasons, 
including: EPA has improperly assessed the toxicity of DDVP; EPA has 
erred in

[[Page 68663]]

estimating dietary and residential exposure to DDVP; and EPA has 
unlawfully removed the additional safety factor for the protection of 
infants and children. This order finds NRDC's claims regarding the DDVP 
tolerances to be without merit and, accordingly, denies that aspect of 
NRDC petition. The other aspects of NRDC's petition are addressed in 
another EPA action.

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

    Under section 408(d)(4) of the FFDCA, EPA is authorized to respond 
to a section 408(d) petition to revoke tolerances either by issuing a 
final rule revoking the tolerances, issuing a proposed rule, or issuing 
an order denying the petition. (21 U.S.C. 346a(d)(4)).

III. Statutory and Regulatory Background

A. Statutory Background

    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 and the U. S. Department of Agriculture. 
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.
    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 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)).
    Section 408(b)(2)(C) requires EPA to give special consideration to 
risks posed to infants and children. Specifically, this provision 
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 further 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, the 
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 affected party has 60 days to file objections with EPA 
and seek an evidentiary hearing on those objections. (21 U.S.C. 
346a(g)(2)). EPA's final order on the objections is subject to judicial 
review. (21 U.S.C. 346a(h)(1)).
    4. Tolerance Reassessment and FIFRA Reregistration. The FQPA 
requires, among other things, that EPA reassess the safety of all 
pesticide tolerances existing at the time of its enactment. (21 U.S.C. 
346a(q)). In this reassessment, EPA is 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 is generally handled in 
conjunction with a similar program involving reregistration of 
pesticides under FIFRA. (7 U.S.C. 136a-1). Reassessment and 
reregistration decisions are generally combined in a document labeled a 
Reregistration Eligibility Decision (``RED'').
    5. Estrogenic Substances Screening Program. Section 408(p) of the 
FFDCA creates the estrogenic substances screening program. This 
provision gives EPA 2 years from enactment of the FQPA to ``develop a 
screening program ... to determine whether certain substances may have 
an effect in humans that is similar to an effect produced by a 
naturally occurring

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estrogen, or such other endocrine effect as the Administrator may 
designate.'' This screening program must use ``appropriate validated 
test systems and scientifically relevant information.'' (21 U.S.C. 
346a(p)(1)). 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 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. Setting and Reassessing Pesticide Tolerances Under the FFDCA

    1. In general. The process EPA follows in setting and reassessing 
tolerances under the FFDCA includes two steps. First, EPA determines an 
appropriate residue level value for the tolerance taking into account 
data on levels that can be expected in food. Second, EPA evaluates the 
safety of the tolerance relying on toxicity and exposure data and 
guided by the statutory definition of ``safety'' and requirements 
concerning risk assessment. Only on completion of the second step can a 
tolerance be established or reassessed. Both stages of this process are 
relevant to EPA's analysis of petitions to revoke tolerances based on 
risk concerns because both stages bear on the assessment of risk.
    2. Choosing a tolerance value. In the first step of the tolerance 
setting or reassessment process (choosing a tolerance value), EPA 
evaluates 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. 2 and 3). 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. 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. 4). (As discussed below, the safety of the 
tolerance value chosen is separately evaluated.).
    There are three main reasons for closely linking tolerance values 
to the maximum value that could be present from maximum label usage of 
the pesticide. First, EPA believes it is important to coordinate its 
actions under the two statutory frameworks governing pesticides. (See 
61 FR 2378, 2379 (January 25, 1996)). It would be illogical for EPA to 
set a pesticide tolerance under the FFDCA without considering what 
action is being taken under FIFRA with regard to registration of that 
pesticide use. (Cf. 40 CFR 152.112(g) (requiring all necessary 
tolerances to be in place before a FIFRA registration may be granted)). 
In coordinating its actions, one basic tenet that EPA follows is that a 
grower who applies a pesticide consistent with the FIFRA label 
directions should not run the risk that his or her crops will be 
adulterated under the FFDCA because the residues from that legal 
application exceed the tolerance associated with that use. Crop field 
trials require application of the pesticide in the manner most likely 
to produce maximum residues to further this goal. Second, choosing 
tolerance values based on FIFRA label rates helps to ensure that 
tolerance levels are established no higher than necessary. If tolerance 
values were selected solely in consideration of health risks, in some 
circumstances, tolerance values might be set so as to allow much 
greater application rates than necessary for effective use of the 
pesticide. This could encourage misuse of the pesticide. Finally, 
closely linking tolerance values to FIFRA labels helps EPA to police 
compliance with label directions by growers because detection of an 
over-tolerance residue is indicative of use of a pesticide at levels, 
or in a manner, not permitted on the label.
    3. The safety determination - risk assessment. Once a tolerance 
value is chosen, EPA then evaluates the safety of the pesticide 
tolerance using the process of risk assessment. To assess risk of a 
pesticide, EPA combines information on pesticide toxicity with 
information regarding the route, magnitude, and duration of exposure to 
the pesticide.
    In evaluating toxicity or hazard, EPA examines both short-term 
(e.g., ``acute'') and longer-term (e.g., ``chronic'') adverse effects 
from pesticide exposure. (Ref. 2 at 8-10). EPA also considers whether 
the ``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. 2 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 carcinogenesis have 
increasingly led EPA to conclude that some pesticides that cause 
carcinogenic effects only cause such effects above a certain threshold 
of exposure. EPA has traditionally considered adverse effects on the 
endocrine system to be a threshold effect; that determination is being 
reexamined in conjunction with the endocrine disruptor screening 
program.
    Once the hazard for a durational scenario is identified, EPA must 
determine the toxicological level of concern and then compare estimated 
human exposure to this level of concern. This comparison is done 
through either calculating a safe dose in humans (incorporating all 
appropriate safety factors) and expressing exposure as a percentage of 
this safe dose (the reference dose (``RfD'') approach) or dividing 
estimated human exposure into an appropriate dose from the relevant 
studies at which no adverse effects from the pesticide are seen (the 
margin of exposure (``MOE'') approach). How EPA determines the level of 
concern and assesses risk under these two approaches is explained in 
more detail below. EPA's general approach to estimating exposure is 
also briefly discussed.
    a. Levels of concern and risk assessment--i. Threshold effects. In 
assessing the risk from a pesticide's threshold effects, EPA evaluates 
an array of toxicological 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 in 
estimating the level of concern for humans. In estimating and 
describing the level of

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concern, however, the chosen NOAEL is at times manipulated differently 
depending on whether the risk assessment addresses dietary or non-
dietary exposures.
    For dietary risks, EPA uses the chosen NOAEL to calculate a safe 
dose or RfD. The RfD is calculated by dividing the chosen NOAEL by all 
applicable safety or uncertainty factors. Typically, a combination of 
safety or uncertainty factors providing a hundredfold (100X) margin of 
safety is used: 10X to account for uncertainties inherent in the 
extrapolation from laboratory animal data to humans and 10X for 
variations in sensitivity among members of the human population as well 
as other unknowns. Additional safety factors may be added to address 
data deficiencies or concerns raised by the existing data. Further, 
under the FQPA, an additional safety factor of 10X is presumptively 
applied to protect infants and children, unless reliable data support 
selection of a different factor. 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.
    To quantitatively describe risk using the RfD/PAD approach, 
estimated exposure is expressed as a percentage of the RfD/PAD. Dietary 
exposures lower than 100 percent of the RfD are generally not of 
concern.
    For non-dietary, and often for combined dietary and non-dietary, 
risk assessments of threshold effects, the toxicological level of 
concern is not expressed as a safe dose or RfD/PAD but rather as the 
margin of exposure (MOE) that is necessary to be sure that exposure to 
a pesticide is safe. A safe 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 interspecies differences, 10X factor for intraspecies differences, 
and 10X factor for FQPA, the safe or target MOE would be a MOE of at 
least 1,000. To calculate the MOE for a pesticide, human exposure to 
the pesticide is divided into the lowest NOAEL from the available 
studies. In contrast to the RfD/PAD approach, the higher the MOE, the 
safer the pesticide. Accordingly, if the level of concern for a 
pesticide is 1,000, MOEs exceeding 1,000 would generally not be of 
concern. Like RfD/PADs, specific MOEs are calculated for exposures of 
different durations. For non-dietary exposures, EPA typically examines 
short-term, intermediate-term, and long-term exposures. Additionally, 
non-dietary exposure often involves exposures by various routes 
including dermal, inhalation, and oral.
    The RfD/PAD and MOE approaches are fundamentally equivalent. For a 
given risk and given exposure of a pesticide, if the pesticide were 
found to be safe under an RfD/PAD analysis it would also pass under the 
MOE approach, and vice-versa.
    ii. Non-threshold effects. For risk assessments for non-threshold 
effects, EPA does not use the RfD/PAD or MOE approach if quantitation 
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 model that assumes that any amount of exposure will 
lead to some degree of risk. The slope of the dose-response curve can 
then be used to estimate the probability of occurrence of additional 
adverse effects as a result of exposure to the pesticide. For non-
threshold cancer risks, EPA generally is concerned if the probability 
of increased cancer cases exceeds the range of 1 in 1 million.
    b. Estimating human exposure. Equally important to the risk 
assessment process as determining the toxicological level of concern 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. (A) In General. 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 
U.S. Department of Agriculture. (Ref. 2 at 12). Information on residue 
values comes from a range of sources including crop field trials, data 
on pesticide reduction 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, conducts its exposure assessment using the extreme 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. 
Second, as discussed above, the tolerance value is set above the 
highest value observed in crop field trials using maximum use rates. 
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. (Id. 
at 17-28).

[[Page 68666]]

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 
Food and Drug Administration, the U.S. Department of Agriculture, 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. Although 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 maximum residue values for acute risk assessment tends to 
greatly overstate exposure in narrow increments of time where it 
matters how much of each treated food a given consumer eats and what 
the residue levels are in the particular foods consumed. 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.
    (B) Computer modeling of dietary exposure. EPA uses a computer 
program known as the Dietary Exposure Evaluation Model - Food Commodity 
Intake Database (``DEEM-FCID'') to estimate exposure by combining data 
on human consumption amounts with residue values in food commodities. 
DEEM-FCID also compares exposure estimates to appropriate RfD/PAD 
values to estimate risk. DEEM-FCID can estimate exposure for the 
general U.S. population as well as 32 subgroups based on age, sex, 
ethnicity, and region. DEEM-FCID is closely modeled on its predecessor 
program DEEM. DEEM-FCID includes the DEEM software modeling program but 
has revised inputs bearing on consumption patterns that were developed 
by EPA to insure that all underlying aspects of the model are publicly 
available. (Ref. 6).
    EPA uses a computer program to make exposure and risk estimates 
because EPA has great volumes of data on human consumption amounts and 
residue levels. Matching consumption and residue data can be done more 
efficiently by computer. Additionally, certain risk assessment 
techniques involve thousands of repeated analyses of the consumption 
database and this cannot practically be done by hand. However, the 
actual structure and logic of DEEM-FCID is relatively simple.
    DEEM-FCID contains consumption and demographic information on the 
individuals who participated in the USDA's Continuing Surveys of Food 
Intake by Individuals (``CSFII'') in 1994-1996 and 1998. The 1998 
survey was a special survey required by the FQPA to supplement the 
number of children survey participants. DEEM-FCID also contains 
translation factors that convert foods as consumed (e.g., pizza) back 
into their component raw agricultural commodities. This is necessary 
because residue data are generally gathered on raw agricultural 
commodities rather than on finished ready-to-eat food. Data on residue 
values for a particular pesticide and the RfD/PADs for that pesticide 
have to be inputted into the DEEM-FCID program to estimate exposure and 
risk.
    DEEM-FCID can make three types of risk estimates: a single point 
estimate; a simple distribution; or a probabilistic distribution. A 
point estimate provides a single exposure and risk value for each 
population subgroup. Generally, these exposure and risk values are 
derived by combining single values for consumption and residue amount 
on consumed commodities. For example, point estimates are commonly 
computed for chronic exposure and risk by combining data on average 
consumption with data on average residue levels. (Ref. 7-).
    In contrast to a point estimate, DEEM-FCID can also do two types of 
distributional analyses. A simple distribution combines a single 
residue value for each food with the full range of data on individual 
consumption amounts to create a distribution of exposure and risk 
levels. More specifically, DEEM-FCID creates this distribution by 
calculating an exposure value for each reported day of consumption per 
person (``person/day'') in CSFII assuming that all foods potentially 
bearing the pesticide residue contain such residue at the chosen value. 
The exposure amounts for the thousands of person/days in the CSFII are 
then collected in a frequency distribution.
    Added complexity is introduced if DEEM-FCID computes a distribution 
taking into account both the full range of data on consumption levels 
and the full range of data on potential residue levels in food. 
Combining these two independent variables (consumption and residue 
levels) into a distribution of potential exposures and risk requires 
use of probabilistic techniques.
    The probabilistic technique that DEEM-FCID uses to combine 
differing levels of consumption and residues involves the following 
steps:
    1. for each person/day in the CSFII, identification of any food(s) 
that could possibly bear the residue of the pesticide in question;
    2. calculation of an exposure level for each person/day based on 
the foods identified in Step 1 by randomly selecting residue 
values for the foods from the residue database;
    3. repetition of Step 2 one thousand times for each 
person/day; and
    4. collection of all of the hundreds of thousands of potential 
exposures estimated in Steps 2 and 3 in a frequency 
distribution.
    In this manner, a probabilistic assessment presents a range of 
exposure/risk estimates.
    Point estimates are used for chronic risk assessments. EPA does not 
use DEEM-FCID to calculate distributional assessments for chronic risk 
because EPA's current view is that its consumption database is not 
sufficiently robust to support a distributional analysis for chronic 
exposure. Both simple and probabilistically-derived distributions are 
used for acute risk assessment. EPA generally estimates exposure and 
risk from a simple distribution based on the 95th percentile of such a 
distribution. EPA's reason for relying on the 95th percentile with 
simple distribution assessments is that for these assessments EPA 
typically uses very conservative assumptions regarding residue levels 
(100 percent of the crop is treated and all treated food bears residues 
at the tolerance level) and thus the 95th percentile is protective of 
the general population as well as all major, identifiable population 
subgroups. Because probabilistic assessments generally use more 
realistic residue levels, EPA's starting point for estimating exposure 
and risk for such assessments is the 99.9th percentile.

[[Page 68667]]

This value can change depending on the degree of conservatism in the 
residue estimates. (Ref. 8).
    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 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.
    EPA has developed models for estimating exposure in both surface 
water and ground water. EPA uses a two-tiered approach to modeling 
pesticide exposure in surface water. In the initial tier, EPA uses the 
FQPA Index Reservoir Screening Tool (FIRST) model. FIRST replaces the 
GENeric Estimated Environmental Concentrations (GENEEC) model that was 
used as the first tier screen by EPA from 1995-1999. If the first tier 
model suggests that pesticide levels in water may be unacceptably high, 
a more refined model is used as a second tier assessment. The second 
tier model is actually a combination of the models, Pesticide Root Zone 
Model (PRZM) and the Exposure Analysis Model System (EXAMS). For 
estimating pesticide residues in groundwater, EPA uses the Screening 
Concentration In Ground Water (SCI-GROW) model. Currently, EPA has no 
second tier groundwater model.
    EPA's water exposure models have been extensively peer-reviewed 
and/or validated, and have proved highly conservative in practice. In 
fact, an evaluation conducted in conjunction with NRDC objections to 
tolerances for other pesticides found that EPA's surface water models 
never under-estimated the highest values measured in monitoring 
studies, and that EPA's groundwater model had only rarely under-
estimated such results, and those underestimations were relatively 
small. (69 FR at 30061-30064).
    Whether EPA estimates pesticide exposure in drinking water through 
monitoring data or modeling, EPA uses the higher of the two values from 
surface and ground water in quantifying overall exposure to the 
pesticide. In most cases, pesticide concentrations in surface water are 
significantly higher than in groundwater.
    iii. Residential exposures. Generally, in assessing residential 
exposure to pesticides EPA relies on its Residential Standard Operating 
Procedures (``SOPs''). 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.

C. EPA Policy on Cholinesterase Inhibition as a Regulatory Endpoint

    On August 18, 2000, EPA issued a science policy document entitled 
``The Use of Data on Cholinesterase Inhibition for Risk Assessments of 
Organophosphorous and Carbamate Pesticides.'' (Ref. 9). Although 
assessing the risk from organophosphorous and carbamate pesticides was 
a primary reason for updating EPA guidance on cholinesterase 
inhibition, the policy addressed the topic generally and not just in 
the context of these two families of pesticides.
    Cholinesterase inhibition is a disruption of the normal enzymatic 
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 enzyme, 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 the policy explains, ``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.'' (Id. 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.
    The cholinesterase inhibition policy statement explains EPA's 
approach to evaluating the hazard posed by cholinesterase-inhibiting 
pesticides. The policy focuses on three types of effects associated 
with cholinesterase-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 a safe 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. Due 
to strict ethical limitations, however, 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

[[Page 68668]]

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).
    The policy advises that, in selection of a Point of Departure for 
deriving a RfD/PAD, all data on clinical signs and cholinesterase 
inhibition should be considered in a weight-of-the-evidence analysis. 
This weight-of-the-evidence analysis should focus, according to the 
policy, on (1) ``[a] comparison of the pattern of doses required to 
produce physiological and behavioral effects and cholinesterase 
inhibition'' in the central and peripheral nervous systems and in 
blood; (2) ``comparisons of the temporal aspects (e.g., time of onset 
and peak effects and duration of effects) of each relevant endpoint;'' 
and (3) ``the potential for differential sensitivity/susceptibility of 
adult versus young animals (i.e., effects following perinatal or 
postnatal exposures).'' (Id. at 35). This analysis can lead EPA to 
``select as the critical effects any one or more of the behavioral and 
physiological changes or enzyme measures listed above.'' (Id.). In 
comparing studies across the entire database to select an endpoint for 
the Point of Departure, the policy stresses that ``parallel analyses of 
the dose-response (i.e., changes in magnitude of enzyme inhibition or 
of a different effect with increasing dose) and the temporal pattern of 
all relevant effects will be compared across all of the different 
compartments affected (e.g., plasma, RBC, peripheral nervous system, 
brain), and for the functional changes to the extent the database 
permits.'' (Id. at 38). Further, the policy states that ``[t]he 
consistency (or, the lack thereof) of LOAELs, NOAELs, or BMDs for each 
category of effects (e.g., clinical signs, cholinesterase inhibition in 
the various compartments, etc.) for the test species/strains/sex 
available and for each duration and route of exposure should be 
noted.'' (Id.).

D. 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 
differences between animals and humans when relying on studies in 
animals (inter-species safety factor) and differences among humans 
(intra-species safety factor) as well as the additional 10X children's 
safety factor added by the FQPA.
    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).

E. Endocrine Disruptor Screening Program

    To aid in the design of the endocrine screening 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. 10). 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 androgenic and 
thyroid effects as well. (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

[[Page 68669]]

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, 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. 
(Endocrine Disruptor Screening and Testing Advisory Committee Final 
Report, 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 these assays, 
however, is not yet 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.
    Recently, 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.)

IV. DDVP Tolerances

A. Regulatory Background

    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. 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 108.235 for DDVP on agricultural (food and 
feed) crops and animal commodities. DDVP is 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.
    DDVP is closely related to the pesticides naled and trichlorfon. 
Naled and trichlorfon both metabolize or degrade to DDVP in food, 
water, or the environment. All three pesticides 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 and thus, in 
addition to assessing the risks posed by exposure to these pesticides 
individually, EPA has assessed the potential cumulative effects from 
concurrent exposure to organophosphate pesticides.

B. FFDCA Tolerance Reassessment and FIFRA Pesticide Reregistration

    As required by the Food Quality Protection Act of 1996, EPA 
reassessed the safety of the DDVP tolerances under the new safety 
standard established in the FQPA. In the Interim Reregistration 
Eligibility Document (``IRED'') for DDVP, EPA determined that aggregate 
exposure to DDVP as a result of use of DDVP, naled, and trichlorfon, 
complied with the FQPA safety standard. (Ref. 11). Separately, EPA 
determined that cumulative effects from exposure to all organophosphate 
residues were safe. (Ref. 12). 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 the only technical 
product registrant, Amvac Corporation (``Amvac''), an irrevocable 
request to cancel certain uses and include additional pest strip label 
restrictions on the DDVP technical 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. Additionally, in early March, 2007, Amvac requested the voluntary 
cancellation of all its pet 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)).

C. Toxicity Overview

    Animal and human studies with DDVP demonstrate that the toxic 
effect of concern for DDVP is inhibition of cholinesterase activity. 
These studies showed decreases in cholinesterase activity in plasma, 
red blood cell, and the brain. These effects were consistently found 
whether the exposure duration was acute or chronic and across all 
tested routes of exposure. Studies involving in utero, as well as pre- 
and post-natal, exposure of young animals showed no evidence of 
increased sensitivity in the young to these effects. Cholinesterase 
inhibition was also the effect used to assess potential cumulative 
effects from exposure to organophosphate pesticides. Based on numerous 
cancer studies with DDVP, EPA has classified the evidence

[[Page 68670]]

on DDVP's potential carcinogenicity as ``suggestive;'' however, due to 
the lack of relevance to humans of the tumors identified, EPA has 
determined that DDVP poses a negligible cancer risk to humans.

D. Exposure Overview

    Exposure to DDVP can occur through the consumption of food treated 
with DDVP, naled, or trichlorfon, consumption of drinking water bearing 
DDVP residues, or from exposure in the residential setting from use of 
DDVP or trichlorfon. EPA has extensive food monitoring data on DDVP. 
These data show that with one exception, strawberries, DDVP is rarely 
found at detectable amounts in food. About 5 percent of sampled 
strawberries have shown detectable DDVP residues. These monitoring 
results are consistent with metabolism data on DDVP which shows that it 
is rapidly degraded into non-toxic substances. EPA has limited water 
monitoring data showing no detectable residues of DDVP. Due to the fact 
that these data do not identify whether they were collected from areas 
of DDVP, naled, or trichlorfon usage and the lack of data from shallow 
groundwater wells, EPA has relied upon conservative modeling estimates 
of drinking water. EPA has estimated residential exposure to DDVP based 
primarily on one of several monitoring studies conducted using DDVP 
pest strips in houses.

V. The Petition to Revoke Tolerances

    On June 2, 2006, the Natural Resources Defense Council (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 SAP 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. 1). Shortly after the petition was filed, on 
June 30, 2006, EPA released the Interim Reregistration Eligibility 
Decision (``IRED'') for DDVP which addressed DDVP's eligibility for 
reregistration under FIFRA and assessed 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. 13).
    NRDC asserted numerous grounds as to why the DDVP tolerances do not 
meet the FQPA safety standard and should be revoked. EPA has divided 
NRDC's grounds for revocation into four categories - toxicology; 
dietary exposure; residential exposure; and risk characterization - and 
addressed separately each claim under these categories. Each specific 
claim of NRDC is summarized in Unit VII immediately prior to EPA's 
response to the claim.

VI. Public Comment

    In response to the aspects of the petition addressing the DDVP 
tolerances, 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, the party holding the registration for DDVP under 
FIFRA. (Ref. 14). Amvac's comments on the specific claims by NRDC are 
summarized