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 eCFR 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 EPAHQOPP20020302 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 EPAHQOPP20020302, by one of the following methods:

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
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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 nonoccupational 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 postnatal 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. 136a1). 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. 300j17).
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 preharvest 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 nondetectable 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 overtolerance 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 shortterm (e.g., ``acute'') and longerterm (e.g., ``chronic'') adverse effects from pesticide exposure. (Ref. 2 at 810). EPA also considers whether the ``effect'' has a threshold a level below which exposure has no appreciable chance of causing the adverse effect. For nonthreshold 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 nonthreshold effect. (Ref. 2 at 89). Not all carcinogens, however, pose a risk at any exposure level (i.e., ``a nonthreshold 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 assessmenti. 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 1316). 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 nondietary, and often for combined dietary and nondietary, 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 nondietary exposures, EPA typically examines shortterm, intermediateterm, and longterm exposures. Additionally, nondietary 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 viceversa.

ii. Nonthreshold effects. For risk assessments for nonthreshold 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 doseresponse curve for the nonthreshold 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 doseresponse 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 nonoccupational 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 worstcase 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 1728).
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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 highend 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 shortterm 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 (``DEEMFCID'') to estimate exposure by combining data on human consumption amounts with residue values in food commodities. DEEMFCID also compares exposure estimates to appropriate RfD/PAD values to estimate risk. DEEMFCID can estimate exposure for the general U.S. population as well as 32 subgroups based on age, sex, ethnicity, and region. DEEMFCID is closely modeled on its predecessor program DEEM. DEEMFCID 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 DEEMFCID is relatively simple.

DEEMFCID contains consumption and demographic information on the individuals who participated in the USDA's Continuing Surveys of Food Intake by Individuals (``CSFII'') in 19941996 and 1998. The 1998 survey was a special survey required by the FQPA to supplement the number of children survey participants. DEEMFCID 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 readytoeat food. Data on residue values for a particular pesticide and the RfD/PADs for that pesticide have to be inputted into the DEEMFCID program to estimate exposure and risk.

DEEMFCID 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, DEEMFCID 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, DEEMFCID 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 DEEMFCID 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 DEEMFCID 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 DEEMFCID 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 probabilisticallyderived 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.
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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, 3005830065 (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 twotiered 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 19951999. 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 (SCIGROW) model. Currently, EPA has no second tier groundwater model.

EPA's water exposure models have been extensively peerreviewed 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 underestimated 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 3006130064).

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 postapplication exposures in a residential setting where pesticidespecific 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 pesticidespecific 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 cholinesteraseinhibiting pesticides. The policy focuses on three types of effects associated with cholinesteraseinhibiting 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 cholinesteraseinhibiting 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 cholinesteraseinhibiting 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
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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 cholinesteraseinhibiting 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 90day exposures.'' (Id. at 27).

Cholinesterase inhibition in the blood is one step further removed from the direct harmful consequences of cholinesteraseinhibiting 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 cholinesteraseinhibiting 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 weightofthe 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 weightoftheevidence analysis. This weightoftheevidence 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 doseresponse (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 (interspecies safety factor) and differences among humans (intraspecies 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 postnatal toxicity. In examining these factors, EPA strives to make sure that its choice of a safety factor, based on a weightofthe evidence evaluation, does not understate the risk to children. (Id. at 2425, 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 twotier 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 7155471555).

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 shortterm in vitro and in vivo assays for the Tier 1 screening exercise. (63 FR at 7155071551). 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 longerterm 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, 2dichlorovinyl 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 nonfood areas of foodhandling 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 cholinesteraseinhibiting 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 nonoccupational 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 postnatal, 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
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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 nontoxic 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 inhome 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. Cancera. 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 weightoftheevidence 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; 85:24952) 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):658591) found that these me

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 204600001; telephone number: (703) 6030065; email address: bartow.susan@epa.gov.