

[Federal Register: December 5, 2007 (Volume 72, Number 233)]
[Rules and Regulations]               
[Page 68661-68698]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr05de07-21]                         


[[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


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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 http://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 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 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 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. 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: http://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 in Unit VII immediately following the summary of NRDC's 
claim but prior to EPA's response to the claim.

VII. Ruling on Petition

    This order addresses NRDC's petition to revoke DDVP tolerances. As 
noted, in responding to NRDC's petition, EPA has broken the issues into 
four categories -- toxicology; dietary exposure; residential exposure; 
and risk characterization. Below, EPA addresses each of the claims 
raised in these categories and explains why they do not support 
revocation of the tolerances.
    EPA has not addressed claims that concern DDVP uses that have been 
canceled since the time of the petition. Specific uses cancelled were 
the largest (100 gram) pest strip; lawn, turf, and ornamentals; pet 
collars; and in-home crack and crevice. Additionally, the remaining 
``large'' pest strips (80 and 65 grams) were limited to unoccupied 
portions of the home. The only pest strips permitted in occupied areas 
were smaller strips (16, 10.5, 5.25 grams) for use in closets, 
wardrobes, and cupboards.

A. Toxicological Issues

    1. Cancer--a. NRDC's claims. NRDC claims that ``the rejection by 
EPA of the `probable carcinogen' cancer classification of previous 
Agency reviews is inadequately supported .. ..'' (Ref. 1 at 17). 
According to NRDC, EPA has not explained why its prior analysis was 
``flawed,'' and the reasons EPA has given for the change in cancer 
classification are ``speculative, at best.'' (Id.). NRDC urges EPA to 
drop its new classification of DDVP as having ``suggestive'' evidence 
of carcinogenicity and restore the ``original classification.'' (Id. at 
18).
    Specifically, NRDC argues with EPA's decision to discount, in its 
weight-of-the-evidence evaluation for DDVP, mononuclear cell leukemia 
(MCL) seen in a rat study and forestomach tumors identified in a mouse 
study. NRDC claims that EPA's assertion that a finding of MCL in the 
Fischer rat is of limited usefulness due to variability of occurrence 
of this cancer in the Fischer rat ``may be an artifact of the design of 
such studies and is not an adequate basis for ignoring a positive 
result.'' (Id. at 17). NRDC suggests that a larger scale study could 
have resolved this issue. As to forestomach tumors, NRDC disputed EPA's 
conclusion that these tumors have limited relevance to humans given 
that humans do not have forestomachs. NRDC notes that all animals have 
some difference in their organs and tissues and thus the lack of a 
forestomach in humans does not ``automatically mean that the effect is 
irrelevant to humans.'' (Id.). According to NRDC, EPA ``must provide 
convincing explanations based on reliable data that their rejection of 
forestomach tumors is a reasonable certainty and will adequately 
protect the public health.'' (Id.).
    NRDC also suggests that a study in Denver, Colorado ``specifically 
linked'' DDVP pest strips to leukemia in children under 15 (Leiss, 
J.K., Savitz, D.A. ``Home pesticide use and childhood cancer: a case-
control study,'' American Journal of Public Health 1995; 85:249-52) and 
a study of adult men with leukemia in Iowa and Minnesota (Brown, L.M., 
Blair, A., Gibson, R., et al. ``Pesticide exposures and other 
agricultural risk factors for leukemia among men in Iowa and 
Minnesota,'' Cancer Research 1990;50(20):6585-91) found that these men 
were twice as likely to have a history of exposure to DDVP.
    b. Amvac's comments. Disagreeing with NRDC's claims, Amvac argues 
that NRDC has ignored an extensive DDVP cancer database and the 
confounding effect that corn oil played in the two positive studies 
relied upon by NRDC. (Ref. 14 at 27-28). Amvac asserts that 11 cancer 
studies have been performed with DDVP, involving both oral and 
inhalation exposure routes, and that the only two positive studies were 
gavage studies in which the DDVP was administered by gavage in corn 
oil.

[[Page 68671]]

Amvac claims that it is well-recognized that corn oil as a confounding 
factor in cancer studies and that, in fact, the National Toxicology 
Program (``NTP'') has found corn oil to be carcinogenic. Finally, Amvac 
cites to a recent review by the European Food Safety Agency, which 
Amvac asserts concluded, after reviewing all of the evidence, ``that 
the carcinogenic risk from exposure to DDVP is very low.'' (Ref. 15).
    c. EPA's response. Initially, EPA responds to NRDC's claims 
regarding EPA's cancer classification by noting that NRDC's request to 
amend the cancer classification is not a sufficient ground for seeking 
revocation of the DDVP tolerances. A cancer classification does not 
determine whether a pesticide is safe or not; rather, a cancer 
classification is one step in a multi-stage risk assessment process 
that ascertains and examines not only the toxicological effects a 
pesticide causes, but also the potency of the pesticide and the extent 
of human exposure to the pesticide. A pesticide found to be a 
``probable'' human carcinogen may nonetheless meet the FFDCA section 
408 safety standard if it has a low potency and/or low exposure. NRDC's 
petition contains no arguments or evidence that if DDVP is reclassified 
as a probable human carcinogen, a cancer risk assessment would show 
that DDVP is not safe. Accordingly, EPA denies NRDC's petition to 
revoke DDVP tolerances to the extent that the petition cites EPA's 
alleged cancer misclassification of DDVP as grounds for such a 
revocation.
    Nonetheless, to clarify the issue, EPA will explain the basis for 
its revision of the cancer classification of DDVP. EPA's Cancer 
Assessment Review Committee (CARC) in the Health Effects Division of 
the Office of Pesticide Programs has held six cancer reviews for DDVP 
over the past two decades. These multiple reviews have been necessary 
due to the development of new information on DDVP as well as on 
carcinogenicity generally. What these reviews show is that EPA has 
taken a conservative approach to the cancer classification of DDVP, 
only weakening the classification (i.e., adopting a classification of 
lower human carcinogenic potential) upon the repeated advice of 
independent expert scientific panels.
    EPA's reviews bridge two versions of its cancer assessment 
guidelines. These guidelines have slightly different descriptive 
categories for classifying chemicals as to their carcinogenic 
potential. In its 1986 Cancer Assessment Guidelines, EPA created the 
following categories regarding cancer potential: ``human carcinogen'' 
(Group A), ``probable human carcinogen'' (Group B), ``possible human 
carcinogen'' (Group C), ``not classifiable as to human 
carcinogenicity'' (Group D), and ``evidence of non-carcinogenicity for 
humans'' (Group E). (51 FR 33992 (September 24, 1986)). Under the 1986 
Guidelines, Group B was further subdivided into Groups B1 and B2 with 
the former for chemicals categorized on the basis of data from humans 
and the latter based on data in animals. In an update to these 
guidelines in 2005, EPA adopted the following classifications: 
``carcinogenic to humans,'' ``likely to be carcinogenic to humans,'' 
``suggestive evidence of carcinogenic potential,'' ``inadequate 
information to assess carcinogenic potential,'' and ``not likely to be 
carcinogenic to humans.'' (70 FR 17765, April 7, 2005). The revised 
guidelines dropped the alphabetic labeling of the classifications.
    In its first review of DDVP in June 1987, the CARC's predecessor, 
the Carcinogenicity Cancer Peer Review Committee [hereinafter referred 
to as the CARC for simplicity], classified DDVP as a probable human 
carcinogen (Group B2), under EPA's 1986 cancer classification system. 
(Ref. 16). The CARC's classification of DDVP as a probable human 
carcinogen was based on its conclusion that the evidence showed DDVP 
satisfied two separate criteria for a ``probable human carcinogen:'' 
(1) carcinogenicity seen in multiple species; and (2) carcinogenicity 
seen in an unusual degree in a single experiment. To show cancer in 
multiple species, the CARC cited (1) a finding of statistically 
significant dose-related trend and statistically significant increase 
in forestomach tumors (combined papillomas and carcinomas) in female 
mice in a cancer study in the mouse conducted by the National 
Toxicology Program (NTP); and (2) a finding of a statistically 
significant dose-related trend and statistically significant increase 
in mononuclear cell leukemia (MCL) and pancreatic acinar adenomas in 
male rats in a cancer study in the rat conducted by the NTP. These two 
findings were supported by a significant positive trend for forestomach 
tumors in male mice in the NTP mouse study and a finding of 
statistically significant increased (but overall numbers within the 
range of historical controls) lung adenomas and combined mammary 
fibroadenomas and carcinomas in male and female rats, respectively, in 
the NTP rat study. To satisfy the criterion of cancer in an unusual 
degree in a single study, the CARC noted that forestomach tumors are a 
rare tumor in the female mouse. Finally, the CARC relied on positive in 
vitro mutagenicity data in support of the ``probable human carcinogen'' 
classification.
    In September, 1987, the CARC's classification was evaluated by the 
FIFRA Scientific Advisory Panel (``SAP''), an independent expert panel 
created by statute for the purpose of providing EPA advice on 
scientific matters concerning pesticides. The SAP disagreed with EPA's 
classification and recommended that DDVP be classified as only a 
possible human carcinogen (Group C) based on its conclusions that: (1) 
DDVP only induced benign tumors; (2) the tumors did not show a dose-
related trend; and (3) DDVP was not mutagenic in in vivo assays. (Ref. 
17).
    The CARC met for a second time on DDVP in September, 1987, to take 
the SAP's view into consideration. The CARC refused to alter its Group 
B2 carcinogen classification. It cited essentially the same reasons 
from the first review and emphasized the following evidence of 
malignancy to explain its difference with the SAP: (1) MCL is 
considered a malignant tumor; (2) both the pancreatic adenomas in rats 
and forestomach papillomas in mice had the potential to progress to 
malignancies; and (3) the presence of ``some'' rare forestomach 
carcinomas in female mice. (Id.)
    A third meeting of the CARC was held in July, 1988 to review a 
report from the NTP Panel of Experts on the classification of DDVP. 
(Ref. 18). NTP scientists had reexamined the pancreata of the rats in 
the NTP rat study and concluded that the statistically significant 
increase in pancreatic lesions was diminished. For this reason, the NTP 
recommended that the evidence for carcinogenicity in male rats be 
downgraded from ``clear'' evidence to ``some'' evidence. Nonetheless, 
the CARC again refused to change DDVP's cancer classification relying 
on the MCL finding in rats, findings of multiple benign tumors in rat 
and mouse NTP studies, and DDVP's mutagenic properties. The CARC noted 
this classification was interim until new cancer and mutagenicity data 
could be reviewed.
    A fourth meeting of the CARC in September, 1989, again reviewed the 
reanalysis of the pancreatic lesions in the rat, and also examined new 
cancer studies. (Ref. 19). The CARC noted that, although the NTP 
reexamination had found pancreatic tumors in treated rats to be 
statistically increased, albeit to a diminished degree than first 
thought, a new statistical review by EPA using two common statistical 
procedures found no statistical significance at all. Further, the CARC 
examined a DDVP inhalation cancer study in rats and two cancer

[[Page 68672]]

studies in which DDVP was administered in drinking water. The 
inhalation study was negative for cancer effects. The drinking water 
studies had several deficiencies making quantitative analysis 
inappropriate but had qualitative evidence that showed some of the 
tumors seen in previous studies. Taking this information into account, 
as well as new information questioning the relevance of MCL in rats and 
forestomach tumors in mice to humans, the CARC downgraded DDVP to a 
possible human carcinogen (Group C). Nonetheless, the CARC maintained 
that a quantitative cancer assessment was warranted using the geometric 
mean of the tumor rates of MCL in rats and forestomach tumors in mice.
    The fifth meeting of the CARC, in March 1996, considered new 
information from Amvac including an evaluation of the severity of the 
MCL seen in the NTP rat study, studies on the mechanism of forestomach 
tumors, and in vivo mutagenicity testing. (Ref. 20). The evaluation of 
the severity of the rat MCL in the NTP study showed that there was no 
statistically significant difference in the severity of the MCL between 
control and treated animals. (Ref. 21 at 10). Further, the new in vivo 
testing was negative. The CARC, however, rejected Amvac's argument that 
the studies it submitted demonstrated the mechanism of tumor formation 
for the mouse forestomach tumors. Weighing all of this information, the 
CARC retained the possible human carcinogen classification (Group C) 
and recommendation for quantitative low dose linear cancer assessment. 
Based on its conclusion that the MCL in rats but not the forestomach 
papillomas are malignant tumors, however, the CARC concluded that the 
linear low dose extrapolation should be based on the MCL in rats alone.
    The sixth cancer review, finalized in February, 2000, principally 
focused on the significance of the MCL in the rat NTP study taking into 
account three new analyses of this cancer. (Ref. 22). The first was a 
report submitted by Amvac titled ``An Evaluation of the Potential 
Carcinogenicity of Dichlorvos: Final Report of the Expert Panel.'' 
(Ref. 23). That report was prepared by various experts in the field, 
primarily academics, who had been assembled by a consulting firm hired 
by Amvac. The report describes the steps taken to avoid conflicts of 
interest and to insure that the substance of the report was not 
influenced by its sponsor. The report concludes that the ``incidence of 
MCL in the NTP DDVP rat study (1989) . . . does not support a 
conclusion of carcinogenicity.'' (Id. at 21). The report summarized the 
main reasons for this conclusion as follows:
    1. The results are species-, strain-, and sex-specific.
    2. The endpoint is dramatically affected by administration of corn 
oil by gavage.
    3. There was no significant effect on the relative severity of the 
disease, time-to-tumor latencies or percentage of rats surviving to 
study termination.
    4. The data do not demonstrate a classic dose-response.
    5. The results are not replicated in a very large number of 
carcinogenicity studies on DDVP and related substances (e.g., 
Trichlorfon, Metrifonate, Naled).
    6. Many other studies are more appropriate to estimate human risks 
since the routes of administration employed more closely approximated 
potentially hazardous routes in man (e.g., inhalation, dietary or in 
drinking water) rather than the gavage method employed in the NTP 
study.
    7. The incidences are similar to normal background rates that are 
increasing over time.
(Id.). The report further stated that effects seen in the NTP rat study 
showed ``the extremely wide variability that is typically observed with 
this tumor.'' (Id.). The finding of a lack of carcinogenicity, the 
report asserted, is consistent with ``similar positions taken by other 
organizations (e.g., Joint FAO/WHO Panel of Experts on Pesticide 
Residues, NTP, and OSTP).'' (Id.). Additionally, the report concluded 
that ``metabolic considerations and the genotoxic potential of DDVP'' 
do not support a finding of carcinogenicity. Finally, the report 
concluded that DDVP does cause forestomach tumors in mice but that this 
``endpoint has no relevance to man and therefore, should not be 
employed for extrapolation to human risk.'' (Id.).
    The second new analysis was from the SAP review of the CARC's 
fourth review of the carcinogenicity of DDVP. (Ref. 24). The SAP 
concluded that ``[t]here is compelling evidence to disregard MCL in the 
Fischer rat.'' The SAP gave several reasons for this conclusion based 
both on general information on MCL in Fischer rats and specific 
information on the NTP rat cancer study with DDVP. In terms of general 
evidence, the SAP explained that (1) ``MCL is one of the most common 
background tumor types'' in the Fischer rat; (2) that there is a high 
variability in MCL in Fischer rats; and (3) MCL is a strain specific 
cancer. (Id. at 17). On this last point, the SAP noted that MCL ``has 
been referred to as Fischer rat leukemia . . . [and] [o]ther rat 
strains and mice do not develop MCL, and there is no human correlate to 
this disease.'' (Id.). Turning to the NTP rat study with DDVP, the SAP 
noted that (1) although MCL was seen at both the low and high doses in 
the study there was no clear dose-response relationship seen in the 
study; and (2) chemically-related increases in MCL are marked by 
advanced severity of the MCL but that the NTP rat study ``showed no 
significant increase in severity of the MCL with increasing dose, 
indicating that these lesions are background.'' (Id.).
    The SAP also ratified the CARC's earlier position that the 
forestomach tumors in the NTP mouse study should not be relied upon to 
estimate risk to humans. The SAP explained that these tumors are 
``likely due to the chronic irritancy, inflammation, and cytotoxicity 
during chronic bolus dosing, resulting in extraordinary high local 
concentration of the chemical.'' (Id.). Such conditions would not exist 
outside of the laboratory. Further, such tumors have only limited 
relevance to humans because ``the forestomach in rodents acts as a 
storage site where irritant chemicals in food have prolonged contact 
with the sensitive squamous epithelium lining, a situation that does 
not pertain to humans.'' (Id.).
    The SAP reached an overall conclusion that ``the weight of the 
evidence suggests carcinogenicity in animals treated with DDVP with a 
non-linear dose-response. However, the compound is considered a weak 
carcinogen acting via a secondary or indirect mechanism.'' (Id. at 
18.).
    The third new analyses was a short memorandum summarizing a 
conversation with Dr. Gary Boorman of the NTP. (Ref. 25). Dr. Boorman 
opined that the MCL ``tumor type in males[] [Fisher rats] had a high 
and variable background.'' (Id.). Further, Dr. Boorman is cited as 
stating that although ``this tumor type can not be dismissed as 
[ir]relevant to humans, [] it does seem to be found mainly in the 
Fisher rat and does not appear to be the same type of leukemia as found 
in [human] adults or children.'' (Id.).
    Relying heavily on the advice of these expert scientific opinions 
(particularly, the views of the SAP), the CARC in its sixth report 
softened its view regarding the importance of the MCL seen in the NTP 
rat study and reaffirmed its view that the forestomach tumors in the 
NTP mouse study were a localized tumor of limited relevance to humans. 
Although the CARC maintained that the MCL in the rat study could ``not 
be totally disregarded,'' it accepted the advice of the expert panel of 
the SAP and as well

[[Page 68673]]

as the report commissioned by Amvac that the evidence on MCL did not 
warrant use of this cancer to quantitatively estimate cancer risk to 
humans using a low-dose linear extrapolation. The CARC specifically 
cited the high background rates and variability of MCL in the Fischer 
rat, the lack of a dose-response effect in the NTP rat study, and 
negative results in other cancer studies as justifying its decision to 
change the cancer classification of DDVP from a ``possible human 
carcinogen'' to ``suggestive evidence of carcinogenic potential'' and 
to recommend that the data did not support a quantitative cancer risk 
assessment.
    To recap, EPA's initial DDVP cancer classification of ``probable 
human carcinogen'' was based on a MCL and pancreatic adenomas in the 
rat, forestomach papillomas in the mouse, and positive in vitro 
mutagenicity data. EPA only downgraded this classification following: 
(1) a re-analysis of the rat study showed no statistically significant 
increase in pancreatic adenomas; (2) presentation of strong evidence 
concerning the non-relevance of MCL in rats and forestomach tumors in 
mice to humans; (3) submission of a negative DDVP cancer study in rats 
by the inhalation route; (4) submission of in vivo data showing a lack 
of mutagenicity for DDVP; and (5) repeated recommendations from 
independent scientific groups to downgrade the DDVP cancer 
classification.
    A recent review by the European Food Safety Agency (``EFSA'') 
supports EPA's DDVP cancer assessment. (Ref. 15). The EFSA found the 
only treatment-related tumors from the DDVP studies to be the mouse 
forestomach tumors: ``[The Scientific Panel on Plant health, Plant 
protection products and their Residues] concludes that with the 
exception of tumours of the forestomach in the mouse, there was no 
convincing evidence for a compound-related, relevant tumour response. 
Tumours observed in other tissues (pancreas, mammary, mononuclear 
leukaemia) showed no dose-response, were inconsistent between studies 
and sexes, were reduced in control animals relative to historical 
control data, or were unique to the experimental conditions of the 
assay.'' (Id. at 33). Further, the EFSA found the forestomach tumors to 
be ``a site of contact effect, and a consequence of the very high, 
sustained concentrations of dichlorvos to the forestomach that would be 
achieved by gavage dosing in corn oil.'' (Id.). These tumors, the EFSA 
concluded, were subject to a threshold dose unlikely to be exceeded in 
humans due to cholinesterase inhibition effects at a much lower 
threshold. (Id. at 34).
    NRDC is wrong to suggest that variability in MCL occurrence alone 
drove EPA's decision to change its views regarding the importance of 
the MCL findings. To the contrary, variability along with several other 
factors were considered in EPA's weight of the evidence approach. If 
anything, EPA took a more conservative approach to this cancer than its 
scientific advisory panel. Further, EPA did not discount the 
forestomach tumors simply because humans do not have forestomachs. 
Rather, both EPA and the SAP explained why the unique aspects of the 
rodent forestomach in connection with the artificial condition of corn 
oil bolus dosing are likely to produce results of limited relevance to 
humans.
    Further, NRDC's reliance on epidemiological studies by Liess and 
Brown is misplaced. EPA reviewed the Liess study and identified biases 
and confounders in the studies that are a more likely explanation for 
the findings of increased cancer than exposure to pest strips. (Ref. 11 
at 142). As to the Brown study, EPA has rejected it as inadequate 
because the subjects were exposed to other pesticides in addition to 
DDVP and there was no adjustment made for these other exposures. Other 
confounders such as multiple statistical comparisons were identified as 
well. (Ref. 26).
    2. NOAEL/LOAEL--a. NRDC's claims. NRDC notes that a NOAEL for 
cholinesterase inhibition was not established in a mouse oncogenicity 
study relied upon by EPA. NRDC claims that failure to identify a NOAEL 
not only renders the mouse oncogenicity study invalid but ``undermines 
the entire risk assessment and precludes the Agency from finding that 
the DDVP tolerances are safe . . . .'' (Ref. 1 at 47). NRDC argues that 
if there is no NOAEL identified in a study, the LOAEL from that study 
is ``virtually meaningless information.'' (Id.). Finally, NRDC argues 
that EPA cannot legally make the reasonable certainty of no harm 
finding for DDVP or any other pesticide if EPA is relying on a LOAEL 
rather than a NOAEL.
    b. EPA's response. EPA has repeatedly rejected NRDC's legal 
arguments concerning reliance on LOAELs in making safety findings under 
FFDCA section 408. (70 FR 46706, 46729; 69 FR 30042, 30066-30067; Ref. 
27 at 165-166). EPA incorporates those prior responses herein. Further, 
EPA disagrees with NRDC's contention that a LOAEL in a study that does 
not identify a NOAEL provides ``virtually meaningless information.'' 
Depending on the severity and consistency of the effect at the LOAEL as 
well as the severity and consistency at higher doses, the LOAEL can 
provide substantial information bearing on the no adverse effect level. 
It is for this reason that EPA and FDA, as well as other public health 
agencies, have long relied on LOAELs, in appropriate circumstances, in 
making safety findings. (69 FR at 30066; Ref. 28).
    EPA relied upon a LOAEL in assessing the risk posed by DDVP for the 
following exposure scenarios: short-term incidental oral; short-, 
intermediate-, and long-term dermal; short- and intermediate-term 
inhalation. The LOAEL was from a single blind, placebo controlled, 
randomized study to investigate the effects of multiple oral dosing on 
erythrocyte cholinesterase inhibition in healthy male volunteers and 
involved a dose of 0.1 milligrams/kilogram of body weight/day (``mg/kg/
day''). This value was adjusted with a safety factor of 3X to 
approximate the value of a NOAEL. The LOAEL provided sufficient 
information to estimate the NOAEL (using a 3X safety factor) because 
the study measured the severity of the cholinesterase inhibition 
response observed. Cholinesterase inhibition is a continuous endpoint 
where no fixed generic percentage of change from baseline separates 
potential adverse effects from non-adverse effects. Generally, 
cholinesterase inhibition of 20 percent from baseline is regarded as 
showing a potential for adverse effects on the nervous system with 
lower levels evaluated on a case-by-case basis. (Ref. 9 at 37-38). In 
the DDVP human study, the cholinesterase inhibition fell at the very 
low end of the scale (cholinesterase inhibition in individuals varied 
from baseline within a range from 8 to 23 percent at the end of the 
study) indicating that the NOAEL was not significantly lower.
    NRDC is mistaken to claim that the mouse oncogenicity study was 
invalid for failure to identify a NOAEL. Oncogenicity (carcinogenicity) 
studies are not designed to produce NOAELs but rather to examine the 
cancer responses at high doses. EPA relies on chronic studies in the 
rodent and non-rodent (generally the rat and dog, respectively) to 
evaluate and define the level of threshold chronic, non-cancer effects. 
(40 CFR 158.340(a)). Acceptable chronic rat and dog studies are 
available for DDVP. (Ref. 11). NRDC also errs in contending that EPA, 
by examining cholinesterase effects in the mouse oncogenicity study, 
indicates that it does not have valid and reliable chronic toxicity 
data. As noted, EPA does not specifically require a chronic toxicity

[[Page 68674]]

study in the mouse and it has an acceptable study meeting the 
requirement for a chronic study in rodents. Nonetheless, where an 
oncogenicity study in the mouse does shed light on effects seen in 
chronic studies, EPA certainly will consider that information in its 
overall weight-of-the-evidence evaluation for the pesticide.
    3. Human studies--a. NRDC's claims. NRDC asserts that none of the 
DDVP human studies satisfy the standards in EPA's human testing rule 
because they ``violate the Nuremburg Code and fail to satisfy the 
standards in EPA's human testing rule.'' (Ref. 1 at 26.). Therefore, 
NRDC petitions EPA to reject all intentional dosing human studies for 
DDVP as unethical and unscientific.
    NRDC raises various specific concerns as to a particular human 
study commonly referred to as the Gledhill study (MRID  
44248801). Citing a draft report by EPA's Human Studies Review Board 
(HSRB), NRDC claims that this study is ``statistically meaningless'' 
because it had too few test subjects. Further, NRDC argues that the 
variability in the cholinesterase inhibition in the study demonstrates 
that ``even greater than the customary numbers of test subjects would 
be required to permit detection of effects caused by the test substance 
above background variation.'' (Ref. 13 at 15). Other scientific defects 
in the Gledhill study alleged by NRDC include failing to promptly 
measure red blood cell (``RBC'') effects; failing to measure blood 
plasma effects; not restricting subjects in controlled conditions for 
living and eating; and failing to properly obtain informed consent. 
NRDC claims the study was ethically deficient because reference in the 
consent form to DDVP as a drug made it impossible to obtain informed 
consent and study conductors failed to monitor the health of subjects 
after the conclusion of the study. Finally, NRDC argues that if EPA 
relies on the study, EPA cannot conclude that the DDVP tolerances are 
safe because the LOAEL for humans in the study (reported by NRDC to be 
0.01 mg/kg/day) is well below the lowest LOAEL in animal studies (0.1 
mg/kg/day).
    NRDC also objects to EPA's reliance on a number of other human 
studies which NRDC describes as ``ethically repugnant'' due to 
involvement of children as test subjects.
    b. Amvac's comments. In its comments, Amvac argues that ``there is 
a large body of human data from a variety of sources that provide 
information directly relevant to the DDVP risk assessment process.'' 
(Ref. 14 at 32). According to Amvac these human studies show that the 
most sensitive endpoint for DDVP is inhibition of red blood cell 
cholinesterase; DDVP operates by a common mechanism in animals and 
humans; DDVP inhibits RBC cholinesterase at similar levels in animals 
and humans; and DDVP has similar effects no matter what the route of 
exposure. (Id. at 33). As to the Gledhill study, Amvac disputes NRDC's 
criticisms of its scientific value and ethics. (Id. at 37). Amvac 
claims that ``[t]he number of subjects employed, six per dose, is . . . 
a standard number of test subjects sufficient to provide statistical 
power in human studies.'' (Id. at 38). Measuring plasma cholinesterase 
was not essential, according to Amvac, because RBC cholinesterase ``is 
relevant to assessing the risk of inhibition of the toxicologically 
important brain cholinesterase enzyme.'' (Id. at 37).
    c. EPA's response. In responding to the petition, EPA would first 
note that the petition simply asks EPA not to rely on any of the DDVP 
human studies but does not contend that reliance on animal studies 
instead of the human studies will show the DDVP tolerances to be 
unsafe. Subsequent to NRDC's petition, EPA did rely on the Gledhill 
study in assessing the risk posed by DDVP. (Ref. 11 at 133). To clarify 
the basis for EPA's decision to rely on the Gledhill study, EPA has 
described its decision-making process below.
    EPA decisions regarding the ethics and scientific value 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 Research Rule rests on the 
basic principle that EPA will not, in its actions, rely on data derived 
from unethical research. The rule divides human studies into two 
groups: ``new'' studies--those initiated after April 7, 2006--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).
    Whether the data are ``new'' or ``old,'' the Human Research Rule 
forbids EPA to rely on data from any study involving intentional 
exposure of pregnant women, fetuses, or children. (40 CFR 26.1704).
    To aid EPA in making ethical determinations under the Human 
Research Rule, the rule established an independent Human Studies Review 
Board (HSRB) to review both proposals for new research and reports of 
covered human research on which EPA proposes to rely. (40 CFR 26.1603). 
The HSRB is 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 intends to rely on the 
results from ``old'' human research, 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).
    In the risk assessment for DDVP, EPA has relied upon one human 
study for several exposure scenarios. The study, conducted by A.J. 
Gledhill, involved a single blind, randomized placebo-controlled oral 
study in which 6 healthy male volunteers were administered a daily dose 
of DDVP for 21 days at approximately 0.1/mg/kg/day and 3 volunteers 
were administered a placebo

[[Page 68675]]

(Ref. 11 at 133). Prior to relying on the Gledhill study in the IRED, 
EPA presented this study as well as 10 other DDVP human studies to the 
HSRB for review. In its presentation to the HSRB, EPA stated that it 
had concluded that the Gledhill study ``is sufficiently robust for 
developing a Point of Departure for estimating dermal, incidental oral, 
and inhalation risk from exposure to DDVP'' for the purpose of 
assessing DDVP by itself but not for conducting a cumulative assessment 
of DDVP and other organophosphate pesticides. (Ref. 29 at 19). EPA 
recommended that the other 10 studies should not be used. (Id. at 20).
    As part of the public participation procedures that have been 
adopted by the HSRB, NRDC appeared before the HSRB when DDVP was being 
considered to make the points it has raised in this petition. (Ref. 
30).
    The HSRB agreed with EPA on the appropriateness of using the 
Gledhill study after a detailed evaluation of the scientific merit of 
the study as well as an evaluation of other ethical considerations. 
(Ref. 31). In examining scientific merit, the HSRB identified both 
strengths and weaknesses of the Gledhill study. Identified as strengths 
were: 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. Weaknesses seen included: use 
of a single dose; preventing establishment of a dose-response 
relationship; small sample size and use of males subjects only; 
measurement of RBC cholinesterase inhibition at 24 hours after dosing 
which may have missed peak inhibition; no analysis of plasma 
cholinesterase; sampling and analysis of enzyme inhibition ended 3 days 
before the end of dosing; lack of clarity as to whether steady state 
inhibition was achieved; and lack of follow-up with subjects following 
completion of dosing. After carefully considering these factors, the 
HSRB concluded that despite the ``numerous technical difficulties'' 
with the study that it ``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.'' (Id. at 
41). The HSRB's reasoning was that ``[a]lthough a study using a single 
dose level is not ideal for establishing a LOAEL, there was general 
consensus that RBC cholinesterase is a well-characterized endpoint for 
compounds that inhibit acetylcholinesterase activity and therefore, 
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.'' (Id.).
    Turning to other ethical considerations, the HSRB examined whether 
there was clear and convincing evidence that prevailing ethical 
standards had been violated. Specifically, the HSRB considered whether 
informed consent had been compromised by certain references in test 
subject disclosure forms to DDVP as a ``drug,'' or by deficiencies in 
the monitoring of subjects both during and after conclusion of the 
study. Ultimately, the HSRB concluded that although the study ``failed 
to fully meet the specific ethical standards prevalent at the time the 
research was conducted, . . . [t]here was no clear and convincing 
evidence that the research was fundamentally unethical--intended to 
seriously harm participants or that informed consent was not 
obtained.'' (Id. at 46). The 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.'' (Id.). Deficiencies 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. (Id.).
    The HSRB also agreed with EPA that the technical difficulties 
identified with the Gledhill study limited its usefulness in the 
organophosphate cumulative assessment. (Id. at 41). Finally, the HSRB 
agreed with EPA that there were scientific value or other ethical 
considerations that precluded reliance by EPA on the other ten DDVP 
human studies. (Id. at 41-42).
    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. In fact, NRDC has not raised in its petition any 
arguments not considered and rejected by the HSRB.
    EPA would add the following further information regarding NRDC's 
criticisms of the Gledhill study's use of males only, the number of 
test subjects in the study, the 24-hour period between dosing and 
measurement of cholinesterase inhibition, the failure to measure plasma 
cholinesterase, and purported increased sensitivity in humans 
demonstrated by the study.
    As to the use of males only, EPA would note that no sex differences 
were observed in the comparative cholinesterase studies in animals. 
(Ref. 32). With regard to statistical significance of the study results 
due to the number of test subjects, EPA strongly disagrees with the 
claims of NRDC. The results of the repeated dose study of 9 subjects (6 
DDVP and 3 placebo) in the Gledhill study were analyzed statistically 
for significance in addition to being analyzed for biological 
significance. Although 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. Indeed, all of the 6 dosed 
subjects exhibited statistically significant (with respect to their 
pre-dose levels) RBC cholinesterase depression on one or more days. One 
of the three placebo controls exhibited statistically significant 
depression on one day. However, the group means of RBC cholinesterase 
activity in treated subjects are statistically below the group means of 
the placebo controls on days 7, 11, 14, 16 and 18 by repeated measures 
analysis of variance. (Ref. 33). The statistics of the study clearly 
show the ability to demonstrate a statistically significant response. 
For the sake of comparison it is worth noting that use of 6 male test 
subjects exceeds the long-standing EPA recommendation for 4/sex/dose 
subjects in non-rodent (usually dog) animal studies. (Ref. 34). Nor 
does EPA agree with NRDC that the variability in cholinesterase 
inhibition for test subjects shows that more subjects are required to 
detect effects above background variations. First, the variability seen 
in the study (cholinesterase inhibition in individuals varied from 
baseline within a range from 8 to 23 percent at the end of the study) 
is not large, particularly since the percentage inhibition in all 
instances was at the marginal end of the range. Second, EPA concluded, 
and the HSRB agreed, that the study did identify an effect above 
background. Moreover, an intra-species safety factor of 10X was applied 
to the study results to address variability in human sensitivity.
    As to failure of the study to assess inhibition of plasma 
cholinesterase, EPA does not believe that this deficiency has much 
significance. Although the study should have had measurements of both 
RBC and plasma cholinesterase, the use of RBC cholinesterase findings 
provides a more

[[Page 68676]]

useful regulatory estimate for assessing the effects of DDVP on brain 
and peripheral cholinesterase depression in humans. In its policy on 
use of data on cholinesterase inhibition in assessing the risk of 
organophosphates and carbamates, EPA made clear that ``[r]ed blood cell 
measures of acetylcholinesterase inhibition, if reliable, generally are 
preferred over plasma data.'' (Ref. 9 at 29). 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.). Although testing 
for plasma inhibition may have provided additional information, given 
that the study identified statistically significant effects on RBC at a 
marginal level, data on a less preferred endpoint such as plasma 
cholinesterase adds little meaningful information.
    With regard to the study procedure of waiting 24 hours after dosing 
to measure cholinesterase inhibition, the study was designed to 
evaluate the cumulative effect of repeat dosing with DDVP. While a 
shorter interval between dosing and measurement would have provided 
more information about acute effects of DDVP, this study has not been 
relied upon to assess acute risks.
    Finally, NRDC is mistaken to claim that the Gledhill study showed 
humans to be more sensitive than test animals. The LOAEL from the 
Gledhill study is 0.1 mg/kg/day, not 0.01 mg/kg/day, as claimed by 
NRDC. (Ref. 11 at 133). The correct LOAEL is similar to the LOAEL from 
animal studies.
    4. Mutagenicity--a. NRDC's claim. NRDC claims that EPA cannot find 
the DDVP tolerances are safe because EPA has not ``reliably 
establish[ed] the bounds of risk posed by the mutagenic potential of 
DDVP.'' (Ref. 1 at 47). NRDC notes that EPA has found DDVP to be 
mutagenic in in vitro assays and asserts EPA has not taken this 
mutagenic risk into account in assessing the safety of DDVP.
    b. Amvac's Comment. Amvac claims that NRDC has focused on in vitro 
assays to the exclusion of the more important in vivo studies. These 
later studies, Amvac asserts ``provide[] support for the lack of in 
vivo carcinogenic activity seen in the DDVP animal bioassays.'' (Ref. 
14 at 31). According to Amvac, ``[p]harmacokinetic data have 
demonstrated that DDVP is quickly metabolized and this likely accounts 
for the difference in the in vitro and in vivo response in the 
mutagenicity testing.'' (Id.).
    c. EPA's response. NRDC's claim that EPA has not taken mutagenic 
risk into account is mistaken. EPA has fully examined the data on 
DDVP's potential for mutagenic effects and concluded that these data do 
not raise a safety concern.
    Mutagenicity data on DDVP shows the following: (1) DDVP does 
produce positive in vitro results in the absence of activation by rat 
derived liver enzymes; (2) these positive results generally disappear 
in the presence of activation by liver enzymes; (3) there is some 
evidence that DDVP is a weak mutagen in in vivo testing; and (4) an in 
vivo chromosome aberrations study requested to address the in vivo 
mutagenicity study was negative. (Refs. 11, 20 at 13, 35 and 36).
    Mutagenicity data are considered by EPA both as evidence bearing on 
a pesticide's carcinogenic potential and on whether the pesticide can 
result in heritable mutagenic effects. As described in Unit VII.A.1.c., 
EPA fully considered the mutagenicity data in its cancer evaluation. As 
to DDVP's potential to cause heritable mutagenic effects, EPA 
specifically requested that an in vivo chromosome aberrations study be 
performed in which germ cells as well as somatic cells were examined to 
address this question. This study was negative resolving any concern 
with heritable mutagenic effects. (Ref. 20 at 13). One agency reviewer 
suggested a further mutagenicity study at higher doses addressing 
heritable effects but EPA has not required such testing because 
existing testing already tests at the maximum tolerated dose. (Ref. 
37).
    5. Endocrine effects--a. NRDC's claim. NRDC asserts that EPA has 
failed to assess the endocrine disruption effects of DDVP. NRDC notes 
that the statute requires EPA to consider, in making safety 
determinations as to tolerances, whether a pesticide has an effect that 
mimics estrogen or has other endocrine effects, (see 21 U.S.C. 
346a(b)(2)(D)(viii)), and to establish an endocrine screening program, 
(see 21 U.S.C. 346a(p)), but that EPA has not collected any data under 
this program. NRDC claims that ``[i]n light of [EPA's] failure to carry 
out its mandatory statutory duty to investigate the potential of DDVP 
to cause endocrine disruption, EPA cannot conclude that . . . the 
[DDVP] tolerances are safe.'' (Ref. 1 at 49).
    b. Amvac's Comment. Amvac, in its comments, notes that EPA has 
already indicated that it will rely on several studies currently 
required for pesticides to assess endocrine effects and that EPA has 
these studies for DDVP. (Ref. 14 at 74-75).
    c. EPA's response. In a prior order adjudicating a petition to 
revoke tolerances, EPA has rejected the argument that data gathered 
under the Endocrine Disruptor Screening Program (``EDSP'') is a 
prerequisite to a safety determination under FFDCA section 408. (71 FR 
43906, 43919-43921 (August 2, 2006)). There, EPA noted that the 
proposed study to be used for chemicals that initial screening suggests 
may have the potential to interact with the endocrine system (the two 
generation reproduction study in rats) is a study that is currently 
required for approval of agricultural or other food use pesticides. 
(Id. at 43920). Additionally, EPA pointed out that several other 
toxicological studies required for pesticides provide information 
relevant to potential endocrine disruption.
    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 estrous cycling in females and 
sperm number, motility, and morphology in males. The study did identify 
an adverse effect on estrous 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 
estrous 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.
    Finally, based on a comprehensive evaluation of the testicular 
toxicity of dichlorvos in rats, a recent publication reported that 
there were no testicular effects, except for slightly decreased

[[Page 68677]]

sperm motility, at doses causing significant inhibition of 
cholinesterase. (Ref. 38). The NOAEL for dichlorvos with respect to 
reproductive organ weights, sperm counts, sperm morphology, plasma 
testosterone, and testes histopathology was 4 mg/kg, the highest dose 
tested.
    Given that EPA has (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, EPA believes it has adequate data to make a 
safety finding as to DDVP's potential endocrine-related effects.
    6. Neurotoxicity--a. NRDC's claim. NRDC notes that in the 2000 
preliminary risk assessment, EPA imposed a 3X uncertainty factor 
because there was no measurement for cholinesterase inhibition in an 
acute neurotoxicity rat study. NRDC contends that in light of the 
failure to measure cholinesterase inhibition, EPA should have required 
the study to be redone and that in the absence such data, EPA cannot 
make its FFDCA safety finding. (Ref. 1 at 47-48). NRDC also faults the 
Agency for failing to explain why, in these circumstances, a 3X 
uncertainty factor is safe.
    b. EPA's response. Subsequent to the 2000 preliminary risk 
assessment, EPA has received additional acute neurotoxicity data in the 
rat which measured cholinesterase inhibition and thus the deficiency in 
the prior acute neurotoxicity study has been cured. (Ref. 11 at 130). 
Accordingly, the Agency has removed the 3X uncertainty factor that had 
been retained due to the deficiency in the prior study.
    7. Translation of oral study to dermal endpoint--a. NRDC's claim. 
NRDC asserts that EPA cannot make a safety finding for DDVP because EPA 
relied on a rabbit oral study to derive a safe level of acute dermal 
exposure. (Ref. 1 at 48). According to NRDC, this approach is ``based 
on unwarranted and unsubstantiated assumption that the toxicology and 
pharmacokinetics of oral exposure are the same as for dermal 
exposure.'' (Id.) Moreover, NRDC argues that even if it were 
appropriate to use oral data in place of dermal data, the ``inherent'' 
uncertainty requires the imposition of a properly supported uncertainty 
factor. (Id.). Similarly, NRDC argues that using an oral dog study for 
an intermediate-term dermal toxicity scenario is legally inappropriate 
and scientifically unsupportable.
    b. Amvac's comments. Amvac states that ``[i]t is common practice in 
risk assessments . . . to extrapolate across exposure routes if the 
characteristics of the chemical being considered, and the available 
data, support such extrapolation.'' (Ref. 14 at 40). Amvac argues that 
extrapolation from the oral route to the dermal route is appropriate 
for DDVP because the data show that both DDVP's metabolism and types of 
toxicity it causes are consistent across all routes of exposure. (Id.). 
Additionally, Amvac asserts that the greater absorption of DDVP in oral 
studies than in dermal studies makes it more likely that oral studies 
will show DDVP-related effects than dermal studies.
    c. EPA's response. Initially, EPA would note that in the IRED EPA 
relied upon an oral rat and oral human study for assessing dermal 
risks. Presumably, however, NRDC would have similar objections to 
reliance on translation of these oral data to the dermal route.
    Use of oral studies to assess dermal risks is, and has been, a 
common practice at EPA for some time. (Ref. 39). Data specific to DDVP 
confirm that this is a reasonable approach for this pesticide. First, 
numerous toxicity studies have been performed with DDVP, involving both 
acute and chronic dosing and dosing by all routes of exposure. These 
studies consistently show that DDVP is an inhibitor of cholinesterase, 
if doses are high enough, regardless of the duration or route of 
exposure. Similar results are consistently found across the class of 
organophosphate pesticides. (See, e.g., Refs. 40 and 41). Second, oral 
metabolism studies indicate both that DDVP is well-absorbed from the 
gastro-intestinal tract and that there are no significant differences 
in excretion of DDVP doses given orally and intravenously. (Refs. 42 
and 43). Accordingly, an orally-administered dose is a reliable 
prediction of systemic dose. Thus, it is reasonable to use a RfD 
derived from an oral DDVP study to evaluate the safety of systemic 
exposures occurring as a result of dermal absorption of DDVP. Moreover, 
there are two reasons to believe that EPA's use of a dermal absorption 
factor of 11 percent for DDVP in translating the oral RfD into dermal 
RfD tends to overstate dermal absorption, exposure, and risk. (Ref. 
44). First, dermal absorption studies with volatile chemicals such as 
DDVP are likely to overstate the degree of absorption because such 
studies attempt to minimize losses of the chemical through evaporation. 
Outside of the laboratory, there are usually no such barriers to 
evaporation. Second, human skin is generally less permeable than the 
rat skin (largely due to species differences in epidermal anatomy, such 
as skin thickness, sebaceous secretions, and the density of hair 
follicles, (Ref. 45), and thus dermal absorption studies with the rat, 
such as the DDVP dermal absorption study, tend to overstate absorption 
in humans.
    For all of these reasons, EPA concludes that using oral DDVP 
studies in assessing risk from dermal DDVP exposures is a well-
supported scientific assessment technique that would not underestimate 
risks from dermal DDVP exposure. Consequently, the application of an 
additional safety factor to account for uncertainty of the route to 
route extrapolation is not necessary.
    8. Degradates--a. NRDC's claim. NRDC asserts that the Agency has an 
incomplete database regarding degradates of DDVP. (Ref. 1 at 9). 
Specifically, NRDC contends that degradates identified by the Agency 
were never searched for ``or even detectable in the various monitoring 
and metabolism studies relied upon by the Agency.'' (Id.). Further, 
NRDC states that ``[t]here is no indication whether these degradates 
were ever separately subjected to toxicological testing.'' (Id.). Based 
upon this assumption, NRDC contends that it is impossible for EPA to 
find that the DDVP tolerances are ``safe.''
    b. Amvac's comments. Amvac claims that NRDC has failed to consider 
whether the DDVP degradates are toxicologically significant. (Ref. 14 
at 68). According to Amvac, ``[i]t is clear just from the structures of 
some of these degradates that they are either not toxicologically 
significant, and/or, based on structure activity relationships and 
knowledge concerning mechanisms of toxicity, that these degradates have 
much lower toxicity than the parent compound.'' (Id.).
    c. EPA's response. NRDC's concern that EPA has not searched for 
DDVP's major metabolites in magnitude of the residue studies is 
misplaced because EPA has determined that these metabolites are rapidly 
degraded to harmless chemicals in the normal course of plant and 
mammalian metabolism. The residue of concern is DDVP and that is the 
chemical identified by DDVP's analytical method.
    EPA has a robust understanding of DDVP's metabolites and degradates 
derived from multiple metabolism studies in several different animal 
and

[[Page 68678]]

plant species. (Refs. 46, 47, 48, 49, 50 and 51). In animals, DDVP's 
primary metabolites are dichloroacetaldehyde or (minor pathway) des-
methyl DDVP. Des-methyl DDVP also breaks down into 
dichloroacetaldehyde. Dichloroacetaldehyde is rapidly dechlorinated and 
oxidized and either expelled from the body through respiration as 
carbon dioxide or through excretion in the urine and feces as urea or 
hippuric acid or converted into basic carbon compounds which are 
incorporated in amino acids (e.g., glycine, serine) and proteins. In 
metabolism studies using radioactive-labeled DDVP, little or no DDVP or 
its primary metabolites were found in animal tissues and milk.
    In plants, DDVP is hydrolyzed to dimethyl phosphate and 
dichloroacetaldehyde. Dimethyl phosphate is sequentially degraded to 
monomethyl phosphate and inorganic phosphates. Dichloroacetaldehyde is 
converted to 2,2-dichloroethanol which is conjugated and/or 
incorporated into naturally-occurring plant components after additional 
metabolism.
    9. Inerts--a. NRDC's claims. NRDC asserts that the ``apparent 
absence of data on the risks posed by the inert ingredients and 
impurities in all DDVP end-use products compels . . . the revocation of 
all DDVP tolerances.'' (Ref. 1 at 68).
    b. EPA's response. If an inert ingredient that is combined with 
DDVP in an end-use product poses a risk of concern, then there would be 
grounds for modifying or revoking the tolerance or tolerance exemption 
pertaining to the inert ingredient. It would not be grounds for 
revoking the DDVP tolerance, which is evaluated based on the safety of 
DDVP. All impurities in technical active ingredient DDVP, which would 
be included at lower levels in DDVP end use products, were tested as 
part of the technical active ingredient when the toxicology tests on 
the technical active ingredient DDVP were conducted.
    10. Other allegedly missing toxicity data--a. NRDC's claims. NRDC 
contends that the Agency cannot make its statutory determination of 
safety for DDVP dependent upon the submission of data. Specifically, 
NRDC asserts that in the absence of a dermal sensitization study and a 
developmental neurotoxicity test (DNT) study, EPA cannot make a safety 
finding for DDVP under the FFDCA.
    b. EPA's response. EPA has received and reviewed a DNT study for 
DDVP. (Ref. 11 at 127). Additionally, NRDC is incorrect in asserting 
that EPA does not have any dermal sensitization data for DDVP. On the 
contrary, the Agency has four dermal sensitization studies for DDVP. 
(Refs. 52, 53, 54 and 55). The DDVP dermal sensitization studies were 
conducted with formulations, containing varying levels of technical 
DDVP. All four of the studies were negative for sensitization in guinea 
pigs. Although none of the studies tested DDVP in isolation, sufficient 
information was obtained from the four studies to define the dermal 
sensitization toxicity of DDVP.

B. Dietary Exposure Issues

    1. Revised dietary exposure and risk assessment. NRDC's petition 
challenges numerous aspects of EPA's 2000 proposed dietary exposure and 
risk assessment of DDVP. This exposure and risk assessment was 
incorporated into the 2006 DDVP IRED without major changes. In 
responding to NRDC's petition, EPA has updated the DDVP dietary 
exposure and risk assessment. The main changes in the revised 
assessment include: (1) use of EPA's current dietary assessment 
program, DEEM-FCID, instead of DEEM; (2) incorporation of residue 
estimates for drinking water directly into the DEEM-FCID program; (3) 
updated monitoring data (principally from the USDA-Pesticide Data 
Program (``PDP'')) and percent crop treated data; and (4) incorporation 
of estimated exposure from use of naled as a wide area treatment for 
mosquitoes. A summary of the revised dietary risk assessment is 
presented in this unit and NRDC's specific comments are responded to 
individually below. (Ref. 56).
    The estimated risk levels, presented in Table 1, are largely 
unchanged from the 2006 IRED when both food and water are considered. 
Although this risk assessment is highly refined as to some commodities 
it still contains numerous conservatisms. More details concerning the 
revised risk assessment are provided in responding to NRDC's specific 
objections.

                          Table 1.--Dietary (Food and Water) Exposure and Risk for DDVP
----------------------------------------------------------------------------------------------------------------
                                      Acute Dietary (99.9 Percentile)                 Chronic Dietary
                                 -------------------------------------------------------------------------------
       Population Subgroup         Dietary Exposure                        Dietary Exposure
                                      (mg/kg/day)           % aPAD            (mg/kg/day)           % cPAD
----------------------------------------------------------------------------------------------------------------
General U.S. Population           0.001313            16                  0.000060            *COM041*12
----------------------------------------------------------------------------------------------------------------
All Infants (<  1 year old)        0.003735            47                  0.000116            23
----------------------------------------------------------------------------------------------------------------
Children 1-2 years old            0.001523            19                  0.000111            22
----------------------------------------------------------------------------------------------------------------
Children 3-5 years old            0.001312            16                  0.000103            21
----------------------------------------------------------------------------------------------------------------
Children 6-12 years old           0.000911            11                  0.000069            14
----------------------------------------------------------------------------------------------------------------
Youth 13-19 years old             0.000967            12                  0.000048            10
----------------------------------------------------------------------------------------------------------------
Adults 20-49 years old            0.001475            18                  0.000057            11
----------------------------------------------------------------------------------------------------------------
Adults 50+ years old              0.000929            12                  0.000051            10
----------------------------------------------------------------------------------------------------------------
Females 13-49 years old           0.001000            13                  0.000050            10
----------------------------------------------------------------------------------------------------------------

    2. Drinking water models--a. NRDC's claims. NRDC argues that the 
DDVP tolerances are unsafe because EPA has inadequate data on DDVP 
levels in drinking water. (Ref. 1 at 40). NRDC notes that EPA has 
limited groundwater monitoring data and no surface water monitoring 
data for DDVP, naled, and trichlorfon. In the absence of DDVP

[[Page 68679]]

water monitoring data, NRDC claims EPA cannot find the DDVP tolerances 
to be safe. Further, NRDC claims that the surface water exposure model 
used by EPA in the preliminary risk assessment (PRA), GENEEC, has not 
been properly validated, and that ``EPA has failed to demonstrate that 
the surrogate data [in the model] are properly matched to DDVP and that 
the model's assumptions and parameters are justified.'' (Id. at 54). 
NRDC makes similar claims regarding the matching of surrogate 
groundwater data to DDVP through the operation of the SCI-GROW ground 
water model. (Id. at 55). According to NRDC, ``if the SCI-GROW model 
employed surrogate data [on DDVP], it cannot be assumed to be reliable 
unless full disclosure of its construction and inputs is made and this 
information demonstrates its reliability.'' (Id.).
    In its comments on the DDVP IRED, NRDC raised similar issues. (Ref. 
13 at 9). Citing a number of alleged uncertainties pertaining to the 
SCI-GROW model, NRDC argues that because ``[n]one of these 
uncertainties is quantitatively bounded ... the Agency has not or 
cannot determine with reasonable certainty that the risks from 
groundwater contamination by DDVP will not harm people.'' (Id.). 
Additionally, NRDC claims the assessment for groundwater is incomplete, 
because EPA has not aggregated DDVP in groundwater resulting from uses 
of DDVP, naled, and trichlorfon. (Id.).
    Finally, in its petition, NRDC asserts that EPA's conclusion that 
DDVP will not be persistent in surface waters is mere speculation. 
(Ref. 1 at 44).
    b. Amvac's comments. Amvac disputes NRDC's criticism of EPA's 
drinking water models stating ``NRDC appears to not understand the 
underlying assumption and highly conservative nature of these models.'' 
(Ref. 14 at 63). Further, Amvac argues that, because of the highly 
conservative nature of the models, the targeted monitoring data NRDC 
calls for would show that DDVP exposure in drinking water is lower than 
projected. (Id. at 70-71). Amvac further notes that targeted monitoring 
data has limited applicability and would be unlikely ``to be 
representative of potential exposure on a wider geographical scale.'' 
(Id. at 71).
    c. EPA's response. NRDC's general claims regarding EPA's drinking 
water models are addressed for the most part in a prior EPA order 
denying NRDC objections to use of these models in making a safety 
finding for a pesticide tolerance. (69 FR 30042, 30058-30065 (May 24, 
2006). In that order, EPA explained in detail as to each of the models: 
(1) the basic principles on which the model is based; (2) the data 
underlying the models; (3) the numerous conservatisms built in to each 
of the models; (4) the extensive independent peer review used in the 
development of the models; and (5) the external and internal testing of 
the accuracy of the models. After this extensive analysis, EPA 
concluded the models ``are based on reliable data and have produced 
estimates that EPA can reliably conclude will not underestimate 
exposure to pesticides in drinking water.'' (Id. at 30065). Not only 
does this order provide a detailed description of the models and data 
underlying the models but it referenced the many SAP reviews and Agency 
policy documents that further explained the models. Additionally, it 
should be noted that detailed information concerning the models is 
available on EPA's website. EPA has recently updated this information 
to insure that the website provides not only the ability to run the 
models but also a description of the how the models work and the 
underlying codes included in the structure of the model. (Ref. 57)
    NRDC's more specific allegations are also without merit. First, EPA 
took the characteristics of DDVP, naled, and trichlorfon into account 
in modeling DDVP levels in drinking water. Specific information 
concerning these pesticides' mobility and persistence was combined with 
information pertaining to application amounts in use of PRZM-EXAMS to 
model surface water DDVP levels and SCI-GROW to model groundwater DDVP 
levels. In addition, information on soil properties, cropping 
characteristics, and weather appropriate to use of these pesticides was 
incorporated in the PRZM-EXAMS model run. (Ref. 58). Second, EPA has 
adequately addressed uncertainties in the PRZM-EXAMS model through peer 
review and validation. NRDC claims that EPA has not quantified the 
uncertainties in the SCI-GROW model and thus cannot rely on it; 
however, NRDC's listing of uncertainties (e.g., small drinking water 
reservoir, runoff prone soils) applies to considerations relative to 
the surface water model PRZM-EXAMS not SCI-GROW. These apparent 
criticisms of the PRZM-EXAMS model are without merit. As noted above, 
while EPA has not specifically quantified each individual uncertainty 
associated with the model, the overall model has been extensively peer-
reviewed and validated, and has proved very conservative in practice. 
Third, EPA's estimation of surface water DDVP levels is not flawed for 
failure to combine exposures from DDVP, naled, and trichlorfon. The 
highest estimated surface water DDVP levels are from the naled use on 
brassica and the trichlorfon use on turf ((33 parts per billion 
(``ppb'') and 60 ppb, respectively, for acute exposure and 1.83 ppb and 
1.56 ppb, respectively, for chronic exposure). These estimates are 
based on the conservative assumption that 87 percent of the area of the 
watershed is cropped to either brassica or turf and all of the brassica 
or turf is treated with naled or trichlorfon, respectively. The figure 
of 87 percent is based on the fact that ``87 percent cropped was the 
largest cropped area in any 8-digit hydrologic unit in the continental 
United States.'' (69 FR 30042, 30060 (May 26, 2004)). Thus, there is no 
reason to combine these estimates. A watershed may be 87 percent turf 
or 87 percent brassica but not both. Moreover, the available data 
indicate that both trichlorfon and naled are used relatively 
infrequently on turf and brassica, respectively; thus, the water level 
estimate is overstated to begin with. (Refs. 56 and 59). In theory, the 
DDVP use producing the highest estimated surface water levels (wide 
area treatment for mosquitoes) could overlap somewhat with these uses 
but not only is estimated water concentration from the DDVP use 
insignificant compared to the levels used to assess acute and chronic 
drinking water exposure (10X and 20X lower, respectively) but relevant 
survey data show no report of DDVP for this use. (Ref. 60).
    EPA has chosen to rely on modeling estimates of DDVP in drinking 
water because the drinking water modeling data it has were not 
necessarily collected in areas of DDVP, naled, or trichlorfon usage and 
there is inadequate data on drinking water from shallow, groundwater 
wells. Nonetheless, the sampling data give some indication of the 
conservativeness of the modeling estimates. USDA's Pesticide Data 
Program (``PDP'') collected finished drinking water samples from 
California and New York in 2001 (214 samples) and from California, 
Colorado, Kansas, New York, and Texas in 2002 and 2003 (371 and 699 
samples, respectively). In 2004, PDP sampled raw and finished water 
from 171 community water systems from Michigan, North Carolina, Ohio, 
Oregon, Pennsylvania, and Washington (234 samples). Although the 
samples were analyzed for DDVP, no detectable residues of DDVP were 
found in any sample. The limits of detection for these

[[Page 68680]]

monitoring data were between 0.4 and 22.5 parts per trillion (ppt). By 
comparison, the estimates from EPA's drinking water models that EPA is 
using in the DDVP risk assessment are 60 ppb for acute risk and 1.83 
ppb for chronic risk. (Ref. 11). In parts per trillion, these values 
would be 60,000 ppt and 1,830 ppt.
    As to NRDC's claims that EPA is simply speculating in stating that 
DDVP is unlikely to persist in surface water, NRDC is mistaken. The 
conclusion that DDVP will not be persistent in surface water is based 
on the physical and chemical properties of DDVP and the results of the 
suite of environmental fate and transport studies on the compound. As 
EPA noted in the DDVP IRED, ``dichlorvos should not be persistent in 
any surface waters due to its susceptibility to rapid hydrolysis and 
volatilization.'' (Ref. 11 at 152).
    2. Dietary exposure models--a. NRDC's claims. NRDC contends that 
the Dietary Exposure Model (DEEM) cannot be used to demonstrate the 
safety of the DDVP tolerances because ``[t]he model is secret in that 
the codes, internal structure and assumptions have not been made 
available to the public for scrutiny and comment.'' (Ref 1 at 44). 
Additionally, NRDC argues that the model cannot be relied upon because 
it has never been validated. (Id.).
    b. Amvac's comments. Amvac notes that EPA has used DEEM for many 
years and claims that the DEEM ``software and its use have received 
many peer reviews ....'' (Ref. 14 at 57). Further, Amvac asserts that 
``[t]his model and the other models that EPA uses to assess dietary 
risk (i.e., LifelineTM and CARES) have all been made available to the 
public and their computer codes are available for public review and 
comment.'' (Id. at 57-58).
    c. EPA's response. DEEM and its successor, DEEM-FCID, are not 
secret models. As explained in Unit III.B.3.b.i.(B)., these dietary 
assessment models use relatively simple formulas to combine consumption 
information with residue levels in food to estimate exposure and risk. 
In 2000, the company that developed DEEM made a detailed explanation of 
the model public so that the model could be reviewed by the FIFRA SAP. 
(Ref. 7). That explanatory paper documented the data included in DEEM 
and the algorithms DEEM uses to manipulate that data to estimate 
exposure and risk. In addition to the algorithms, the paper contained a 
full delineation of underlying computer segment codes that comprise the 
DEEM program. In response to the SAP's concern that the DEEM paper did 
not make public the ``recipes'' used to translate the CSFII consumption 
data back to the precursor agricultural commodities (e.g. translating 
pizza into tomatoes, wheat, cheese, etc.), EPA contracted to have a new 
set of translations produced that would not be subject to proprietary 
restrictions. Those new translations have been completed and 
incorporated into DEEM-FCID, DEEM's successor, and are fully available 
to the public. (Ref.61).
    Thus, NRDC is wrong in its assertion that DEEM is a ``secret'' 
model. The fundamental logic of this model is available to the public 
(including both the algorithms and computer codes) and data on food 
recipes is available on DEEM's successor DEEM-FCID, the model used to 
run EPA's latest dietary risk assessment for DDVP. NRDC's concerns 
regarding validation are misplaced as well in that DEEM and DEEM-FCID 
have been reviewed by the SAP and produce similar results to other 
publicly-available dietary exposure models. (See, e.g., 70 FR 77363 
(December 30, 2005); 70 FR 40202 (July 13, 2005)). Accordingly, NRDC's 
request that the DDVP tolerances be revoked because of reliance on DEEM 
is denied.
    3. Percent crop treated data--a. NRDC's claims. NRDC asserts that 
EPA has used percent crop treated data in calculating aggregate 
exposure for DDVP without making the findings required by section 
408(b)(2)(F). (Ref. 1 at 39). That section imposes certain conditions 
upon EPA's use of percent crop treated data when assessing chronic 
dietary risk. Among the specified conditions are the requirements that 
EPA find (1) ``the data are reliable and provide a valid basis to show 
what percentage of the food derived from such crop is likely to contain 
such pesticide chemical residue;'' (2) ``the exposure estimate does not 
understate exposure for any significant subpopulation group;'' and (3) 
``if data are available on pesticide use and consumption of food in a 
particular area, the population in such area is not dietarily exposed 
to residues above those estimated by [EPA].'' (21 U.S.C. 
346a(b)(2)(F)). Finally, if EPA does rely on percent crop treated data 
EPA must provide for the periodic reevaluation of the estimate of 
anticipated dietary exposure. (Id.). NRDC claims that EPA, having 
failed to make the foregoing findings cannot rely on percent crop 
treated in making a safety finding for the DDVP tolerances.
    b. Amvac's comments. Amvac asserts that adequate data are available 
on percent crop treated referring to an EPA memorandum (Hummel, 2000). 
(Ref. 14 at 47-48). According to Amvac, ``[t]hat memorandum describes 
the source of the data and states that the upper end of the range was 
assumed for acute dietary exposure analysis and that the typical or 
average was used for the chronic dietary exposure analysis, as is 
typical EPA practice.'' (Id.).
    c. EPA's response. EPA conducted a comprehensive evaluation of the 
usage of DDVP, naled, and trichlorfon for the DDVP IRED. That 
evaluation was described in the memorandum cited by Amvac and the 
memorandum was included in the docket and on EPA's website page for 
DDVP. In response to NRDC's petition EPA has updated its analysis of 
percent crop treated information. Specifically, in its revised analysis 
EPA used percent crop treated data in estimating exposure from use of: 
(1) DDVP on livestock; (2) trichlorfon on turf; (3) DDVP and naled as a 
mosquito (wide area) treatment; and (4) naled on agricultural crops.
    Based on the findings below, EPA concludes that its consideration 
of usage or percent crop treated data to estimate percent crop treated 
conforms to the requirements in section 408(b)(2)(F).
    i. Reliable data. The primary source of data for estimating the 
percent of a commodity treated with a pesticide is the United States 
Department of Agriculture's National Agricultural Statistics Service 
(``NASS''). NASS collects data on a wide variety of agricultural topics 
including pesticide usage. NASS uses the Agricultural Resources 
Management Survey (``ARMS'') as well as other surveys to collect data 
on pesticide usage and other agricultural topics. These surveys are 
designed to produce statistically representative estimates of pesticide 
usage on targeted crops in the surveyed States using a 
probabilistically-based sampling procedure. (See http://www.usda.gov/nass/nassinfo/surveyprograms/index.htm
 and https://arms.ers.usda.gov/

GlobalDocumentation.htm ).
    ARMS is a multi-phase, multi-frame, stratified, probability-
weighted sampling design. There are three phases to the annual survey: 
a screening phase to update data and help target sampling for phases 
two and three; a second phase that collects information on agricultural 
practices and chemical usage; and a third phase that collects costs and 
financial information. ARMS consists of two ``frames'' collecting farms 
and ranches. The main frame is the ``list frame'' that is intended to 
contain the names and addresses of all farms and ranches in the 
continental United States along with the acreage of the farms/ranches 
and the crops grown or livestock raised. The list frame is compiled 
based on the Census of Agriculture as well as numerous other

[[Page 68681]]

surveys and governmental and non-governmental sources. The list frame 
is back-stopped by the ``area frame'' which is constructed from 
satellite images of the continental United States broken down into 
segments based upon degree and type of cultivation. Both frames are 
divided into different strata such as crop type. Due to the complexity 
of the sample design, ARMS uses a weighting system to adjust data 
gathered in reports from sampling of the frames.
    Data is gathered by a statistically-designed sampling of the list 
and area frames. The sampling is done on a state basis with the focus 
for any particular crop on the major production states. Generally, 
samples are conducted in states representing 90 percent or better of 
the production acreage. Reports are usually prepared based on face-to-
face interviews with the identified growers. Surveys for field crops 
are conducted annually with the crops varying each year. (See http://usda.mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID=1560
) 

Surveys for fruits and surveys for vegetables are conducted in 
alternating years with fruits surveyed in odd years and vegetables in 
even years. (See http://usda.mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID=1567 and http://

usda.mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID=1572). 
There is some variation in the crops sampled in each survey. NASS data 
on pesticide use on livestock are published periodically by USDA (1999 
(summary of 1997 livestock and general farm survey), 2000 (summary of 
1999 swine and swine facilities survey), 2001 (summary of 2000 sheep 
and sheep facilities survey), 2002 (summary of 2001 dairy cattle and 
dairy cattle facilities survey), and 2006 (summary of 2005 swine and 
swine facilities survey), see http://usda.mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID=1569
).

    To estimate percent crop treated for pre-harvest pesticide uses, 
EPA has created a database containing NASS data from the years 1999-
2005. Also included in this database is data from a private service, 
Doane Marketing Research, Inc., now known as dmrkynetec. This database 
was used for making the majority of the percent crop treated estimates 
for the DDVP assessment, namely, the estimates pertaining to the use of 
naled as an agricultural pesticide. The 2007 estimates show that naled 
is generally used on a very small percentage of crop acreage. This is 
consistent with the estimates made for the 2000 dietary risk 
assessment. Most estimates from the two assessments were similar with a 
few crops showing declining use over time and one crop (strawberries) 
showing increased use. (Refs. 62 at 27-30; 56 at 29).
    Dmrkynetec is a market research company. Originally, it focused on 
providing market and tracking data to agribusiness but has expanded its 
services to a wide range of industry sectors. In the agriculture area, 
dmrkynetec gathers information by survey research on, among other 
things, crop acres grown, pesticide active ingredients used, total 
acres treated with pesticides, pesticide application rates and timing, 
number of pesticide applications, and pesticide prices. For over 30 
years, EPA has purchased dmrkynetec's proprietary database, which 
provides pesticide usage information for over 50 crops. As part of 
EPA's contract with dmrkynetec, EPA requires both a quality management 
plan and a quality assurance project plan to insure that dmrkynetec's 
survey practices and data compilation are well-designed and reliably 
executed. Data from dmrkynetec is relied upon not only by EPA but by 
other Federal agencies and private industry. (Ref.63).
    For one commodity, poultry, for which sufficient NASS and 
dmrkynetec data were not available, EPA followed a different approach 
in estimating percent crop treated. EPA interviewed agricultural 
extension agents and professors in agricultural colleges in major 
poultry-producing states and reviewed crop profiles compiled by USDA 
and other literature from the extension services to obtain rough 
estimates of usage. Because this information was not based on 
statistically-designed surveys, EPA used it in a very conservative 
manner to estimate worst case percent crop treated estimates. 
Information gathered on broilers indicated that, DDVP was rarely, if 
ever used in broiler production in most of the major producing states. 
The one exception is Georgia, the largest broiler producing state, 
where approximately 1/3 of the broiler flock is treated with a product 
containing DDVP. As to layers (egg producers), DDVP is also not used in 
significant amounts in most of the major producing states. However, an 
expert in California (fourth in egg production among states) indicated 
that a product containing DDVP was used on approximately 75 percent of 
the state's layers. As a very conservative estimate, EPA assumed that 
75 percent of the broilers and layers nationwide are treated with DDVP. 
(Ref. 64).
    Estimates of the percent of crops that receive incidental treatment 
with naled or DDVP as a result of these pesticides' usage as a wide 
area treatment for the control of mosquitoes was based on a combination 
of data from NASS and Kline and Company, Inc., a private market 
research firm. Data from NASS' Census of Agriculture was used to 
determine the total farm acreage in the United States. Data from Kline 
provided information on the poundage of naled and dichlorvos used for 
mosquito treatment. This information was combined in a very 
conservative fashion with the data on total crop acreage in the United 
States. EPA calculated what percentage of the total crop acreage could 
have been treated with the naled and DDVP used for mosquito control and 
assumed that every crop in the United States was treated to that extent 
(3 percent). Although some treatment of agricultural crops will occur 
from the mosquito usage, a significant part, if not most, of the 
treatment area will be in wetlands, forest, urban and suburban land, 
and other non-crop areas. Even where agriculture land is treated, such 
treatment may occur when no crop is present or, even if a crop is 
present, at such a time that all residues would be expected to degrade 
prior to harvest. Estimates of percent crop treated for turf uses was 
also based on data from Kline. This information was not used to 
quantitatively estimate exposure but simply to qualitatively 
characterize the conservativeness of the drinking water concentration 
estimates from turf usage produced by EPA's drinking water model.
    NASS's Census of Agriculture is as the name would suggest a 
complete count of United States farms and ranches. Additionally, the 
Census collects information on land use and ownership, agricultural 
practices, and farm income and costs. The Census is conducted every 5 
years by law and involves individual contact with all farmers and 
ranchers in the United States. (See http://www.agcensus.usda.gov ).

    Kline, like dmrkynetec, conducts market research through surveys on 
a wide range of products. EPA has been purchasing data on non-
agricultural pesticide usage from Kline for over 20 years. As with the 
dmrkynetec contract, EPA has required both a quality management plan 
and a quality assurance project plan to insure that Kline's survey 
practices and data compilation are well-designed and reliably executed. 
Data from Kline is relied upon not only by EPA but by other federal 
agencies and private industry. (Ref. 63).

[[Page 68682]]

    EPA concludes these data sources provided reliable data for the 
percent crop treated estimates that were used by EPA.
    ii. Significant subpopulation group. EPA considered DDVP exposure 
to the general population as well as 32 subpopulation groups based on 
regional location, ethnicity, and age. Reliance on the estimates of 
percent crop treated discussed above will not underestimate exposure 
for any of these population subgroups.
    iii. Data on pesticide use and consumption. EPA takes information 
on regional consumption patterns into account in estimating exposure to 
significant subpopulation groups. EPA's information on percent crop 
treated is primarily national in scope and does not indicate that 
regional groups have greater exposures to DDVP than estimated by EPA.
    iv. Periodic evaluation. The statute provides that EPA shall 
periodically reevaluate the estimate of anticipated dietary exposure. 
This is a prospective requirement. Although it may do so sooner, EPA 
expects that the exposure estimates will be reevaluated periodically 
through the registration review process. (21 U.S.C. 346a(b)(2)(F); Ref. 
65).
    To evaluate the sensitivity of dietary risk assessment to EPA's 
percent crop treated findings, EPA conducted an alternate dietary 
assessment assuming 100 percent crop treated for all commodities. (Ref. 
56). As Table 2 shows, even using this very conservative assumption, 
dietary exposure is well below the RfD/PAD for DDVP.

                     Table 2.--Dietary (Food and Water) Exposure and Risk for DDVP Incorporating 100 Percent CT for All Commodities
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                               Acute Dietary(99.9 Percentile)                            Chronic Dietary
                                                     ---------------------------------------------------------------------------------------------------
                 Population Subgroup                  Dietary Exposure (mg/kg/                          Dietary Exposure (mg/kg/
                                                                day)                    % aPAD                    day)                    % cPAD
--------------------------------------------------------------------------------------------------------------------------------------------------------
General U.S. Population                                              0.002274                       28                 0.000112                       22
--------------------------------------------------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                                            0.004152                       52                 0.000154                       31
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 1-2 years old                                               0.004663                       58                 0.000252                       50
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 3-5 years old                                               0.003533                       44                 0.000214  .......................
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 6-12 years old                                              0.002677                       33                 0.000138                       28
--------------------------------------------------------------------------------------------------------------------------------------------------------
Youth 13-19 years old                                                0.001660                       21                 0.000092                       18
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 20-49 years old                                               0.001850                       23                 0.000102                       20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 50+ years old                                                 0.001437                       18                 0.000088                       18
--------------------------------------------------------------------------------------------------------------------------------------------------------
Females 13-49 years old                                              0.001603                       20                 0.000097                       19
--------------------------------------------------------------------------------------------------------------------------------------------------------

    4. Anticipated residues-- a. NRDC's claims. NRDC asserts that 
because EPA relied upon anticipated residue data, EPA must issue a data 
call-in to demonstrate that actual residues are not higher than the 
anticipated residues relied upon by the Agency. (21 U.S.C. 
346a(b)(2)(E)(ii)).
    b. EPA's response. This is a prospective requirement. To the extent 
that NRDC is claiming that EPA must revoke all DDVP tolerances because 
the FFDCA provides that EPA must require the registrant to submit data 
in the next 5 years pursuant to section 408(f), that claim is rejected.
    5. Trichlorfon and naled--a. NRDC's claims. Based solely upon EPA's 
statement in the prelimanry risk assessment that ``[n]on-detectable 
Dichlorvos residues in livestock commodities are expected as a result 
of Trichlorfon use[,]'' NRDC speculates that the method for detecting 
DDVP in beef may not be sensitive enough to detect toxicologically 
significant residues. (Ref. 1 at 40). Based on this speculation, NRDC 
claims that the DDVP tolerances do not comply with the requirement in 
section 408(b)(3) that ``a tolerance ... shall not be established at 
... a level lower than the limit of detection of the method for 
detecting and measuring the pesticide chemical residue ... .'' (21 
U.S.C. 346a(b)(3)(B)). Further, NRDC claims that EPA has not explained 
its conclusion that residues from trichlorfon use are estimated not to 
increase residues from the use of DDVP. (Ref. 1 at 51). In addition, 
NRDC contends that the Agency's analysis of DDVP residues from the use 
of naled (which also degrades into DDVP) for mosquito control is 
inadequate.
    b. EPA's response-- i. Trichlorfon. Trichlorfon degrades in plants 
and livestock and one of the products (metabolites) that forms is 
dichlorvos. Trichlorfon livestock feeding studies did not detect 
residues of dichlorvos using a level of detection (``LOD'') of 0.05 
ppm. The trichlorfon RED concluded that dichlorvos was not a 
significant residue in the cattle based on the feeding study and a 
metabolism study. The metabolism study found DDVP in subcutaneous fat 
at 4 percent of the total radioactive residue (TRR), and less than 1 
percent of the TRR in loin muscle (0.006 ppm). (Ref. 66). Subcutaneous 
fat is not used for human consumption, and often has residues higher 
than that in fat more distal from the site of application. Thus, it is 
highly unlikely that livestock will contain residues of dichlorvos from 
the use of trichlorfon. In any event, the residue monitoring data on 
DDVP includes DDVP as a degradate of trichlorfon and thus any DDVP in 
beef from use of trichlorfon would be captured by the monitoring data.
    The Agency has substantial data showing that residues of dichlorvos 
as a result of trichlorfon use will be non-detectable in beef. USDA-
FSIS has sampled for trichlorfon and dichlorvos in the past. Although 
there is no U.S. registration for trichlorfon on cattle, there are 
tolerances so that foreign cattle can be treated and imported to the 
United States. From 1993 through 1997, FSIS monitored over 12,000 
samples of beef. (Ref. 67). No residues of dichlorvos

[[Page 68683]]

or trichlorfon were detected at a LOD of 0.2 ppm. However, detectable 
residues of other organophosphates were found.
    In addition, monitoring data from PDP were available for milk at 
the time the last anticipated residues were determined for the 2000 
IRED, and were used in the dietary exposure assessment for the IRED. 
One detectable residue was reported at 0.003 ppm out of 1,881 samples, 
with an LOD of 0.001 - 0.002 ppm (avg. 0.0014 ppm). (Ref. 62 at 12). 
Since that time, PDP collected over 300 samples of beef fat, liver, and 
muscle from 2001 to 2002 and found no detectable dichlorvos at a LOD of 
1.0 ppb; over 300 samples of pork in 2005 and found no detectable 
dichlorvos residues at an LOD of 0.9 ppb in fat; and LOD of 0.45 ppb in 
pork muscle; and over 600 samples of poultry commodities in 2000-2001 
with no detectable residues of dichlorvos at an LOD of 6.3 ppb. PDP 
also analyzed over 100 samples of heavy cream, and found no detectable 
residues of dichlorvos at a LOD of 1-2 ppb. Finally, no detects of DDVP 
were found 1,485 samples of milk analyzed in 2004-2005, at an LOD of 
0.06 ppb. (Refs. 56 at 13; and 68).
    NRDC is mistaken to claim that the detection method for DDVP in 
meat is not adequately sensitive. Generally, the Agency accounts for 
non-detectable residues by using [frac12] the LOD or LOQ in its 
calculations. (Ref. 69). If this calculation shows a potential risk 
problem, then the limits of detection must be lowered. In the case of 
dichlorvos, no risks of concern were identified for livestock 
commodities when they were assessed at [frac12] the LOD. In fact, total 
dietary risk from DDVP in food is just a small fraction of the RfD. 
Thus, the LODs are low enough to be below the level of risk concern and 
to ensure detection of toxicologically significant metabolites.
    ii. Naled. DDVP exposure from use of naled to control mosquitoes 
through wide area treatment is likely to be very low to non-existent 
for two reasons: (1) The treatment rate is very low--0.25 lb ai naled/
Acre, compared to the usual application rate for field crops of 1.8 lb 
ai naled/Acre; (2) residues from treatment degrade rapidly; and (3) the 
usage rate indicates few crops will be impacted by the mosquito use. 
Residue data from field trials showed most samples to be 0.03 ppm or 
less. One DDVP residue from the wide area treatment with naled was as 
high as 0.27 ppm, with the duplicate of this sample having a residue of 
0.08 ppm (average residue 0.18 ppm DDVP). (Ref. 70). Additional data 
show that residues of DDVP are formed 1-3 days after field treatment 
with naled, and decline to non-detectable within 7 days of treatment 
with naled. (Ref. 71). Further, PDP data showed no detectable levels of 
DDVP in crops not registered to be treated with naled out of roughly 
10,000 samples. (Ref. 56 at 19-20).
    Despite these data suggesting there will be little to no exposure 
in the diet from use of naled to control mosquitoes, EPA took a very 
conservative approach to estimating exposure from the naled mosquito 
use in its revised risk assessment. (Ref. 56). First, EPA examined 
usage data to determine a rough estimate of the acreage treated with 
naled for mosquito control. (Ref. 72). EPA assumed that all acres 
treated were cropped farmland and not wetlands, woodlands, urban or 
suburban areas, or other non-cropped areas. This acreage was then 
expressed as a percentage of the overall farm acreage in the United 
States. That percentage (3 percent) was the value used in estimating 
the percent crop treated for all crops grown in the United States. If 
DDVP or naled is not registered for use on a crop, EPA assumed that 
three percent of that crop was treated. If DDVP or naled are registered 
on a crop and EPA has data on the percent of that crop treated as an 
agricultural use with DDVP or naled, EPA summed the percentages from 
the agricultural use and the mosquito use in estimating percent crop 
treated. Finally, if DDVP or naled are registered on a crop and EPA 
does not have data on the percent of that crop treated as an 
agricultural use with DDVP or naled, EPA assumed 100 percent of the 
crop was treated with DDVP or naled. In the latter circumstance, EPA 
considered but rejected somehow incorporating the mosquito use as an 
overlapping use because, for among other reasons, exposure from crops 
was based not on data from field trials but from monitoring data.
    6. Translation of reside levels--a. NRDC's claims. NRDC contends 
that EPA cannot make the safety finding for DDVP because EPA has 
translated data from grain dust to soybean aspirated grain fractions 
and data from cattle to swine based on speculation and not validated 
data. Indeed, NRDC argues that every translation of data from one plant 
or species to another is a major data gap that cannot be addressed 
through worst case or default assumptions because plant or animal 
metabolism can produce metabolites that are more toxic than the parent 
compound.
    b. EPA's response. EPA's translation of other residue data to 
soybean aspirated grain fractions is reasonable. EPA translated 
magnitude of the residue data from wheat and corn aspirated grain 
fractions to soybean aspirated grain fraction. Another name for 
``aspirated grain fractions'' is ``grain dust.'' This is the dust that 
is removed from the grain by the rubbing of the grains together during 
storage. Residues in grain dust are generally surface residues and thus 
grain crops that have otherwise similar residues tend to have similar 
residue levels in grain dust. This is especially the case for DDVP 
given that it is applied in equal amounts to all grains post-harvest. 
Post-harvest application generally results in surface residues, and 
there would be no reason to expect different levels of residues across 
grains. For similar reasons, metabolism of the pesticide in the crop, 
which can play a role in residue levels, is unlikely to be a factor 
with DDVP grain dust residues because metabolism occurs primarily when 
a plant incorporates a pesticide through uptake and not when the 
pesticide is applied to the crop surface post-harvest. Thus, EPA's 
analysis is not based upon mere speculation, but rather a reasoned 
analysis of the similarity between commodities and how DDVP is used.
    EPA's treatment of potential residue levels in swine is also 
reasonable. EPA requires radio-labeled metabolism studies in a few 
plant and animal commodities to identify all potential metabolites. 
(Ref. 73). Then magnitude of the residue studies are generally required 
for each treated plant and animal commodity for the purpose of 
selecting tolerance values and, in the absence of monitoring data, 
assessing risk.
    EPA has all required animal metabolism studies for DDVP. EPA has 
required an additional study on the magnitude of DDVP residues in 
swine. These data are needed to verify that a proper tolerance value 
has been identified for pork commodities. In the absence of those data, 
EPA has relied on data on cattle and poultry products because it is 
likely that the residues will be similar to those in cattle and poultry 
commodities. These additional magnitude of the residue data are not 
needed for risk assessment because EPA has monitoring data on swine 
commodities. These data show no detectable residues.
    7. Food monitoring data--a. NRDC's claims. NRDC asserts that the 
FDA and USDA monitoring programs are inadequate because the number of 
samples examined in these programs is too small to be representative of 
the total quantity of food potentially having DDVP residues. (Ref. 1 at 
49, 61-62). In addition, NRDC claims that the monitoring data are old 
and, therefore,

[[Page 68684]]

do not represent current use patterns. NRDC also asserts that the 
consumption data are insufficient because they have a limited number of 
individuals in the age group of infants less than one year old. NRDC 
further notes that samples collected from the FDA Total Diet Study were 
collected in supermarkets in only four cities per year and residues in 
other locations may be different and very little monitoring data are 
available for fumigated commodities, requiring extensive translation 
from one fumigated commodity to another. Moreover, NRDC raises the 
concern that some of the FDA data were generated with an analytical 
methodology that is not capable of detecting ``early eluters'' such as 
DDVP and EPA has not taken this fact into account. Finally, NRDC 
contends that residues potentially present at roadside produce stands 
or farmer's markets are not represented and, additionally, that EPA 
failed to consider such consumers major identifiable subgroup of 
consumers. NRDC therefore concludes that EPA does not have reliable 
food monitoring data and argues that EPA should use the default 
assumption of 100 percent crop treated for all foods which may be 
treated with DDVP as well as the default assumption of tolerance level 
DDVP residues in all treated commodities.
    In a related comment on the IRED, NRDC takes issue with EPA's 
decision not to sum potential residues resulting from multiple 
treatments of a food with DDVP at different stages of the food 
production process. (Ref. 13 at 8). NRDC claims EPA's conclusion that 
sufficient time would pass between such treatments that only the last 
treatment needs to be considered in estimating exposure is arbitrary 
and capricious.
    b. EPA's response. In general, EPA disagrees that the monitoring 
data are unreliable. To the contrary, EPA believes that the monitoring 
data provide for an appropriately conservative risk assessment.
    i. Adequacy of data - Age and number of samples and sample 
location. Contrary to NRDC's characterization, FDA and USDA each 
analyze thousands of samples per year. FDA analyzed several hundred 
samples per year for DDVP, but now analyzes less than 100. USDA 
analyzes most of their samples for DDVP, generally 350 to 700 samples 
per commodity per year, although sometimes only about 175 samples per 
commodity per year. FDA targets their monitoring toward commodities 
which have historically had residue problems. USDA-PDP uses a more 
random sampling plan, which is statistically designed to be 
representative of the U. S. food supply.
    In response to NRDC's concerns regarding the age of the monitoring 
samples, EPA has updated its dietary risk assessment based almost 
exclusively on USDA PDP data from the years 2000 to 2005. In the 
updated assessment, FDA monitoring data was used for only one 
commodity, berries (not including strawberries). The updated assessment 
confirms what the earlier assessment found: DDVP residues are rarely 
found in food commodities. Not including strawberries, PDP data showed 
only 20 samples with detectable residues of DDVP out of more than 
43,000 samples from 34 commodities which could potentially bear DDVP 
residues. Even focusing on foods covered by registered agricultural 
uses for DDVP or naled, there were only 20 samples with DDVP residues 
out of approximately 33,000 samples (not including strawberries). In 
the PDP data, strawberries were the only commodity with more than a 
marginal number of detections - with 104 samples showing DDVP out of 
1,986 samples. (Ref. 56 at 19-20).
    ii. Infant consumption. NRDC objects to EPA's reliance on an 
alleged lack of infant consumption data. In response, EPA notes that 
there is no more comprehensive a consumption survey in the United 
States than the CSFII surveys. Moreover, the revised dietary assessment 
relies upon more recent and updated CSFII data. Specifically, the FQPA 
required additional sampling of infant and children for information on 
their consumption has been completed. The results of the additional 
sampling were incorporated into DEEM and DEEM-FCID. These surveys are 
available to the public. (Ref. 6).
    iii. Fumigant monitoring data. EPA believes it has adequate data on 
the fumigant use of DDVP. EPA has data from residue studies conducted 
in warehouses with packaged and bagged commodities for the following 
foods: flour, cocoa beans, coffee, dry beans, walnuts, and soybeans. 
(Ref. 74). These studies were conducted by fumigating pallets 
containing these commodities at a maximum rate and then sampling both 
the outside layer and interior of the foods on the pallet. These data 
were translated to other packaged and bagged commodities based on 
starch and moisture content. Although translating these data to other 
commodities creates some uncertainty as to the residue estimate, this 
uncertainty is more than offset by other factors. First, the studies 
used maximum treatment rates and sampled the commodities 6 hours after 
treatment. Not only does this approach overstate residues that would 
occur from lower treatment rates but it does not take into account the 
rapid disappearance of DDVP that occurs due to its volatile nature. 
Second, EPA assumed 100 percent of bagged and packaged commodities were 
treated.
    iv. Early eluter. Because DDVP is an early eluter (i.e., DDVP will 
avoid detection unless samples are analyzed under low temperature 
chromatographic conditions), fewer samples are analyzed by FDA for DDVP 
than are typically analyzed by the Luke multiresidue method. In its 
prior dietary DDVP assessment EPA relied heavily on FDA monitoring but 
only used monitoring that used early eluter conditions which are known 
to detect DDVP. This issue has limited relevance given EPA's revised 
dietary risk assessment which relies almost entirely on PDP monitoring 
data which uses analytical methods which are known to detect DDVP.
    v. Farmers' markets and roadside produce stands. In an order 
responding to NRDC objections to tolerances for different pesticides, 
EPA has addressed NRDC's claims regarding pesticide exposure to persons 
who purchase food at roadside stands or farmers' markets. (70 FR 
46733). As EPA explained there, whether EPA relies on data from crop 
field trials or monitoring data in estimating pesticide exposure, given 
the sampling methods in field trials and food monitoring, residue 
levels identified from these sources are unlikely to understate residue 
levels at farm stands.
    EPA also rejects NRDC's challenge to EPA's decision not to sum 
residues from treatments of a commodity at different stages of the 
production process. Multiple treatments are a possibility for 
commodities such as grains which may be treated as a bulk commodity and 
later as a bagged and packaged commodity. EPA has estimated DDVP 
exposure based on the treatment of bagged and packaged commodities. 
EPA's decision was based on a number of inter-related considerations. 
First, there are data showing that DDVP is a volatile compound that 
rapidly degrades. Second, general monitoring data consistently show 
very low to non-existent residues in food with the exception of one 
commodity (strawberries) that are marketed very promptly. Third, EPA 
has assumed that 100 percent of all bagged and packaged foods are 
treated with DDVP and EPA's estimate of residue values in these 
commodities is based on a conservative value from sampling of bagged 
and packaged commodities 6 hours after treatment. Finally, the latest 
data from FDA's Total Diet Study, a study measuring pesticide residues 
and other

[[Page 68685]]

contaminants in food as consumed, has shown zero detections of DDVP in 
the time period from the survey conducted in 1991 up until the latest 
survey in 2003. (Ref. 75). The Total Diet Study examines 280 foods, 
including many bagged and packaged foods, that are collected from 
different regions in the United States. DDVP is one of many pesticides 
analyzed for in the study.
    8. Cooking factors--a. NRDC's claims. NRDC takes issue with the 
Agency's practice of using cooking factors to reduce estimates of 
residues for particular commodities as well as the Agency's practice of 
translating these factors to other commodities based upon similarity of 
cooking time and temperature. In particular, NRDC asserts that in the 
absence of empirical data demonstrating that each commodity will be 
affected identically by cooking, EPA cannot use cooking factors in its 
assessment of DDVP residues. In addition, NRDC contends that ``EPA 
apparently failed to take into account vastly different cooking 
practices for different commodities, including consumption of some 
commodities raw.'' (Ref. 1 at 50). As such, NRDC asserts that EPA 
should not assume cooking will result in any reduction in observed 
residue levels.
    b. EPA's response. EPA's use of cooking factors is reasonable. 
Amvac submitted a cooking study which examined residue decline due to 
cooking in the following commodities: cocoa beans, dry pinto beans, 
tomato juice, coffee beans, hamburger meat, eggs, and raw whole milk. 
(Ref. 76 at 34-37). The study showed that DDVP residue reduction was 
time and temperature dependent with dramatic reductions occurring when 
items were cooked at high temperatures for more than a few minutes. For 
example, eggs cooked for 3 minutes at greater than 100 degrees C 
resulted in a residue decline of 38 percent, hamburger cooked at a 
similar temperature for six minutes showed a 70 percent decline in DDVP 
residues, and cocoa beans cooked for 10 minutes at 135 degrees C 
resulted in a residue decline of 99.7 percent. Residue decline factors 
(i.e., cooking factors) were translated from tested items only to 
similar commodities which are cooked in a similar manner. For example, 
data on dry pinto beans was translated to other dried beans and peas 
and to boiled peanuts; data on hamburger was translated to other meats; 
and data on tomato juice was translated to celery juice. EPA believes 
these cooking times and temperatures are reasonable, conservative 
estimates. Although certain of these commodities may occasionally be 
cooked for shorter times or at lower temperatures, EPA expects those 
instances to be infrequent. Moreover, given the conservative 
assumptions on cooking times any variations are very unlikely to be 
``vastly different.'' As to consumption of some of these foods 
uncooked, NRDC's concern about use of cooking factors is unwarranted 
because EPA's consumption database differentiates between amounts of 
foods consumed cooked and uncooked and only applies cooking factors as 
to the former. Further, EPA concludes that its choice of translation 
commodities is also reasonable given the similarity between the cooking 
methods for the tested commodity and the translated commodity and the 
strong relationship shown in the data between cooking time and 
temperature and residue decline.
    In any event, EPA disagrees that it cannot rely on cooking data 
unless it has data on all varieties of cooking practices within the 
United States and its cooking data take that full range of cooking 
practices into account. Implicit in this argument, is the view that EPA 
must adopt a cooking factor that reflects the shortest possible cooking 
time, no matter how infrequently such practice is used. Section 408, 
however, does not take such an extreme approach to assessing exposure. 
Rather, section 408, directs EPA to focus on major, identifiable 
subgroups of consumers not worst case scenarios or maximally-exposed 
individuals. EPA believes that use of reasonable, conservative exposure 
assumptions are consistent with this statutory mandate.
    Additionally, it is important for EPA to adapt the assumptions 
underlying any exposure assessment to the complexity of the assessment. 
For simple assessments - a single pesticide to which a human is exposed 
by a single route (e.g., oral) from a single source (e.g., apples) - a 
more conservative approach to assumptions such as cooking factors may 
be necessary to assure high end exposures are captured because high end 
exposure may be defined by consumption of a single food. This is not 
the case with complex assessments like for DDVP that involve multiple 
pesticides, multiple routes of exposure, and multiple sources of 
exposure within routes. In evaluating exposure to DDVP in food alone, 
EPA's exposure assessment takes into account residues in hundreds of 
food commodities. If EPA were to assume worst case residue values for 
each of these commodities (worst case pesticide usage, worst case 
potential residues on the raw crop, worst case processing values, worst 
case cooking factors, etc.) and then combine that information with the 
assumption of worst case consumption for each commodity, the exposure 
assessment would not reflect reality. Just as no one person, and 
certainly no major subgroup of consumers, is a worst-case consumer of 
every commodity, no one person, or major subgroup of consumers, is 
likely to be consumers of every commodity at its worst-case residue 
amount. To make such assumptions when multiple commodities are involved 
compounds multiple conservatisms and would produce an assessment that 
overstates exposure probably by several orders of magnitude. For this 
reason, EPA's exposure assessment guidance advises using a mixture of 
high end and central tendency assumptions to produce a high end 
exposure assessment. (Ref. 77). Accordingly, EPA's use of conservative, 
but not worst case, cooking factors in the DDVP exposure assessment is 
reasonable.
    9. Missing data--a. NRDC's claims. NRDC claims that various data 
are missing: storage stability data for meat, milk, poultry, and egg 
residue studies; crop field trials on tomatoes; and tomato processing 
studies. (Ref. 1 at 43).
    b. EPA's response. The tomato use has been canceled so no data are 
needed on tomatoes. Although the IRED stated that data are needed on 
storage stability, that statement was in error. (Ref. 11 at 189). In 
fact, storage stability requirements have been met. The IRED noted that 
storage stability data were needed in connection with some of the 
residue data used in the 1987 Registration Standard for DDVP. 
Subsequent to 1987, the registrant submitted new residue data on the 
commodities in question and that residue data met the requirements for 
storage stability data. (See, e.g., Ref. 74 at 10).
    10. Uncertainties in estimating residues in foods--a. NRDC's 
claims. NRDC argues that EPA has identified uncertainties in its 
dietary assessment but fails to take these uncertainties into account. 
Uncertainties cited by NRDC include lack of data on residue values in 
foods sold at farm stands, use of cooking data, the limited sampling 
sites in the FDA Total Diet Study, the reliance on residue trial 
instead of monitoring data for warehouse uses of DDVP, the extensive 
translation between commodities in estimating residues from DDVP 
warehouse uses, and the reliance on field trial data for some 
commodities. (Refs. 1 at 52; and 13 at 8-9).
    b. EPA's response. EPA does take into account any uncertainties in 
its food exposure analysis in determining whether it has estimated risk 
in a manner that is protective of the general

[[Page 68686]]

population and all major identifiable consumer subgroups. For DDVP 
there were a number of factors that might have led to an 
underestimation of exposure levels but these factors are dwarfed by 
considerations indicating that EPA has overestimated exposure. Each of 
the factors highlighted by NRDC as well as others are discussed below:
    i. Food from farm stands. As discussed above, EPA does not believe 
that farm stands are likely to sell food containing a significantly 
different residue profile than found in PDP monitoring data. This 
factor introduces little to no uncertainty concerning the possibility 
of underestimation of residues into EPA's analysis.
    ii. Use of cooking factors. As discussed above, EPA used cooking 
factors in a conservative fashion in estimating exposure. For several 
reasons, EPA believes its use of cooking factors did not fully take 
into account the degree of reduction of DDVP residues that occurs with 
cooking. First, cooking factors were only applied to a relatively small 
number of commodities that may contain DDVP residues. Cooking of other 
commodities containing DDVP residues (e.g., grains and vegetables) will 
undoubtedly decrease residues in those commodities substantially. 
Second, the manner in which EPA translated the residue reduction data 
will tend to exaggerate residue levels in many commodities. For 
example, data on the residue reduction that occurs from cooking 
hamburger for six minutes was translated to all cooked meats. Given 
that most meats are cooked substantially longer than six minutes, this 
use of the cooking data will understate exposure. This factor will 
overestimate exposure to DDVP.
    iii. FDA Total Diet Study. In the updated risk assessment the FDA 
Total Diet Study data was not relied upon to quantitatively estimate 
residues in food. This factor has no bearing on the DDVP exposure 
assessment.
    iv. Residues from warehouse use. EPA did do extensive translation 
of data between commodities for the warehouse use. There was a 
reasonable basis for these translations; nonetheless, some uncertainty 
attends any such translation. However, EPA's estimation of exposure 
from the warehouse use will clearly overstate DDVP exposure for two 
reasons. First, EPA is not relying on monitoring data from warehouses 
but data from residue trials in the warehouse. Invariably, residue 
trials result in findings of higher residue values than monitoring data 
because residue trials involve prompt sampling after treatment whereas 
monitoring can occur days or weeks later. Thus, residue trials do not 
take into account the normal degradation that occurs over time. With 
DDVP, this decline in residues is likely to be exaggerated given the 
data showing both DDVP's volatility and rapid degradation. Monitoring 
data that is available on other commodities confirms the rapid decline 
of residues. Second, EPA assumed that all food in warehouses is treated 
with DDVP. This is a very conservative estimate. Accordingly, this 
factor will tend to significantly overstate exposure to DDVP.
    v. Reliance on field trial data. For many commodities that may be 
legally treated with naled, EPA relied upon field trial data or assumed 
tolerance level residues rather than monitoring data. For the reasons 
noted immediately above, this assumption will significantly overstate 
residues on those commodities.
    vi. Percent crop treated. For many commodities that may be legally 
treated with DDVP or naled (other than in warehouses), EPA assumed that 
100 percent of the commodity is treated. Again, this is a very 
conservative estimate and will significantly overstate DDVP exposure 
from those commodities.
    vii. Default processing factors. For several processed commodities, 
EPA relied on default processing factors in estimating DDVP residues in 
the processed food. EPA's default processing factors project worst case 
levels of pesticides in processed food. (70 FR at 46733-46734). Thus, 
use of default processing factors instead of specific processing data 
for DDVP will overestimate residues in food.
    Considering all of this information, EPA's conclusion is 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.
    In any event, EPA's 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. (Ref. 56). To the extent food is a 
driver, that food is food with residue estimates from its treatment as 
a bagged and packaged food. As explained above, estimates of residues 
in bagged and packaged foods are likely to be a significant 
overestimate due to the assumption of 100 percent treatment and use of 
magnitude of the residue study rather than actual monitoring data.

C. Residential Exposure

    1. Aggregating Exposures. The safety standard in FFDCA section 408 
for tolerances requires that there be a reasonable certainty of no harm 
from ``aggregate exposure to the pesticide chemical residue, including 
all dietary exposures and all other exposure for which there is 
reliable information.'' (21 U.S.C. 346a(b)(2)(A)(ii)). Further, EPA in 
evaluating the safety of tolerances is directed to ``consider ... 
available information concerning the aggregate exposures of consumers 
... to the pesticide chemical residue ... including dietary exposure 
under [all] tolerance[s] ... in effect for the pesticide chemical 
residue and exposure from other non-occupational sources.'' (21 U.S.C. 
346a(b)(2)(D)(vi)).
    Unit VII.B. discusses EPA's assessment of aggregate dietary 
exposure to DDVP from residues in food and water. That assessment 
showed that these aggregate exposure levels were well below the acute 
and chronic RfD/PADs. Although refined, these exposure estimates still 
are likely to overstate exposure and risk. This is particularly 
apparent when it is considered that the commodities that drove the risk 
numbers were those commodities (drinking water and bagged and packaged 
goods) for which the most conservative assumptions were made. (Ref. 
56).
    Pesticide residues to which humans are exposed from residential 
uses of pesticides must be considered as part of section 408's 
aggregate exposure calculus. The concern, of course, is that pesticide 
tolerances should not be established or left in effect if dietary 
exposures, when combined with other sources of exposure, exceed safe 
levels. As the analysis in Unit VII.D.2. shows, however, dietary 
exposures are insignificant compared to residential exposures and thus 
the safety determination turns on an evaluation of the exposure and 
risk from the residential uses of DDVP.
    2. Revised residential exposure - pest strips. In light of the 
numerous issues raised by NRDC concerning EPA's assessment of the risk 
posed by DDVP pest strips, EPA has substantially revised its assessment 
of exposure and risk from this use. EPA first discusses that revised 
assessment before turning to NRDC's specific claims. The changes in the 
assessment come in three areas: (1) analysis of exposure data and 
exposure assumptions used; (2) the types of durational scenarios 
assessed; and (3) the endpoint used for chronic exposure. (Ref. 78).
    Currently, there are four sizes of DDVP pest strips that are 
registered. The largest strip (65-80 grams) may only be used in 
unoccupied areas in and around the house (garage, attic, crawl space,

[[Page 68687]]

shed) where humans are present for no greater than four hours per day. 
There are three smaller strips (16, 10.5, and 5.25 grams) that may be 
used in the home in closets, wardrobes, or cupboards. The IRED 
recommended, and Amvac has accepted, label restrictions for these 
smaller strips which bars use in closets of rooms where infants or 
children or sick or elderly people will be confined for an extended 
period or generally in closets of rooms for which any person will be 
present for extended periods. (Refs. 11 at 161; and 79 ). EPA's risk 
assessments examined each of these pest strips.
    a. Exposure data and assumptions. In assessing exposure from pest 
strips, EPA has relied on a study (Collins and DeVries) measuring air 
concentrations in 15 houses treated with multiple large DDVP pest 
strips hung directly in the living areas of the houses. (Id.). In its 
prior assessment, EPA averaged air concentrations measured in the study 
across houses. To insure its assessment is conservative, EPA, in its 
most recent assessment, estimated risk based on the air concentrations 
in the individual houses. (Id.). Additionally, for chronic risk 
assessment, rather than project exposure from the 91 days of the 
Collins and DeVries study over a period of 120 days (the period for 
which a pest strip is generally designed to be effective), EPA used the 
air concentration measured over the 91 days in the study. This approach 
increases exposure estimates as the data show that DDVP air 
concentrations are higher in the first weeks. Finally, rather than 
calculate MOEs for different time periods in the home for strips used 
in occupied portions of the home, EPA calculated MOEs assuming that 
people are exposed in their homes 24 hours per day and spend 24 hours 
per day in a room with a pest strip. For strips used in unoccupied 
portions of the home, EPA assessed the risk based on 4 hours of 
exposure per day.
    b. Durational scenarios. Previously, EPA focused only on chronic 
exposure to DDVP from pest strips and compared that chronic exposure to 
the chronic RfD/PAD. In its revised risk assessment, EPA assessed risks 
for acute, short/intermediate-term, and chronic exposures. (Id.). The 
acute assessment examined risk based on the air concentrations in the 
15 houses in the Collins and DeVries studies for the first 24 hours 
after the pest strip is installed. The short/intermediate-term 
assessment examined risk based on the air concentrations for the first 
two weeks after installation of a pest strip. Appropriate acute and 
short/intermediate-term endpoints were used.
    c. Chronic endpoint. EPA's prior risk assessment used the benchmark 
dose level of 10 percent (BMDL10) for RBC cholinesterase 
from a chronic inhalation study in rats to assess chronic risk from 
exposure to pest strips. EPA reexamined this choice in light of its 
policy on the use of cholinesterase inhibition in risk assessments. 
Consistent with that policy, EPA determined that it would be more 
appropriate to use the BMDL20 for RBC cholinesterase from 
that study in assessing chronic risk (but not for acute risk). That 
decision was based on the consistent and large difference in doses 
between indications of RBC cholinesterase inhibition at both the 
BMDL10 and the BMDL20 and inhibition of brain 
cholinesterase and clinical signs in numerous studies when exposure was 
for 90 days or greater. (Id.).
    d. Revised risk assessments. EPA's revised assessment shows that 
(1) for the large strips permitted only in unoccupied portions of a 
home, the target MOE is exceeded (i.e., there is not a risk of concern) 
for all homes for four hours of exposure for acute, short/intermediate-
term, and chronic scenarios (Table 3, Table 5, and Table 7); (2) for 
the largest closet strip the target MOE is exceeded for all homes for 
24 hours of exposure for the acute scenario (Table 4); (3) for the 
largest closet strip the target MOE is exceeded for most homes for 24 
hours of exposure for the short/intermediate-term and chronic scenarios 
(Table 6 and Table 8); (4) for the smaller closet strip and the 
cupboard strip the target MOE is all but met or exceeded for all homes 
for acute, short/intermediate-term, and chronic scenarios (Table 9 and 
Table 10); and (5) dietary exposure is insignificant compared to pest 
strip exposure for all scenarios. (Id.). The MOEs for all of these 
scenarios for the large pest strip and the large closet strip are 
presented in the tables below.
    The acute risk assessments for large pest strips (Table 3) and 
closet, wardrobe, and cupboard pest strips (Table 4) use a hazard value 
of 0.800 mg/kg which is the BMDL10 for RBC cholinesterase 
from a rat study. Exposure is based on Day 1 air concentrations in the 
Collins and DeVries study. Four hours of exposure is assumed for the 
large strip and 24 hours of exposure is assumed for the closet, 
wardrobe, and cupboard strips. The MOE of concern is 30, as opposed to 
100, because when exposure is expressed in units of air concentration 
such as part per million (``ppm'') or milligrams/meter3 
(``mg/m3'') (as it is in the Collins and Devries data), then 
the pharmacokinetic component of the interspecies factor is decreased 
from 10X to 3X to account for the different breathing rates between 
species. (Id.).

  Table 3.--Acute Risk from Exposure to Large (65 g) Strips for 4 hours
------------------------------------------------------------------------
                                                    Day 1
          Collins and DeVries Home ID           Concentration     MOE
                                                   (mg/m3)
------------------------------------------------------------------------
6N                                                     0.11           45
------------------------------------------------------------------------
7W                                                     0.11           45
------------------------------------------------------------------------
2C                                                     0.08           61
------------------------------------------------------------------------
14W                                                    0.08           61
------------------------------------------------------------------------
10C                                                    0.07           70
------------------------------------------------------------------------
13W                                                    0.07           70
------------------------------------------------------------------------
5N                                                     0.05           98
------------------------------------------------------------------------
11C                                                    0.05           98
------------------------------------------------------------------------
12N                                                    0.05           98
------------------------------------------------------------------------
3C                                                     0.04          123
------------------------------------------------------------------------
15N                                                    0.04          123
------------------------------------------------------------------------
1W                                                     0.02          245
------------------------------------------------------------------------
4N                                                     0.02          245
------------------------------------------------------------------------
8W                                                     0.02          245
------------------------------------------------------------------------
9C                                                     0.01          490
------------------------------------------------------------------------


 Table 4.-- Acute Risk from Exposure to Large Closet (16 g) Pest Strips
                              for 24 hours
------------------------------------------------------------------------
                                                    Day 1
          Collins and DeVries Home ID           Concentration     MOE
                                                   (mg/m3)
------------------------------------------------------------------------
6N                                                    0.028           30
------------------------------------------------------------------------
7W                                                    0.028           30
------------------------------------------------------------------------
2C                                                    0.020           41
------------------------------------------------------------------------
14W                                                   0.020           41
------------------------------------------------------------------------
10C                                                   0.018           47
------------------------------------------------------------------------
13W                                                   0.018           47
------------------------------------------------------------------------
5N                                                    0.013           66
------------------------------------------------------------------------
11C                                                   0.013           66
------------------------------------------------------------------------
12N                                                   0.013           66
------------------------------------------------------------------------
3C                                                    0.010           82
------------------------------------------------------------------------
15N                                                   0.010           82
------------------------------------------------------------------------
1W                                                    0.005          165
------------------------------------------------------------------------

[[Page 68688]]


4N                                                    0.005          165
------------------------------------------------------------------------
8W                                                    0.005          165
------------------------------------------------------------------------
9C                                                    0.003          329
------------------------------------------------------------------------

    The smaller closet strip and cupboard strip will have higher MOEs. 
Background dietary DDVP exposure when expressed in mg/m3 is 
0.00026 and this value is insignificant compared to the air 
concentration levels in higher concentration houses.
    The short/intermediate-term risk assessments for large pest strips 
(Table 5) and for closet, wardrobe, and cupboard pest strips (Table 6) 
use a hazard value of 0.1 mg/kg/day which is the LOAEL for the human 
repeat dose oral study. Exposure is based on the average air 
concentration of the first 2 weeks of exposure in the Collins and 
DeVries study. Four hours of exposure is assumed for the large strip 
and 24 hours of exposure is assumed for the closet, wardrobe, and 
cupboard strips. The MOE of concern is 30 based on an intraspecies 
safety factor of 10X and an additional safety factor of 3X for reliance 
on a LOAEL.

  Table 5.--Short/Intermediate-term Risk from Exposure to Large (65 g)
                         Strips for 4 hours/day
------------------------------------------------------------------------
                                                    2-Week
                                                   Average
          Collins and DeVries Home ID           Concentration     MOE
                                                   (mg/m3)
------------------------------------------------------------------------
7W                                                    0.074           29
------------------------------------------------------------------------
2C                                                    0.073           29
------------------------------------------------------------------------
10C                                                   0.072           29
------------------------------------------------------------------------
6N                                                    0.066           32
------------------------------------------------------------------------
13W                                                   0.065           32
------------------------------------------------------------------------
14W                                                   0.059           36
------------------------------------------------------------------------
12N                                                   0.048           43
------------------------------------------------------------------------
11C                                                   0.038           55
------------------------------------------------------------------------
3C                                                    0.032           65
------------------------------------------------------------------------
5N                                                    0.030           69
------------------------------------------------------------------------
15N                                                   0.028           74
------------------------------------------------------------------------
8W                                                    0.019          109
------------------------------------------------------------------------
1W                                                    0.019          112
------------------------------------------------------------------------
4N                                                    0.017          126
------------------------------------------------------------------------
9C                                                    0.012          177
------------------------------------------------------------------------
------------------------------------------------------------------------


Table 6.--Short/Intermediate-term Risk from Exposure to Large Closet (16
                     g) Pest Strips for 24 hours/day
------------------------------------------------------------------------
                                                    2-Week
                                                   Average
          Collins and DeVries Home ID           Concentration     MOE
                                                   (mg/m3)
------------------------------------------------------------------------
7W                                                    0.018           19
------------------------------------------------------------------------
2C                                                    0.018           19
------------------------------------------------------------------------
10C                                                   0.018           20
------------------------------------------------------------------------
6N                                                    0.016           21
------------------------------------------------------------------------
13W                                                   0.016           22
------------------------------------------------------------------------
14W                                                   0.015           24
------------------------------------------------------------------------
12N                                                   0.012           29
------------------------------------------------------------------------
11C                                                   0.010           37
------------------------------------------------------------------------
3C                                                    0.008           43
------------------------------------------------------------------------
5N                                                    0.008           46
------------------------------------------------------------------------
15N                                                   0.007           50
------------------------------------------------------------------------
8W                                                    0.005           73
------------------------------------------------------------------------
1W                                                    0.005           75
------------------------------------------------------------------------
4N                                                    0.004           84
------------------------------------------------------------------------
9C                                                    0.003          118
------------------------------------------------------------------------

    The smaller closet strip and cupboard strip will have MOEs of 29 or 
higher. Background dietary DDVP exposure when expressed in mg/
m3 is 0.00026 and this value is insignificant compared to 
the air concentration levels in higher concentration houses.
    For the chronic risk assessments for large pest strips (Table 7) 
and closet, wardrobe, and cupboard pest strips (Table 8, Table 9, and 
Table 10), EPA calculated MOEs for a range of hazard values: the 
BMDL10 and BMDL20 for RBC cholinesterase from a 
2-year chronic rat study, BMDL10 for brain cholinesterase 
from a 90-day rat study, and the NOAEL for clinical signs from a 7-day 
rat study. Exposure is based on the average air concentration for the 
91 days of the Collins and DeVries study. Four hours of exposure is 
assumed for the large strip and 24 hours of exposure is assumed for the 
closet, wardrobe, and cupboard strips. The MOE of concern is 30 for the 
same reason as with the acute exposure assessment.

                                       Table 7.--Chronic Risk from Exposure to Large (65 g) Strips for 4 hours/day
--------------------------------------------------------------------------------------------------------------------------------------------------------
                        Study                                            Rat 2-Year Inhalation                     Rate 90 Day oral     Rate 7 Day oral
--------------------------------------------------------------------------------------------------------------------------------------------------------
                      POD Type                                        BMDL10                        BMDL20              BMDL10               LOAEL
--------------------------------------------------------------------------------------------------------------------------------------------------------
                     POD (mg/m3)                             0.078               0.41                0.196                0.4                 7.3
--------------------------------------------------------------------------------------------------------------------------------------------------------
             Home ID                  CD avg / 6              RBC                Brain                RBC                 RBC            Clincal signs
--------------------------------------------------------------------------------------------------------------------------------------------------------
10C                                         0.00607                  13                  67                  32                  66                1200
--------------------------------------------------------------------------------------------------------------------------------------------------------
2C                                          0.00575                  14                  70                  34                  70                1300
--------------------------------------------------------------------------------------------------------------------------------------------------------

[[Page 68689]]


13W                                         0.00483                  16                  84                  41                  83                1500
--------------------------------------------------------------------------------------------------------------------------------------------------------
7W                                          0.00337                  23                 120                  58                 119                2200
--------------------------------------------------------------------------------------------------------------------------------------------------------
12N                                         0.00330                  24                 123                  59                 121                2200
--------------------------------------------------------------------------------------------------------------------------------------------------------
14W                                         0.00330                  24                 123                  59                 121                2200
--------------------------------------------------------------------------------------------------------------------------------------------------------
6N                                          0.00212                  37                 191                  93                 189                3400
--------------------------------------------------------------------------------------------------------------------------------------------------------
3C                                          0.00212                  37                 191                  93                 189                3400
--------------------------------------------------------------------------------------------------------------------------------------------------------
11C                                         0.00207                  38                 196                  95                 194                3500
--------------------------------------------------------------------------------------------------------------------------------------------------------
15N                                         0.00192                  41                 211                 102                 208                3800
--------------------------------------------------------------------------------------------------------------------------------------------------------
8W                                          0.00161                  48                 251                 122                 248                4500
--------------------------------------------------------------------------------------------------------------------------------------------------------
1W                                          0.00137                  57                 295                 143                 291                5300
--------------------------------------------------------------------------------------------------------------------------------------------------------
9C                                          0.00127                  61                 318                 154                 314                5700
--------------------------------------------------------------------------------------------------------------------------------------------------------
5N                                          0.00109                  71                 370                 179                 366                6700
--------------------------------------------------------------------------------------------------------------------------------------------------------
4N                                          0.00099                  79                 409                 198                 404                7400
--------------------------------------------------------------------------------------------------------------------------------------------------------


               Table 8.--Chronic Risk from Exposure to Large (16 g) Closet Strips for 24 hours/day
----------------------------------------------------------------------------------------------------------------
                   Study                              Rat 2-Year Inhalation            Rate 90 Day   Rate 7 Day
-------------------------------------------------------------------------------------     oral          oral
                 POD Type                             BMDL10               BMDL20    ---------------------------
-------------------------------------------------------------------------------------    BMDL10*        LOAEL
                POD (mg/m3)                     0.078         0.41          0.196    ---------------------------
-------------------------------------------------------------------------------------      0.4           7.3
                                                                                     ---------------------------
           Home ID             CD avg / 4        RBC          Brain          RBC                      Clinical
                                                                                           RBC          signs
----------------------------------------------------------------------------------------------------------------
10C                               0.00910             9            45            22            44           780
----------------------------------------------------------------------------------------------------------------
2C                                0.00862             9            47            23            46           830
----------------------------------------------------------------------------------------------------------------
13W                               0.00725            11            56            27            55           980
----------------------------------------------------------------------------------------------------------------
7W                                0.00506            15            80            39            79          1400
----------------------------------------------------------------------------------------------------------------
12N                               0.00495            16            82            40            81          1400
----------------------------------------------------------------------------------------------------------------
14W                               0.00495            16            82            40            81          1400
----------------------------------------------------------------------------------------------------------------
6N                                0.00318            25           127            62           126          2100
----------------------------------------------------------------------------------------------------------------
3C                                0.00318            25           127            62           126          2200
----------------------------------------------------------------------------------------------------------------
11C                               0.00310            25           131            63           129          2300
----------------------------------------------------------------------------------------------------------------
15N                               0.00288            27           141            68           139          2500
----------------------------------------------------------------------------------------------------------------
8W                                0.00242            32           168            81           166          3000
----------------------------------------------------------------------------------------------------------------
1W                                0.00206            38           196            95           194          3400
----------------------------------------------------------------------------------------------------------------
9C                                0.00191            41           212           103           209          3800
----------------------------------------------------------------------------------------------------------------
5N                                0.00164            48           247           119           244          4100
----------------------------------------------------------------------------------------------------------------
4N                                0.00148            53           273           132           270          4700
----------------------------------------------------------------------------------------------------------------


[[Page 68690]]


              Table 9.--Chronic Risk from Exposure to Small Closet (10.5 g) Strips for 24 hours/day
----------------------------------------------------------------------------------------------------------------
                                 Study                                            Rat 2-Year Inhalation
----------------------------------------------------------------------------------------------------------------
                               POD Type                                           BMDL10               BMDL20
----------------------------------------------------------------------------------------------------------------
                              POD (mg/m3)                                   0.078         0.41          0.196
----------------------------------------------------------------------------------------------------------------
                         Home ID                           CD avg / 6        RBC          Brain          RBC
----------------------------------------------------------------------------------------------------------------
10C                                                           0.00607            13            67            32
----------------------------------------------------------------------------------------------------------------
2C                                                            0.00575            14            70            34
----------------------------------------------------------------------------------------------------------------
13W                                                           0.00483            16            84            41
----------------------------------------------------------------------------------------------------------------
7W                                                            0.00337            23           120            58
----------------------------------------------------------------------------------------------------------------
12N                                                           0.00330            24           123            59
----------------------------------------------------------------------------------------------------------------
14W                                                           0.00330            24           123            59
----------------------------------------------------------------------------------------------------------------
6N                                                            0.00212            37           191            93
----------------------------------------------------------------------------------------------------------------
3C                                                            0.00212            37           191            93
----------------------------------------------------------------------------------------------------------------
11C                                                           0.00207            38           196            95
----------------------------------------------------------------------------------------------------------------
15N                                                           0.00192            41           211           102
----------------------------------------------------------------------------------------------------------------
8W                                                            0.00161            48           251           122
----------------------------------------------------------------------------------------------------------------
1W                                                            0.00137            57           295           143
----------------------------------------------------------------------------------------------------------------
9C                                                            0.00127            61           318           154
----------------------------------------------------------------------------------------------------------------
5N                                                            0.00109            71           370           179
----------------------------------------------------------------------------------------------------------------
4N                                                            0.00099            79           409           198
----------------------------------------------------------------------------------------------------------------


               Table 10.--Chronic Risk from Exposure to Cupboard (5.25 g) Strips for 24 hours/day
----------------------------------------------------------------------------------------------------------------
                                 Study                                            Rat 2-Year Inhalation
----------------------------------------------------------------------------------------------------------------
                               POD Type                                           BMDL10               BMDL20
----------------------------------------------------------------------------------------------------------------
                              POD (mg/m3)                                   0.078         0.41          0.196
----------------------------------------------------------------------------------------------------------------
                         Home ID                           CD avg / 12       RBC          brain          RBC
----------------------------------------------------------------------------------------------------------------
10C                                                           0.00303            26           134            65
----------------------------------------------------------------------------------------------------------------
2C                                                            0.00287            27           141            68
----------------------------------------------------------------------------------------------------------------
13W                                                           0.00242            32           168            81
----------------------------------------------------------------------------------------------------------------
7W                                                            0.00169            46           240           116
----------------------------------------------------------------------------------------------------------------
12N                                                           0.00165            47           245           119
----------------------------------------------------------------------------------------------------------------
14W                                                           0.00165            47           245           119
----------------------------------------------------------------------------------------------------------------
6N                                                            0.00106            74           382           185
----------------------------------------------------------------------------------------------------------------
3C                                                            0.00106            74           382           185
----------------------------------------------------------------------------------------------------------------
11C                                                           0.00103            75           392           190
----------------------------------------------------------------------------------------------------------------
15N                                                           0.00096            81           422           204
----------------------------------------------------------------------------------------------------------------
8W                                                            0.00081            97           503           243
----------------------------------------------------------------------------------------------------------------
1W                                                            0.00069           113           589           285
----------------------------------------------------------------------------------------------------------------
9C                                                            0.00064           123           636           308
----------------------------------------------------------------------------------------------------------------

[[Page 68691]]


5N                                                            0.00055           143           740           358
----------------------------------------------------------------------------------------------------------------
4N                                                            0.00049           158           819           396
----------------------------------------------------------------------------------------------------------------

    Background dietary DDVP exposure when expressed in mg/m3 
is 0.00026 and this value is insignificant compared to the air 
concentration levels in higher concentration houses.
    Despite the fact that some homes from the Collins and DeVries study 
do not have acceptable MOEs for the short/intermediate-term and chronic 
scenarios for the large closet strip, EPA concludes that the pest 
strips do not pose a risk of concern for the following reasons. First, 
use of BMDL20 for RBC cholinesterase is a conservative 
endpoint based on the DDVP database. As Table 7 indicates, target MOEs 
are well exceeded for all homes for chronic risk if the 
BMDL10 for brain cholinesterase or the NOAEL for clinical 
signs are used as the Point of Departure. Second, for short/
intermediate-term risk, EPA has used the results of the human oral 
study in a conservative fashion. The maximum inhibition of RBC 
cholinesterase from the 0.1 mg/kg/day dose used in that study was 16 
percent (group mean) after 18 days of exposure. As discussed above, 
however, 20 percent inhibition is a more appropriate line of 
demarcation for DDVP given, among other things, the wide margin between 
RBC cholinesterase inhibition and clinical effects. If that approach is 
followed the one dose from that study, then 0.1 mg/kg/day would be a 
NOAEL not a LOAEL and the additional 3X safety factor would be 
unnecessary. Without that 3X safety factor, the MOE of concern would 
drop to 10. The conservativeness of the 3X safety factor is also 
supported by the HSRB's conclusion that a dose lower than 0.1 mg/kg/day 
would not be expected to show a significant inhibition response.
    Finally, EPA made numerous conservative assumptions regarding 
interpretation of the Collins and DeVries data in using it to estimate 
exposure, including that: (1) the large strips used in the Collins and 
DeVries study emitted the same amount of DDVP as the largest strip 
currently registered even though the current large strip (65 - 80 
grams) is smaller than the strip used in the Collins and DeVries study 
(100 grams); (2) placement of a strip in a closet is the same as 
hanging it in the adjacent living area; (3) for closet, wardrobe, and 
cupboard strips, exposure is 24 hours per day (despite label 
restrictions barring use in rooms where people would be exposed for 
extended periods); (4) during the 24 hours per day a person is in a 
home that person is continually in a room with a pest strip; and (5) 
strips are replaced every 90 days.
    3. Issues raised by NRDC concerning pest strips--a. NRDC's claims. 
NRDC argues that EPA's exposure assessment for pest strips ``is based 
on unsupported assumptions and inadequate data'' and therefore EPA 
cannot conclude that aggregate exposure to DDVP is safe. NRDC's 
specific allegations are described below.
    i. Reliance on an inadequate exposure study. NRDC notes that EPA 
relied on a single study (Collins and DeVries) monitoring 15 homes in 
one geographic area to estimate residential exposure to DDVP from pest 
strips. NRDC claims this study is inadequate because (1) the number of 
homes monitored is too small to be representative of the housing stock 
in the United States; (2) the study was conducted in only one 
geographic area and at one time of year and thus would not be 
representative of weather conditions (including humidity and 
temperature) in other regions of the United States; (3) sampling in the 
homes was done in only one location and thus the study ``provides no 
information about the movement of residues from room-to-room and [] 
exposure in other rooms in the homes;'' (4) homes were only treated 
with three or four pest strips but homeowners with severe pest problems 
may ``place pest strips in every room or most rooms in the house;'' and 
(5) the study contained insufficient information to estimate exposure 
levels for pest strips of different sizes. (Ref. 1 at 19, 58-59).
    ii. Unsupported assumption that users will not replace pest strips 
more frequently than every 120 days. NRDC claims that EPA's assumption 
that homeowners will not replace pest strips until the strip has been 
in use for at least 120 days is unreasonable because the label does not 
prohibit more frequent replacement and EPA has no empirical data to 
support this assumption. (Id. at 59). NRDC argues that ``[i]n the 
absence of reliable empirical data demonstrating that consumers do not 
... replace the strips more often than is assumed by EPA, at a minimum, 
the labels of these products should be amended to place restrictions on 
use consistent with the assumptions made in the risk assessment.'' 
(Ref. 13 at 10).
    iii. Only considered average exposure over 120 days. NRDC argues 
that EPA erred by averaging exposure levels over a 120-day period. 
According to NRDC, EPA should have considered ``the higher, more 
dangerous exposures that occur when a strip is first hung ....'' (Ref. 
1 at 59). Instead, NRDC asserts, EPA ``should have presented the range 
of risks displayed over time.'' (Id.).
    iv. Failure to consider exposure from use in unoccupied spaces. 
NRDC claims that EPA has not taken into account that DDVP residues 
could migrate from use of the full-size pest strips in attics, crawl 
spaces, and garages to the main living areas of a home. (Ref. 13 at 
10). NRDC notes that EPA has found that use of chlorpyrifos in crawl 
spaces leads to residues in living areas. (Id.). NRDC further contends 
that attics can be part of the air exchange for the living areas in a 
house.
    v. Estimates of exposure durations in homes are too low. While NRDC 
concedes that an estimate of 16 hours/day in a home would be a high end 
estimate for most people, NRDC argues that this estimate ignores 
``several significant population groups'' such as ``[p]eople who work 
or stay at home, retired and elderly people, and pre-school children.'' 
(Id.). Further, NRDC asserts that EPA's low end estimate of 2 hours/day 
in the home is ``absurd on its face.'' (Id.).
    vi. No consideration of incidental oral and dermal exposure. NRDC 
claims that

[[Page 68692]]

EPA had insufficient data to conclude that incidental oral and dermal 
exposure resulting from DDVP residues that settle on home surfaces 
would be minimal. (Id. at 19.). According to NRDC, the only information 
EPA relied upon was data on residues that settle on foodstuffs and such 
data would not be representative of other home surfaces.
    vii. Failure to collect data on consumer use practices with pest 
strips. Echoing comments from the SAP that ``better knowledge of real 
world use practices would serve to improve residential exposure 
analyses,'' NRDC argues that the failure of EPA to collect such data 
``undermines the risk analysis for pest strips.'' (Ref. 1 at 62).
    viii. Failure to consider aggregation of pest strip exposure with 
other residential exposures. NRDC claims that EPA does not support its 
statement that pest strip exposures would not co-occur with high 
dietary exposures. NRDC also argues that EPA should consider co-
occurrence of exposure between pest strips and other DDVP residential 
products. (Ref. 13 at 12-13).
    b. Amvac's comments. Amvac contends that the Collins and DeVries 
study is adequate for assessing exposure from pest strips citing 
several other studies which it states contain similar results. (Ref. 14 
at 45). Further, Amvac argues that ``the estimated time-weighted 
average concentration used by EPA (0.015mg/m3) is higher 
than found in many other studies.'' (Id.). Amvac also defends EPA's use 
of a time-weighted average in estimating risk noting that ``EPA is 
assessing chronic exposure and thus it is appropriate to average over 
the entire period to compare to a chronic endpoint.'' (Id.). Finally, 
Amvac argues that, if EPA assessed acute risk from pest strips, it 
would be appropriate for EPA to use the highest concentration from the 
Collins and DeVries study (0.11 mg/m3) but that this 
exposure level does not show an acute risk concern. (Id.).
    c. EPA's response--adequacy of the Collins and DeVries Study. EPA 
believes this study is sufficiently representative to estimate exposure 
and EPA disagrees with each of NRDC's contentions. First, EPA does not 
believe the study is inadequate due to being performed in a single 
location on 15 houses during a single season of the year. As noted by 
Amvac, there are a number of studies other than Collins and Devries 
that test DDVP pest strips in houses. Specifically, data on DDVP air 
concentrations from the use of pest strips are available for over 100 
homes in the United States, United Kingdom, and France. (Ref. 80). 
There was no major difference in the DDVP air concentration in the 100 
houses and the DDVP air concentration in the study of the 15 houses 
that were used for exposure estimates.
    Second, EPA does not view the study as flawed because it only 
sampled DDVP concentrations in one location in each home. Importantly, 
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. Thus, EPA has assessed 
MOEs in an appropriately conservative fashion given the sampling 
location in the Collins and DeVries study.
    Third, NRDC's suggestion that some homeowners may put a pest strip 
in every room fails to take into account that (1) the label now bars 
use of full-size pest strips except in infrequently-occupied spaces 
(attics, crawl spaces, sheds, and garages); (2) in-home pest strips 
must contain significantly less DDVP than full-size strips and are 
limited to use in closets, wardrobes, and cupboards; and (3) EPA's risk 
assessment assumes a person spends all of their time in a room with a 
closet or cupboard that contains a pest strip. Relevantly, the largest 
closet strip is only labeled as effective in a 200 cubic foot area. 
Areas beyond that efficacious zone of treatment are likely to contain 
significantly lower air concentrations.
    Fourth, the Collins and DeVries study does provide sufficient 
information to estimate exposure from different size strips. The 
Collins and Devries study used a pest strip that was larger than the 
largest size available today and EPA made the conservative assumption 
that the currently-registered large strip would have similar exposure 
to the older, larger version and extrapolated exposure levels for 
smaller strips proportionately based on that conservative assumption.
    Finally, to insure that EPA has the most accurate information 
possible on exposure for pest strips, EPA plans to require as part of 
the data call-in to be issued in connection with reregistration that an 
additional study be conducted that measures DDVP air concentrations in 
houses from use of pest strips.
    i. Replacement of strips. EPA's risk assessment has a built-in 
margin of error in the event strips are replaced more frequently than 
every 120 days because it is based on an average of the first 91 days 
of exposure which was the period of time air concentrations were 
measured in the Collins and DeVries study.
    ii. Use of time-weighted average exposure. EPA believes that use of 
a time-weighted average of the DDVP concentration levels is appropriate 
for chronic risk and does not understand NRDC to be contesting this 
approach to assessing chronic risk. As to acute exposures that occur 
during the first day after a strip is hung, EPA has now expanded its 
risk assessment to address both this scenario and a short/intermediate-
term exposure scenario (exposure for the two weeks after a strip is 
installed).
    iii. Exposure from use in unoccupied spaces. EPA believes it 
unlikely that DDVP residues will migrate from attics, crawl spaces, 
garages, and sheds to living areas within a house because it would be 
unusual for these spaces to be connected to the air exchange for a 
house. On the other hand, basements may be included in a home's air 
exchange system and, for that reason, the large pest strips may not be 
used in a basement. This is likely part of the explanation for the 
result in the cited chlorpyrifos study. In that study, the chlorpyrifos 
was injected into the foundation and migrated to the basement of the 
house. From there, it is likely that chlorpyrifos moved to other rooms 
in the house through air exchange. Further, the chlorpyrifos study 
cited by NRDC has little relevance to pest strips given the vastly 
different amounts of active ingredient involved. (Ref. 81). In the 
chlorpyrifos study, approximately 100 gallons of a solution containing 
1 percent of pesticide product (Dursban TC) was injected into basement 
walls. According to the label, Dursban TC contains 4 pounds per gallon 
of chlorpyrifos. Thus, that study used approximately 4 pounds of 
chlorpyrifos. A large pest strip contains, at most, 80 grams of 
pesticide product, of which 18.6 percent is DDVP. Accordingly, the pest 
strip exposure in unoccupied areas would contain roughly 15 grams of 
DDVP compared to approximately 1,800 grams of chlorpyrifos in the study 
cited.
    iv. Exposure durations in homes. First, EPA believes it is unlikely 
that a person would spend four hours per day, day in and day out for an 
extended period in an attic, crawl space, garage, or shed. In any 
event, the label forbids use of the large pest strips in such locations 
should they be occupied that regularly. Second, as to the closet, 
wardrobe, and cupboard strips, EPA has assumed 24 hours per day 
exposure in calculating margins of exposure. Amvac has agreed to modify 
labels on these products so that they bar use of these strips in 
closets in rooms where infants or children, or sick or elderly people 
are confined for extended periods. Additionally, the label prohibits 
use of

[[Page 68693]]

the strip in any area of the house where people are present for 
extended periods.
    v. Incidental oral and dermal exposure. NRDC is incorrect in its 
assertion that EPA's risk assessment does not take into account 
incidental oral and dermal exposure. Although dermal and incidental 
oral exposure from contact with DDVP adsorbed on solid surfaces was not 
assessed directly, the inhalation study used for assessing inhalation 
risk includes dermal and oral exposure components because the study 
involved continuous whole-body exposure resulting in adsorption of DDVP 
vapors to the animal's fur and food. In other words, the inhalation 
study is actually a total exposure study accounting for exposure by all 
routes when DDVP is delivered as a vapor. Further, the pest strip use 
is unlikely to leave significant DDVP residues on residential surfaces 
leading to dermal or incidental oral exposures. DDVP is highly volatile 
and degrades rapidly. Thus, even if a person repeatedly uses pest 
strips in the home, significant long-term dermal exposure is unlikely. 
The Collins and DeVries study showed very low concentrations of DDVP in 
the air and almost all food sampled in the home had no detectable 
residues. EPA reasonably concluded that any dermal exposures from 
deposit of air residues on surfaces would be negligible compared to 
residues inhaled directly.
    vi. Data on real world use practices. Data on ``real world'' use 
practices of pest strips might make it possible for EPA to determine 
the extent to which EPA is likely overestimating exposure. EPA believes 
its conservative projection of exposure, given the clarity and 
reasonableness of the label directions, as amended, preclude the need 
to require additional data on use practices.
    vii. Aggregating pest strip exposure with other residential 
exposures. In assessing aggregate risks, EPA believes it is unrealistic 
to add high-end exposures from intermittent and unconnected pesticide 
exposures which are likely to affect relatively small population 
groups. Thus, in aggregating dietary exposures to pest strip exposures, 
EPA has compared chronic (rather than acute) dietary exposure levels of 
DDVP as a background exposure to the various pest strip durational 
scenarios (acute, short/intermediate-term, chronic). It should also be 
noted that the dietary exposure estimates for DDVP are driven by high-
end model estimates of residues in drinking water which is an 
additional conservatism.
    For similar reasons, EPA does not believe it is realistic to add 
high-end acute or short-term exposures for the residential use of 
trichlorfon on turf and DDVP as a spot insect treatment by aerosol 
spray. Although dietary exposure to DDVP, and possibly exposure from a 
DDVP pest strip, may be appropriately aggregated as a background 
exposure to the turf or spot treatment uses, assuming that the windows 
for high-end acute exposures from the turf use and the spot treatment 
overlap is overly conservative. In any event, however, even if 
exposures from turf and spot treatment uses are aggregated with each 
other and with background exposures from food and water and pest 
strips, the aggregate exposure still does not show a risk of concern. 
Aggregating the MOEs of 100 for both the turf and spot treatment uses, 
(Ref. 11 at 160, 165), with MOEs for background exposure for dietary 
(900) and pest strips (93) gives an aggregate short-term MOE of 31 for 
the child who simultaneously experiences outdoor exposures from the 
trichlorfon turf use with indoor exposures from DDVP spot treatments 
and pest strips. The target MOE here is 30. This aggregation relies 
upon average dietary exposure for the most highly exposed subgroup 
which may have turf post-application exposures (children aged 1-2) 
compared to the short-term oral Point of Departure and average pest 
strip exposure over 91 days compared to the short-term inhalation Point 
of Departure. (Refs. 11 at 138, 162; 56 at 18).

D. Risk Characterization

    1. 99.9th percentile--a. NRDC's claims. NRDC asserts that EPA has 
failed to provide a rationale for using the 99.9th percentile in the 
DDVP risk assessment for acute population effects. (Ref. 1 at 51). NRDC 
further contends that some 300,000--0.1 percent of the U.S. 
population--will not be considered because they ``fall below the level 
of sensitivity of the calculation method.'' (Id.). NRDC therefore 
argues that EPA cannot make its FFDCA safety finding.
    b. EPA's response. Contrary to NRDC's assertion, EPA has not 
ignored 300,000 of the U.S. population in estimating acute DDVP risks 
through reliance on the 99.9th exposure percentile in the DDVP risk 
assessment. As EPA has repeatedly explained in the past - in science 
policy documents and in responses to NRDC's objections to tolerances - 
``the use of a particular percentile of exposure is a tool to estimate 
exposures for the entire population and population subgroups and not a 
means to eliminate protection for a certain segment of a subgroup.'' 
(69 FR 30070 and 70 FR 46733).
    In examining pesticide exposure, EPA does not have the capability 
of measuring actual exposure to individuals across the population. 
Rather, EPA uses data on factors bearing on exposure such as residue 
levels in food and drinking water, food consumption patterns, and air 
concentration levels and transferable surface residues to estimate 
exposure to hypothetical individuals across major identifiable 
subgroups in the population. These data on exposure factors can range 
from highly conservative values (e.g., assumption that 100 percent of a 
crop is treated with a pesticide) to highly realistic values (e.g., 
market basket monitoring data on pesticide residue levels). In 
interpreting exposure estimates based on such factors, EPA makes 
judgments regarding what exposure level (expressed as a percentile) is 
protective of the relevant population subgroups taking into account the 
relative conservativeness of the factors which are the basis of the 
assessment.
    Generally, EPA uses the 95th percentile exposure as a starting 
point for evaluating the safety of pesticide in circumstances where EPA 
has employed very conservative assumptions on residue values and risk 
assessment techniques. In EPA's judgment, the 95th percentile exposure, 
when calculated using such conservative assumptions, will not 
underestimate exposure for any major identifiable subgroups. However, 
when EPA uses more realistic residue values and refined risk assessment 
techniques, it starts its evaluation of safety at the 99.9th percentile 
of exposure to be sure that it is protecting the entire population and 
all major, identifiable subgroups. EPA uses the 99.9th percentile as 
the starting point for refined assessments rather than the 100th 
percentile because generally its exposure assumptions, even when 
refined, contain residual conservatisms. Thus, whether EPA is relying 
on the 95th percentile, the 99.9th percentile, or some other value, the 
population exposure percentile is a means to an end and not a 
designation of those people worthy of protection. As EPA noted in a 
science policy document on this issue: ``just as when OPP uses the 95th 
percentile with non-probabilistic exposure assessments OPP is not 
suggesting that OPP is leaving 5 percent of the population unprotected, 
OPP is not by choosing the 99.9th percentile for probabilistic exposure 
assessments concluding that only 99.9 percent of the population 
deserves protection.'' (Ref. 8 at 31). Perhaps the best evidence that 
use of population percentiles is not identifying those worthy of 
protection but simply a tool in estimating exposure

[[Page 68694]]

is that refined assessments using the 99.9th percentile invariably 
estimate exposure to be lower for a pesticide than an unrefined 
assessment for that same pesticide using the 95th percentile. (69 FR 
30071). Yet, under NRDC's logic the use of the 95th percentile, by 
itself, would signal that fewer people are being protected than if the 
99.9th percentile was used, and thus an exposure estimate based on the 
95th percentile should necessarily be lower than one based on the 
99.9th percentile.
    2. Inappropriate use of 100% of the RfD/PAD as a ``Bright Line'' 
Rule--a. NRDC's claims. NRDC contends that EPA is unlawfully 
disregarding significant risks by relying on a ``bright line rule'' 
that risks below 100 percent of the acute population adjusted does 
(aPAD) are not of concern and risks above 100 percent are of concern. 
(Ref. 1 at 51-52). Specifically, NRDC argues that (i) EPA treats the 
100 percent threshold as a rule that has not been subject to notice and 
comment rulemakings; (ii) use of a 100 percent threshold is arbitrary 
and capricious; (iii) use of 100 percent threshold improperly excludes 
acute risks unless they exceed 100 percent of the aPAD; and (iv) EPA 
cannot reasonably explain how children aged 1 to 6, the sub-population 
with the highest percentage exposure, will not be harmed.
    b. EPA's response. NRDC appears to be suggesting that EPA's 
approach of comparing estimated DDVP exposure to an EPA-derived safe 
dose for DDVP is unlawful because (1) EPA cannot adopt an analytical 
approach of comparing exposure to the safe dose without a regulation 
that permits such an approach; and (2) EPA has not adequately justified 
that its chosen safe dose is actually safe. Such claims are baseless.
    In assessing risks posed by a pesticide, EPA first examines 
toxicological studies with the pesticide and calculates a safe dose in 
humans (RfD/PAD) based on the results of those studies and 
incorporating appropriate safety factors. This analysis, based on well-
established risk assessment principles used both across the federal 
government and internationally, is designed to establish a dose without 
appreciable risk to humans. EPA then compares estimated aggregate 
exposure to humans to the safe dose to make a determination on the 
safety of the pesticide. EPA believes this type of case-by-case 
assessment of the risk from exposure to a pesticide is precisely what 
section 408 demands. Other than the statutory mandates in FFDCA section 
408, EPA does not follow ``bright line'' rules in making safety 
determinations but rather is guided by what the data show on a 
particular pesticide. Of course, at the end of its pesticide-specific 
analysis EPA must make a safety determination. EPA does not believe it 
needs a rule saying so to conclude that, where it has confidence that 
exposure is below the safe dose, a tolerance is safe. Further, there is 
no merit to NRDC's bald claim that EPA's safe dose determination for 
DDVP is arbitrary and capricious because EPA has failed to explain the 
basis for its safe dose determination. EPA's safe dose determination is 
supported and explained by extensive documentation including the IRED 
and numerous EPA-produced data evaluation and other analytical 
memoranda addressing DDVP as well as long-established and commonly-
employed risk assessment principles. (See, e.g., Ref. 11).
    3. FQPA Safety Factor--a. NRDC's claims. NRDC asserts that the 
Agency has no basis upon which to apply anything lower than a 10X FQPA 
safety factor in the DDVP risk assessment. According to NRDC, ``[t]he 
admitted potential for pre- and post-natal toxicity from exposure to 
DDVP, combined with incomplete data regarding toxicity and exposure to 
infants and children, compel EPA to retain the default FQPA tenfold 
safety factor for DDVP.'' (Ref. 1 at 15). As to pre- and post-natal 
toxicity, NRDC called particular attention to a study in the open 
literature (Mehl et al (1993), which reported brain effects in guinea 
pig pups. (Id. at 15-16). As to missing data, NRDC placed particular 
evidence on the absence of a DNT study. NRDC also criticizes EPA's 
choice of an additional safety factor of 3X arguing that ``[t]he Agency 
did not explain why it chose 3X as opposed to 4X or any other factor.'' 
(Id. at 14).
    b. EPA's response. As discussed above, under the FQPA, EPA 
presumptively applies an additional tenfold margin of safety (i.e., 
safety factor) when assessing the risk of pesticide exposure to 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. FQPA, however, authorizes the Agency to use a 
different margin of safety for pesticide residues if, on the basis of 
reliable data, such a margin will be safe for infants and children. 
When EPA issued its preliminary risk assessment for DDVP, it employed 
an FQPA safety factor of 3X because the Agency lacked an acceptable DNT 
study as well as an FQPA safety factor of 3X for various residential 
risk assessments.
    Since the preliminary risk assessment was issued for public comment 
in 2000, the Agency received two Developmental Neurotoxicity Test (DNT) 
studies. The NOAEL/LOAEL for the two combined DNT studies is 1.0/7.5 
mg/kg/day based on increased auditory startle amplitude in male 
offspring in both studies. The NOAEL is much higher than the points of 
departure used for regulation of dichlorvos: 0.05 mg/kg/day from a dog 
study used to assess long-term effects, and 0.1 mg/kg/day from a human 
study used for short- and intermediate-term scenarios. Now that the DNT 
studies have been submitted, EPA believes it has reliable data showing 
it is safe for infants and children to remove the additional safety 
factor for all risk assessments other than the residential assessments. 
This conclusion is based on:
    (1) The toxicity database is complete.
    (2) There are no residual concerns for pre- and/or postnatal 
toxicity resulting from exposure to dichlorvos. There was no evidence 
for increased susceptibility of the rat and rabbit offspring to 
prenatal or postnatal exposure to dichlorvos. In both rat and rabbit 
developmental studies, no developmental effects were observed. In the 
reproduction study, the parental/systemic NOAEL/LOAEL was 2.3/8.3 mg/
kg/day which was identical to the reproductive/offspring NOAEL/LOAEL. 
The DNT showed evidence of susceptibility in one parameter, auditory 
startle amplitude. However, there are no residual concerns for 
susceptibility from this because the affects in pups were seen at a 
dose well above the points of departure upon which EPA is regulating 
and a clear NOAEL for the effect (again, well above the points of 
departure) was identified. In addition, using a Benchmark Dose Methods 
(BMD) analysis of studies with pup and adult cholinesterase depression 
results did not demonstrate any substantial numerical differences in 
BMDL values for either RBC or brain cholinesterase between young and 
adult animals.
    (3) Although the exposure estimate for DDVP in food is highly 
refined as to some commodities, EPA is confident that its DDVP exposure 
estimate from food, if anything overstates DDVP exposure, given the 
many conservatisms retained in the exposure assessment and DDVP's 
documented volatility and rapid degradation. Additionally, the very 
conservative estimate on DDVP exposure through drinking water based on 
the use of trichlorfon on turf and naled on brassica is likely to 
significantly overstate DDVP exposure. Finally, EPA believes its 
residential exposure estimates will also not underestimate exposure 
given the conservative assumptions used in the

[[Page 68695]]

assessment and in EPA's residential exposure models and the data on 
residential exposure.
    With respect to the Mehl study, NRDC has mischaracterized the 
issue. Although the Mehl study raised an initial concern for potential 
developmental neurotoxicity, this concern was resolved by the 
subsequent DNT studies.
    EPA has retained a FQPA safety factor of 3X for various residential 
risk assessments. This additional safety factor is due to these 
assessments' reliance on a LOAEL rather than a NOAEL. EPA chose a 
safety factor other than 10X based on its evaluation of the study in 
question. EPA determined that 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. The HSRB confirmed EPA's interpretation of this study in its 
review of the scientific merit of the study. Specifically, the HSRB 
concluded that ``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. 31 at 41).
    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. (Ref. 82). 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.
    Without in any way implying that there is anything improper with 
agency decisionmakers making a FQPA safety factor determination, NRDC's 
comments about who made the decision on the FQPA safety factor for DDVP 
can be dismissed because NRDC is referring a prior decision on the FQPA 
safety factor pre-dating the submission of the DNT.

E. Conclusion

    NRDC's petition to revoke all DDVP tolerances is denied. NRDC's 
arguments have not convinced EPA that the DDVP tolerances are unsafe; 
to the contrary, EPA finds that its risk assessments show that the DDVP 
tolerances pose a reasonable certainty of no harm. EPA specifically 
rejects NRDC's claims that (1) EPA has mischaracterized the hazard 
posed by DDVP; (2) dietary and residential exposure to DDVP pose a risk 
of concern; and (3) EPA failed to justify removal of the additional 10X 
safety factor for the protection of infants and children.

VIII. Regulatory Assessment Requirements

    As indicated previously, this action announces the Agency's order 
denying a petition filed, in part, under section 408(d) 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.

IX. 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).

X. References

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W. Hauswirth to George LaRocca, Second

[[Page 68696]]

Peer Review of Dichlorvos -- evalution Following the September 23, 1987 
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0223 (December 3, 1991).
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to George Gray, Subject: April 4-6, 2006 Meeting EPA Human Studies 
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EPA, Memorandum from William Dykstra to Eric Olson, Review of 
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EPA, Memorandum from Jocelyn Stewart to Christina Schletema, Review of 
Toxicity Studies on Dichlorvos Using Human Volunteers(March 24, 1998) 
(MRIDs 44317901, 4416201, 44248801, 44248802).
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EPA, Health Effects Test Guidelines: OPPTS 870.4100 Chronic Toxicity 
(August 1998).
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from Kerry L. Dearfield to Judith Hauswirth, Review of in vivo 
mutagenicity studies concerning Dichlorvos (August 10, 1988).
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Final Report of the Expert Panel (July 22, 1998).
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Irving Mauer to Susan Hummel and Robert McNally/Pamela Noyes, 
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Mutagenicity Potential, Presented by the Blue Ribbon Panel in: An 
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the the Expert Panel (April 6, 1999).
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Toxicity of Dichlorvos in Wistar Rats, Toxicology 213, 129-137 (2005).
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(August 1998).
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Project ID HLA 6274-105. Unpublished study prepared by Hazleton 
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(dichlorvos); Poultry Dermal Metabolism Study (December 17, 1993).
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DDVP -- Review of Metabolism of DDVP in Rats (October 19, 1990).
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(dichlorvos); Goat Metabolism Study Following Dermal Application for 3 
Consecutive Days (July 21, 1993).
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25, 1992).
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to Amy Rispin and William Miller, Registration Standard for Naled (June 
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Shell Chemical Co., Washington, DC; CDL:000935-B).

[[Page 68697]]

    53. Rosenfeld, G. (1984) Guinea Pig Sensitization Study (Buehler): 
Study #1097F. Unpublished study prepared by Cosmopolitan Safety 
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EPA, Memorandum from Ibrahim Abdel-Saheb to Eric Olson and Susan 
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from Naled (PC Code 034401), and from Trichlorfon (PC Code 057901); DP 
Barcode: D288834 (March 16, 2003).
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Criteria and Assessment Office, Office of Health and Environmental 
Assessment, (October 1994).


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List of Subjects

    Environmental protection, pesticides and pest.


    Dated: November 16, 2007
Debra Edwards,
Director, Office of Pesticide Programs.

[FR Doc. E7-23571 Filed 12-4-07; 8:45 a.m.]

BILLING CODE 6560-50-S
