[Federal Register Volume 74, Number 93 (Friday, May 15, 2009)]
[Rules and Regulations]
[Pages 23045-23095]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E9-11396]



[[Page 23045]]

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Part III





Environmental Protection Agency





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40 CFR Part 180



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Carbofuran; Final Tolerance Revocations; Final Rule

Federal Register / Vol. 74, No. 93 / Friday, May 15, 2009 / Rules and 
Regulations

[[Page 23046]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2005-0162; FRL-8413-3]


Carbofuran; Final Tolerance Revocations

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: EPA is revoking all tolerances for carbofuran. The Agency has 
determined that the risk from aggregate exposure from the use of 
carbofuran does not meet the safety standard of section 408(b)(2) of 
the Federal Food, Drug, and Cosmetic Act (FFDCA).

DATES: This final rule is effective August 13, 2009. Written 
objections, requests for a hearing, or requests for a stay identified 
by the docket identification (ID) number EPA-HQ-OPP-2005-0162 must be 
received on or before July 14, 2009, 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: Written objections and hearing requests, identified by the 
docket ID number EPA-HQ-OPP-2005-0162, may be submitted to the Hearing 
Clerk by one of the following methods:
     Mail: U.S. EPA Office of the Hearing Clerk, Mailcode 1900 
L, 1200 Pennsylvania Ave., NW., Washington, DC 20460-0001.
     Delivery: U.S. EPA Office of the Hearing Clerk, 1099 14th 
St., NW., Suite 350, Franklin Court, Washington, DC 20005. Deliveries 
are only accepted during the Office'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 Office's telephone number is (202) 564-6262.
    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-2005-0162, 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.
    Docket: All documents in the docket are listed in the docket index. 
Although listed in the index, some information is not publicly 
available, e.g., 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.
    Submitting CBI. Do not submit this information to EPA through 
regulations.gov or e-mail. Clearly mark the part or all of the 
information that you claim to be CBI. For CBI information in a disk or 
CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM as 
CBI and then identify electronically within the disk or CD-ROM the 
specific information that is claimed as CBI. In addition to one 
complete version of the objection that includes information claimed as 
CBI, a copy of the objection that does not contain the information 
claimed as CBI must be submitted for inclusion in the public docket. 
Information so marked will not be disclosed except in accordance with 
procedures set forth in 40 CFR part 2.

FOR FURTHER INFORMATION CONTACT: Jude Andreasen, Special Review and 
Reregistration Division (7508P), Office of Pesticide Programs, 
Environmental Protection Agency, 1200 Pennsylvania Ave, NW., 
Washington, DC 20460-0001; telephone number: (703) 308-9342; e-mail 
address: [email protected].

SUPPLEMENTARY INFORMATION: 

I. General Information

A. Does This Action Apply to Me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
Potentially affected entities may include, but are not limited to:
     Crop production (NAICS code 111).
     Animal production (NAICS code 112).
     Food manufacturing (NAICS code 311).
     Pesticide manufacturing (NAICS code 32532).
    This listing is not intended to be exhaustive, but rather provides 
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 North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether this action might apply to certain entities. To determine 
whether you or your business may be affected by this action, you should 
carefully examine the applicability provisions in Unit II.A. 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. What Can I Do if I Wish the Agency To Maintain a Tolerance That the 
Agency Has Revoked?

    Any affected party has 60 days from the date of publication of this 
order to file objections to any aspect of this order with EPA and to 
request an evidentiary hearing on those objections (21 U.S.C. 
346a(g)(2)). A person may raise objections without requesting a 
hearing.
    The objections submitted must specify the provisions of the 
regulation deemed objectionable and the grounds for the objection (40 
CFR 178.25). Each objection must be accompanied by the fee prescribed 
by 40 CFR 180.33(i). If a

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hearing is requested, the objections must include a statement of the 
factual issue(s) on which a hearing is requested, the requestor's 
contentions on such issues, and a summary of any evidence relied upon 
by the objector (40 CFR 178.27).
    Although any person may file an objection, the substance of the 
objection must have been initially raised as an issue in comments on 
the proposed rule. As explained in the July 31, 2008 proposed rule (73 
FR 44864) (FRL-8378-8), EPA will treat as waived any issue not 
originally raised in timely submitted comments. Accordingly, EPA will 
not consider any legal or factual issue presented in objections that 
was not presented by a commenter in response to the proposed rule, if 
that issue could reasonably have been raised at the time of the 
proposal.
    Similarly, if you fail to file an objection to an issue resolved in 
the final rule within the time period specified, you will have waived 
the right to challenge the final rule's resolution of that issue (40 
CFR 178.30(a)). After the specified time, issues resolved in the final 
rule cannot be raised again in any subsequent proceedings on this rule. 
See Nader v EPA, 859 F.2d 747 (9th Cir. 1988), cert denied 490 US 1931 
(1989).
    You must file your objection or request a hearing on this 
regulation 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-2005-0162 in the subject line on the first page of 
your submission. All requests must be in writing, and must be received 
by the Hearing Clerk as required by 40 CFR part 178 on or before July 
14, 2009.
    EPA will review any objections and hearing requests in accordance 
with 40 CFR 178.30, and will publish its determination with respect to 
each in the Federal Register. A request for a hearing will be granted 
only to resolve factual disputes; objections of a purely policy or 
legal nature will be resolved in the Agency's final order, and will 
only be subject to judicial review pursuant to 21 U.S.C. 346a(h)(1), 
(40 CFR 178.20(c) and 178.32(b)(1)). A hearing will only be held if the 
Administrator determines that the material submitted shows the 
following: There is a genuine and substantial issue of fact; there is a 
reasonable probability that available evidence identified by the 
requestor would, if established, resolve one or more of such issues in 
favor of the requestor, taking into account uncontested claims to the 
contrary; and resolution of the issue(s) in the manner sought by the 
requestor would be adequate to justify the action requested (40 CFR 
178.30).

II. Introduction

A. What Action Is the Agency Taking?

    EPA is revoking all of the existing tolerances for residues of 
carbofuran. Currently, tolerances have been established on the 
following crops: Alfalfa, forage; alfalfa, hay; artichoke, globe; 
banana; barley, grain; barley, straw; beet, sugar roots; beet, sugar 
tops; coffee bean, green; corn, forage; corn, grain (including 
popcorn); corn, stover; corn, sweet, kernel plus cob; cotton, 
undelinted seed; cranberry; cucumber; grape; grape raisin; grape, 
raisin, waste; melon; milk; oat, grain; oat, straw; pepper; potato; 
pumpkin; rice, grain; rice, straw; sorghum, forage; sorghum, grain 
grain; sorghum, grain, stover; strawberry; soybean, forage; soybean, 
hay; squash; sugarcane, cane; sunflower, seed; wheat, grain; wheat, 
straw.
    As discussed at greater length in Unit VII., on September 29, 2008, 
the sole registrant of carbofuran pesticide products, FMC Corporation 
requested that EPA cancel certain registrations. Consistent with the 
request, the registrant indicated that it no longer seeks to maintain 
the tolerances associated with the domestic use of carbofuran on the 
eliminated crops, and therefore no longer opposes the revocation of 
those tolerances. No other commenter indicated any interest in 
maintaining these tolerances. EPA is therefore revoking the tolerances 
associated with those domestic uses on two separate grounds. The first 
is that the tolerances will no longer be necessary because the 
registrations for these uses have been canceled (74 FR 11551, March 18, 
2009) (FRL-8403-6). The tolerances that EPA is revoking on this basis 
are: Alfalfa, forage; alfalfa, hay; artichoke, globe; barley, grain; 
barley, straw; beet, sugar roots; beet, sugar tops; corn, fresh 
(including sweet); cotton, undelinted seed; cranberry; cucumber; grape; 
grape raisin; grape, raisin, waste; melon; oat, grain; oat, straw; 
pepper; rice, straw; sorghum, forage; sorghum, grain grain; sorghum, 
grain, stover; strawberry; soybean, forage; soybean, hay; squash; 
wheat, grain; and wheat, straw. The second basis is that EPA also 
finds, that as outlined in its July 31, 2008 proposed rule, revocation 
of these tolerances is warranted on the grounds that aggregate exposure 
to residues from these tolerances do not meet the safety standard of 
section 408(b)(2) of the FFDCA. The Agency is therefore revoking 
tolerances for these crops because aggregate dietary exposure to these 
residues of carbofuran, including all anticipated dietary exposures and 
all other exposures for which there is reliable information, is not 
safe.
    The remaining tolerances the commenters seek to retain are: Banana; 
coffee bean; corn, forage; corn, grain; corn, stover; milk; potato; 
pumpkin; rice, grain; sugarcane, cane; and sunflower, seed. EPA has 
determined that aggregate exposure to carbofuran greater than 0.000075 
milligrams/kilogram/day (mg/kg/day) (i.e., greater than the acute 
Population Adjusted Dose (aPAD)) does not meet the safety standard of 
section 408(b)(2) of the FFDCA. For the 11 remaining tolerances, based 
on the contribution from food alone, exposure levels are below EPA's 
level of concern. At the 99.9th percentile of exposure, aggregate 
carbofuran dietary exposure from food alone was estimated to range 
between 0.000020 mg/kg/day for children 6 to 12 years old (29% of the 
aPAD) and 0.000058 mg/kg/day (78% of the aPAD) for children 1 to 2 
years old, the population subgroup with the highest estimated dietary 
exposure. However, EPA's analyses show that those individuals--both 
adults and children--who receive their drinking water from sources 
vulnerable to carbofuran contamination are exposed to carbofuran levels 
that exceed EPA's level of concern--in some cases by orders of 
magnitude. This primarily includes those populations consuming drinking 
water from ground water from shallow wells in acidic aquifers overlaid 
with sandy soils that have had crops treated with carbofuran. Aggregate 
exposures from food and from drinking water derived from ground water 
in vulnerable areas (e.g., from shallow wells associated with sandy 
soils and acidic aquifers) result in significant estimated exceedances. 
The estimates for aggregate food and ground water exposure from such 
sources range between 780% of the aPAD for adults over 50 years, to 
9,400% of the aPAD for infants. Similarly, EPA analyses show 
substantial exceedances for those populations that obtain their 
drinking water from reservoirs (i.e., surface water) located in small 
agricultural watersheds, prone to runoff, and predominated by crops 
that are treated with carbofuran, even though there is more uncertainty 
associated with these exposure estimates. For example, estimated 
aggregate exposures from food and drinking water derived from surface 
water, based on corn use in Nebraska, range between 330% of the aPAD 
for

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youths 13 to 19 years old and 3,900% of the aPAD for infants.
    Every analysis EPA has performed has shown that estimated exposures 
from drinking water from each remaining domestic use significantly 
exceed EPA's level of concern for children. Accordingly, aggregate 
exposures from food and water significantly exceed safe levels. 
Although the magnitude of the exceedance varies depending on the level 
of conservatism in the assessment, the fact that in each case aggregate 
exposures to residues of carbofuran fail to meet the FFDCA section 
408(b)(2) safety standard, including where EPA relied on highly refined 
estimates of risk, using all relevant data and methods, strongly 
corroborates EPA's conclusion that aggregate exposures to residues of 
carbofuran are not safe.

B. Overview of Final Rule

    EPA's final rule preamble is organized primarily into two sections. 
Following a brief summary of the July 31, 2008 proposed rule, EPA 
summarizes the major comments received on the proposed rule, along with 
the Agency's responses in Unit VII. Because EPA only presents a summary 
of all of the comments received, readers are encouraged to also consult 
EPA's Response to Comments Documents, found in the docket for today's 
action (Refs. 111, 112, 113). These documents contain EPA's complete 
responses to all of the significant comments received on this 
rulemaking, and therefore will contain a more detailed explanation on 
many of the issues presented in Unit VII.
    Unit VIII. presents the results of EPA's analyses of carbofuran's 
dietary risks. This Unit generally describes the bases for the Agency's 
conclusions that carbofuran presents unacceptable dietary risks to 
children. Readers are also encouraged to consult EPA's underlying risk 
assessment support documents, identified in the References section, and 
contained in the docket for today's action, for a more detailed 
presentation of EPA's scientific analyses.
    Each of these units is generally organized consistent with the 
structure of a risk assessment. Each unit begins with a discussion of 
carbofuran's toxicity, and EPA's hazard identification, including a 
discussion of the issues surrounding the selection of the children's 
safety factor EPA has applied to this chemical. EPA then discusses 
issues relating to carbofuran's exposures from food and drinking water. 
The final section of each unit relates to EPA's conclusions regarding 
the risks from carbofuran's aggregate (i.e., food + water) exposures.

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

    EPA is taking this action, pursuant to the authority in FFDCA 
sections 408(b)(1)(b), 408(b)(2)(A), and 408(e)(1)(A). 21 U.S.C. 
346a(b)(1)(b), (b)(2)(A), (e)(1)(A).

III. Statutory and Regulatory Background

    A ``tolerance'' represents the maximum level for residues of 
pesticide chemicals legally allowed in or on raw agricultural 
commodities (including animal feed) and processed foods. Section 408 of 
FFDCA, 21 U.S.C. 346a, as amended by the Food Quality Protection Act 
(FQPA) of 1996, Public Law 104-170, authorizes the establishment of 
tolerances, exemptions from tolerance requirements, modifications to 
tolerances, and revocation of tolerances for residues of pesticide 
chemicals in or on raw agricultural commodities and processed foods. 
Without a tolerance or exemption, food containing pesticide residues is 
considered to be unsafe and therefore ``adulterated'' under section 
402(a) of the FFDCA, 21 U.S.C. 342(a). Such food may not be distributed 
in interstate commerce (21 U.S.C. 331(a)). For a food-use pesticide to 
be sold and distributed, the pesticide must not only have appropriate 
tolerances under the FFDCA, but also must be registered under the 
Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) (7 U.S.C. 
136 et seq.). Food-use pesticides not registered in the United States 
must have tolerances in order for commodities treated with those 
pesticides to be imported into the United States.
    Section 408(e) of the FFDCA, 21 U.S.C. 346a(e), authorizes EPA to 
modify or revoke tolerances on its own initiative. EPA is revoking 
these tolerances to implement the Agency's findings made during the 
reregistration and tolerance reassessment processes. As part of these 
processes, EPA is required to determine whether each of the existing 
tolerances meets the safety standard of section 408(b)(2) (21 U.S.C. 
346a(b)(2)). Section 408(b)(2)(A)(i) of the FFDCA requires EPA to 
modify or revoke a tolerance if EPA determines that the tolerance is 
not ``safe'' (21 U.S.C. 346a(b)(2)(A)(i)). Section 408(b)(2)(A)(ii) of 
the FFDCA defines ``safe'' 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). This includes exposure through drinking water 
and in residential settings, but does not include occupational 
exposure.
    Risks to infants and children are given special consideration. 
Specifically, section 408(b)(2)(C) states that EPA:

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

    (21 U.S.C. 346a(b)(2)(C)(i)(II) and (III)).
    This provision 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 final 
rule as the ``children's safety factor.''

IV. Carbofuran Background and Regulatory History

    In July 2006, EPA completed a refined acute probabilistic dietary 
risk assessment for carbofuran as part of the reassessment program 
under section 408(q) of the FFDCA. The assessment was conducted using 
Dietary Exposure Evaluation Model-Food Commodity Intake Database (DEEM-
FCID\TM\, Version 2.03), which incorporates consumption data from the 
United States Department of Agriculture's (USDA's) Nationwide 
Continuing Surveys of Food Intake by Individuals (CSFII), 1994-1996 and 
1998, as well as carbofuran monitoring data from USDA's Pesticide Data 
Program\1\ (PDP), estimated percent crop treated information, and 
processing/cooking factors, where applicable. The assessment was 
conducted applying a

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500-fold safety factor that included a 5X children's safety factor, 
pursuant to section 408(b)(2)(C). That refined assessment showed acute 
dietary risks from carbofuran residues in food above EPA's level of 
concern (Ref. 19). Since 2006, EPA has evaluated additional data 
submitted by the registrant, FMC Corporation, and has further refined 
its original assessment by incorporating more recent 2005/2006 PDP 
data, and by conducting additional analyses. In January 2008, EPA 
published a draft Notice of Intent to Cancel (NOIC) all carbofuran 
registrations, based in part on carbofuran's dietary risks. As mandated 
by FIFRA, EPA solicited comments from the FIFRA Scientific Advisory 
Panel (SAP) on its draft NOIC. Having considered the comments from the 
SAP, EPA initiated the process to revoke all carbofuran tolerances, 
publishing its proposed revocation on July 31, 2008 (73 FR 44864). The 
comment period for the proposed rule closed on September 29, 2008. 
Having considered all comments received by this date, EPA is now 
finalizing the revocation of all existing carbofuran tolerances. As 
noted above, aggregate exposures from food and water to the U.S. 
population at the upper percentiles of exposure substantially exceed 
the safe daily levels and thus are ``unsafe'' within the meaning of 
FFDCA section 408(b)(2) (Ref. 71). It is particularly significant that 
under every analysis EPA has conducted, the levels of carbofuran exceed 
the safe daily dose for children, even when EPA used the most refined 
data and models available. Based on these findings, EPA has decided to 
move expeditiously to address the unacceptable dietary risks to 
children. EPA anticipates issuing the NOIC subsequent to undertaking 
the activities required to revoke the carbofuran tolerances.
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    \1\ USDA's Pesticide Data Program monitors for pesticides in 
certain foods at the distribution points just before release to 
supermarkets and grocery stores.
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V. EPA's Approach to Dietary Risk Assessment

    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. A short summary is provided 
below to aid the reader. For further discussion of the regulatory 
requirements of section 408 of the FFDCA and a complete description of 
the risk assessment process, see http://www.epa.gov/fedrgstr/EPA-PEST/1999/January/Day-04/p34736.htm
    To assess the risk of a pesticide tolerance, EPA combines 
information on pesticide toxicity with information regarding the route, 
magnitude, and duration of exposure to the pesticide. The risk 
assessment process involves four distinct steps: (1) Identification of 
the toxicological hazards posed by a pesticide; (2) determination of 
the exposure ``level of concern'' for humans; (3) estimation of human 
exposure; and (4) characterization of human risk based on comparison of 
human exposure to the level of concern.

A. Hazard Identification and Selection of Toxicological Endpoint

    Any risk assessment begins with an evaluation of a chemical's 
inherent properties, and whether those properties have the potential to 
cause adverse effects (i.e., a hazard identification). EPA then 
evaluates the hazards to determine the most sensitive and appropriate 
adverse effect of concern, based on factors such as the effect's 
relevance to humans and the likely routes of exposure.
    Once a pesticide's potential hazards are identified, EPA determines 
a toxicological level of concern for evaluating the risk posed by human 
exposure to the pesticide. In this step of the risk assessment process, 
EPA essentially evaluates the levels of exposure to the pesticide at 
which effects might occur. An important aspect of this determination is 
assessing the relationship between exposure (dose) and response (often 
referred to as the dose-response analysis). In evaluating a chemical's 
dietary risks EPA uses a reference dose (RfD) approach, which involves 
a number of considerations including:
     A ``point of departure'' (PoD)--the value from a dose-
response curve that is at the low end of the observable data and that 
is the toxic dose that serves as the `starting point' in extrapolating 
a risk to the human population.
     An uncertainty factor to address the potential for a 
difference in toxic response between humans and animals used in 
toxicity tests (i.e., interspecies extrapolation).
     An uncertainty factor to address the potential for 
differences in sensitivity in the toxic response across the human 
population (for intraspecies extrapolation).
     The need for an additional safety factor to protect 
infants and children, as specified in FFDCA section 408(b)(2)(C).
    EPA uses the chosen PoD to calculate a safe dose or RfD. The RfD is 
calculated by dividing the chosen PoD by all applicable safety or 
uncertainty factors. Typically in EPA risk assessments, a combination 
of safety or uncertainty factors providing at least a hundredfold 
(100X) margin of safety is used: 10X to account for interspecies 
extrapolation and 10X to account for intraspecies extrapolation. 
Further, in evaluating the dietary risks for pesticide chemicals, 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 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 children's 
safety factor that does not correspond to one of the traditional 
additional uncertainty/safety factors used in general Agency risk 
assessment. 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. For acute assessments, the 
risk is expressed as a percentage of a maximum acceptable dose or the 
acute PAD (i.e., the acute dose which EPA has concluded will be 
``safe''). As discussed below in Unit V.C., dietary exposures greater 
than 100% of the acute PAD are generally cause for concern and would be 
considered ``unsafe'' within the meaning of FFDCA section 408(b)(2)(B). 
Throughout this document general references to EPA's calculated safe 
dose are denoted as an acute PAD, or aPAD, because the relevant point 
of departure for carbofuran is based on an acute risk endpoint.
    Carbofuran is a member of the class of pesticides called n-methyl 
carbamates (NMCs). The primary toxic effect caused by NMCs, including 
carbofuran, is neurotoxicity resulting from inhibition of the enzyme 
acetylcholinesterase (AChE, See Unit VIII.A.). The toxicity profile of 
these pesticides is characterized by rapid time to onset of effects 
followed by rapid recovery (minutes to hours). Consistent with its 
mechanism of action, toxicity data on AChE inhibition from laboratory 
rats provide the basis for deriving the PoD for carbofuran.

B. Estimating Human Dietary Exposure Levels

    Pursuant to section 408(b) of the FFDCA, EPA has evaluated 
carbofuran's dietary risks based on ``aggregate exposure'' to 
carbofuran. By ``aggregate exposure,'' EPA is referring to exposure to 
carbofuran by multiple pathways of exposure. EPA uses available data 
and standard analytical methods, together with assumptions designed to 
be protective of public health, to produce separate estimates of 
exposure for a highly exposed subgroup of the general population, for 
each potential pathway and route of exposure. For acute risks,

[[Page 23050]]

EPA then calculates potential aggregate exposure and risk by using 
probabilistic \2\ techniques to combine distributions of potential 
exposures in the population for each route or pathway. For dietary 
analyses, the relevant sources of potential exposure to carbofuran are 
from the ingestion of residues in food and drinking water. The Agency 
uses a combination of monitoring data and predictive models to evaluate 
environmental exposure of humans to carbofuran.
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    \2\ Probabilistic analysis is used to predict the frequency with 
which variations of a given event will occur. By taking into account 
the actual distribution of possible consumption and pesticide 
residue values, probabilistic analysis for pesticide exposure 
assessments ``provides more accurate information on the range and 
probability of possible exposure and their associated risk values'' 
(Ref. 101). In capsule, a probabilistic pesticide exposure analysis 
constructs a distribution of potential exposures based on data on 
consumption patterns and residue levels and provides a ranking of 
the probability that each potential exposure will occur. People 
consume differing amounts of the same foods, including none at all, 
and a food will contain differing amounts of a pesticide residue, 
including none at all.
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    1. Exposure from Food. Data on the residues of carbofuran in foods 
are available from a variety of sources. One of the primary sources of 
data comes from federally conducted surveys, including the PDP 
conducted by the USDA. Further, market basket surveys, which are 
typically performed by registrants, can provide additional residue 
data. These data generally provide a characterization of pesticide 
residues in or on foods consumed by the U.S. population that closely 
approximates real world exposures because they are sampled closer to 
the point of consumption in the chain of commerce than field trial 
data, which are generated to establish the maximum level of legal 
residues that could result from maximum permissible use of the 
pesticide. In certain circumstances, when EPA believes the information 
will provide more accurate exposure estimates, EPA will rely on field 
trial data (see below in Unit VIII.E.1.).
    EPA uses a computer program known as the DEEM-FCID\TM\ to estimate 
exposure by combining data on human consumption amounts with residue 
values in food commodities. DEEM-FCID\TM\ also compares exposure 
estimates to appropriate RfD or PAD values to estimate risk. EPA uses 
DEEM-FCID\TM\ to estimate exposure for the general U.S. population as 
well as for 32 subgroups based on age, sex, ethnicity, and region. 
DEEM-FCID\TM\ allows EPA to process extensive volumes of data on human 
consumption amounts and residue levels in making risk estimates. 
Matching consumption and residue data, as well as managing the 
thousands of repeated analyses of the consumption database conducted 
under probabilistic risk assessment techniques, requires the use of a 
computer.
    DEEM-FCID\TM\ contains consumption and demographic information on 
the individuals who participated in the USDA's 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\TM\ 
also contains ``recipes'' that convert foods as consumed (e.g., pizza) 
back into their component raw agricultural commodities (e.g., wheat 
from flour, or tomatoes from sauce). 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 or PADs for that pesticide are inputs to the 
DEEM-FCID\TM\ program to estimate exposure and risk.
    For carbofuran's assessment, EPA used DEEM-FCID\TM\ to calculate 
risk estimates based on a probabilistic distribution. DEEM-FCID\TM\ 
combines the full range of residue values 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\TM\ 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 a value selected randomly from the 
concentration data sets. The exposure amounts for the thousands of 
person-days in the CSFII are then collected in a frequency 
distribution. EPA also uses DEEM-FCID\TM\ to compute 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 consumption and residue levels into a distribution of 
potential exposures and risk requires use of probabilistic techniques.
    The probabilistic technique that DEEM-FCID\TM\ uses to combine 
differing levels of consumption and residues involves the following 
steps:
    (1) Identification of any food(s) that could bear the residue in 
question for each person-day in the CSFII.
    (2) Calculation of an exposure level for each of the thousands of 
person-days in the CSFII database, 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.
    (4) Collection of all of the hundreds of thousands of potential 
exposures estimated in Steps  2 and 3 in a frequency 
distribution.
    The resulting probabilistic assessment presents a range of 
exposure/risk estimates.
    2. Exposure from water. EPA may use field monitoring data and/or 
simulation water exposure models to generate pesticide concentration 
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 the 
specific agricultural or residential pesticide practices in specific 
locations, under the environmental conditions associated with a 
sampling design (i.e., the locations of sampling, the times of the year 
samples were taken, and the frequency by which samples were collected). 
Although monitoring data can provide a direct measure of the 
concentration of a pesticide in water, it does not always provide a 
reliable basis for estimating spatial and temporal variability in 
exposures because sampling may not occur in areas with the highest 
pesticide use, and/or when the pesticides are being used and/or at an 
appropriate sampling frequency to detect high concentrations of a 
pesticide that occur over the period of a day to several days.
    Because of the limitations in most monitoring studies, EPA's 
standard approach is to use simulation water exposure models as the 
primary means to estimate pesticide exposure levels in drinking water. 
Modeling is a useful tool for characterizing vulnerable sites, and can 
be used to estimate peak pesticide water concentrations from 
infrequent, large rain events. EPA's computer models use detailed 
information on soil properties, crop characteristics, and weather 
patterns to estimate water concentrations in vulnerable locations where 
the pesticide could be used according to its label (69 FR 30042, 30058-
30065, May 26, 2004) (FRL-7355-7). These models calculate estimated 
water concentrations of pesticides using laboratory data that describe 
how fast the pesticide breaks down to other chemicals and how it moves 
in the environment at these vulnerable locations. The modeling provides 
an estimate of pesticide concentrations in ground water and surface 
water. Depending on the modeling algorithm (e.g., surface water 
modeling scenarios), daily concentrations can be estimated

[[Page 23051]]

continuously over long periods of time, and for places that are of most 
interest for any particular pesticide.
    EPA relies on models it has developed for estimating pesticide 
concentrations in both surface water and ground water. Typically EPA 
uses a two-tiered approach to modeling pesticide concentrations in 
surface and ground water. 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 for 
surface water is actually a combination of two models: The Pesticide 
Root Zone Model (PRZM) and the Exposure Analysis Model System (EXAMS). 
The second tier model for ground water uses PRZM alone.
    A detailed description of the models routinely used for exposure 
assessment is available from the EPA OPP Water Models web site: http://www.epa.gov/oppefed1/models/water/index.htm. These models provide a 
means for EPA to estimate daily pesticide concentrations in surface 
water sources of drinking water (a reservoir) using local soil, site, 
hydrology, and weather characteristics along with pesticide application 
and agricultural management practices, and pesticide environmental fate 
and transport properties. Consistent with the recommendations of the 
FIFRA SAP, EPA also considers regional percent cropped area factors 
(PCA) which take into account the potential extent of cropped areas 
that could be treated with pesticides in a particular area. The PRZM 
and EXAMS models used by EPA were developed by EPA's Office of Research 
and Development (ORD), and are used by many international pesticide 
regulatory agencies to estimate pesticide exposure in surface water. 
EPA's use of the PCA area factors and the Index Reservoir scenario was 
reviewed by the FIFRA SAP in 1999 and 1998, respectively (Refs. 37 and 
38).
    In modeling potential surface water concentrations, EPA attempts to 
model areas of the country that are vulnerable to surface water 
contamination rather than simply model ``typical'' concentrations 
occurring across the nation. Consequently, EPA models exposures 
occurring in small highly agricultural watersheds in different growing 
areas throughout the country, over a 30-year period. The scenarios are 
designed to capture residue levels in drinking water from reservoirs 
with small watersheds with a large percentage of land use in 
agricultural production. EPA believes these assessments are likely 
reflective of a small subset of the watersheds across the country that 
maintain drinking water reservoirs, representing a drinking water 
source generally considered to be more vulnerable to frequent high 
concentrations of pesticides than most locations that could be used for 
crop production.
    EPA uses the output of daily concentration values from tier two 
modeling as an input to DEEM-FCID\TM\, which combines water 
concentrations with drinking water consumption information in the daily 
diet to generate a distribution of exposures from consumption of 
drinking water contaminated with pesticides. These results are then 
used to calculate a probabilistic assessment of the aggregate human 
exposure and risk from residues in food and drinking water.
    3. Aggregate exposure analyses. Using probabilistic analyses, EPA 
combines the national food exposures with the exposures derived for 
individual region and crop-specific drinking water scenarios to derive 
estimates of aggregate exposure. Although food is distributed 
nationally, and residue values are therefore not expected to vary 
substantially throughout the country, drinking water is locally derived 
and concentrations of pesticides in source water fluctuate over time 
and location for a variety of reasons. Pesticide residues in water 
fluctuate daily, seasonally, and yearly as a result of the timing of 
the pesticide application, the vulnerability of the water supply to 
pesticide loading through runoff, spray drift and/or leaching, and 
changes in the weather. Concentrations are also affected by the method 
of application, the location and characteristics of the sites where a 
pesticide is used, the climate, and the type and degree of pest 
pressure.
    EPA's standard acute dietary exposure assessment calculates total 
dietary exposure over a 24-hour period; that is consumption over 24 
hours is summed and no account is taken of the fact that eating and 
drinking occasions may spread out exposures over a day. This total 
daily exposure generally provides reasonable estimates of the risks 
from acute dietary exposures, given the nature of most chemical 
endpoints. Due to the rapid recovery associated with carbofuran 
toxicity (AChE inhibition), 24-hour exposure periods may or may not, a 
priori, be appropriate. To the extent that a day's eating or drinking 
occasions leading to high total daily exposure might be found close 
together in time, or to occur from a single eating event, minimal AChE 
recovery would occur between eating occasions (i.e., exposure events). 
In that case, the ``24-hour sum'' approach, which sums eating events 
over a 24-hour period, would provide reasonable estimates of risk from 
food and drinking water. Conversely, to the extent that eating 
occasions leading to high total daily exposures are widely separated in 
time (within 1 day) such that substantial AChE recovery occurs between 
eating occasions, then the estimated risks under any 24-hour sum 
approach may be overstated. In that case, a more sophisticated approach 
- one that accounts for intra-day eating and drinking patterns and the 
recovery of AChE between exposure events -- may be more appropriate. 
This approach is referred to as the ``Eating Occasions Analysis'' and 
it takes into account the fact that the toxicological effect of a first 
dose may be reduced or tempered prior to a second (or subsequent) dose.
    Thus, rather than treating a full day's exposure as a one-time 
``bolus'' dose, as is typically done in the Agency's assessments, the 
Eating Occasion Analysis uses the actual time of eating or drinking 
occasion, and amounts consumed as reported by individuals to the USDA 
CSFII. The actual CSFII-recorded time of each eating event is used to 
``separate out'' the exposures due to each eating occasion; in doing 
so, this ``separation'' allows the Agency to distinguish between each 
intake event and account for the fact that at least some partial 
recovery of AChE inhibition attributable to the first (earlier) 
exposure occurs before the second exposure event. For chemicals for 
which the toxic effect is rapidly reversible, the time between two (or 
more) exposure events permits partial to full recovery from the toxic 
effect from the first exposure and it is this ``partial recovery'' that 
is specifically accounted for by the Eating Occasion Analysis. More 
specifically, an estimated ``persisting dose'' from the first exposure 
event is added to the second exposure event to account for the partial 
recovery of AChE inhibition that occurs over the time between the first 
and second exposures. The ``persisting dose'' terminology, and this 
general approach were originally offered by the FIFRA SAP in the 
context of assessing AChE inhibition from cumulative exposures to 
organophosphorous pesticides (OPs) (Ref. 40).

C. Selection of Acute Dietary Exposure Level of Concern

    Because probabilistic assessments generally present a realistic 
range of residue values to which the population may be exposed, EPA's 
starting point for estimating exposure and risk for such aggregate 
assessments is the 99.9th percentile of the population under

[[Page 23052]]

evaluation, which represents one person out of every 1,000 persons. 
When using a probabilistic method of estimating acute dietary exposure, 
EPA typically assumes that, when the 99.9th percentile of acute 
exposure is equal to or less than the aPAD, the level of concern for 
acute risk has not been exceeded. By contrast, where the analysis 
indicates that estimated exposure at the 99.9th percentile exceeds the 
aPAD, EPA would generally conduct one or more sensitivity analyses to 
determine the extent to which the estimated exposures at the high-end 
percentiles may be affected by unusually high food consumption or 
residue values. To the extent that one or a few values seem to 
``drive'' the exposure estimates at the high end of exposure, EPA would 
consider whether these values are reasonable and should be used as the 
primary basis for regulatory decision making (Ref. 101).

VI. Summary of the Proposed Rule

    EPA proposed to revoke all of the existing tolerances for residues 
of carbofuran on the grounds that aggregate exposure from all uses of 
carbofuran fail to meet the FFDCA section 408 safety standard (73 FR 
44864). Based on the contribution from food alone, EPA calculated that 
dietary exposures to carbofuran exceeded EPA's level of concern for all 
of the more sensitive subpopulations of infants and children. At the 
99.9th percentile, carbofuran dietary exposure from food alone was 
estimated at 0.000082 mg/kg/day (110% of the aPAD) for children 3-5 
years old, the population subgroup with the highest estimated dietary 
exposure (Ref. 16). In addition, EPA's analyses showed that those 
individuals--both adults as well as children--who receive their 
drinking water from vulnerable sources are also exposed to levels that 
exceed EPA's level of concern--in some cases by orders of magnitude. 
This primarily included those populations consuming drinking water from 
ground water from shallow wells in acidic aquifers overlaid with sandy 
soils that have had crops treated with carbofuran. It also included 
those populations that obtain their drinking water from reservoirs 
located in small agricultural watersheds, prone to runoff, and 
predominated by crops that are treated with carbofuran, although there 
was more uncertainty associated with these exposure estimates. The 
proposal discussed a number of sensitivity analyses the Agency had 
conducted in order to further characterize the potential risks to 
children. Every one of these sensitivity analyses determined that 
estimated exposures significantly exceeded EPA's level of concern for 
children.

VII. Summary of Public Comments and EPA Responses

    This section presents a summary of some of the significant comments 
received on the proposed rule, as well as the Agency's responses. More 
detailed responses to these comments, along with the Agency's responses 
to other comments received can be found in the Response to Comments 
Documents, located in the docket for this rulemaking (Refs. 111, 112, 
and 113).

A. Tolerances Associated With Voluntarily Canceled Uses

    On September 29, 2008, the registrant, FMC Corporation requested 
EPA to eliminate several uses from their end-use products. Consistent 
with this request, the registrant has indicated that it no longer seeks 
to maintain the tolerances associated with the domestic use of these 
products, and therefore no longer opposes the revocation of those 
tolerances. No other commenter indicated any interest in maintaining 
these tolerances. EPA is therefore revoking the tolerances associated 
with those domestic uses, on two separate grounds. The first ground is 
that the tolerances will no longer be necessary because the 
registrations for these uses have been canceled. The tolerances that 
EPA is revoking on this basis are: Alfalfa, forage; alfalfa, hay; 
artichoke, globe; barley, grain; barley, straw; beet, sugar roots; 
beet, sugar tops; corn, fresh (including sweet); corn, popcorn; cotton, 
undelinted seed; cranberry; cucumber; grape; grape raisin; grape, 
raisin, waste; melon; oat, grain; oat, straw; pepper; rice, straw; 
sorghum, forage; sorghum, grain grain; sorghum, grain, stover; 
strawberry; soybean, forage; soybean, hay; squash; wheat, grain; and 
wheat, straw.
    EPA also finds, however, that revocation of these tolerances is 
warranted on the grounds that aggregate exposures to these residues of 
carbofuran do not meet the safety standard of section 408(b)(2) of the 
FFDCA. The Agency is therefore revoking tolerances for these crops 
because aggregate dietary exposures to residues of carbofuran, 
including all anticipated dietary exposures and all other exposures for 
which there is reliable information, are not safe.
    As noted in the proposed rule, based on the contribution from only 
the foods bearing residues resulting from all of these tolerances, 
dietary exposures to carbofuran would be unsafe for the more sensitive 
children's subpopulations. At the 99.9th percentile, carbofuran dietary 
exposure from food alone was estimated at 0.000082 mg/kg/day (110% of 
the aPAD) for children 3-5 years old, the population subgroup with the 
highest estimated dietary exposure (Ref. 70). In addition, as discussed 
in more detail, both in the proposed rule, and in Unit VIII.E.2. below, 
drinking water residues of carbofuran contribute significantly to 
unsafe aggregate exposures. Accordingly, it has not been shown that 
exposures from these uses would meet the FFDCA safety standard.

B. Comments Relating to EPA's Toxicology Assessment

    1. Comments relating to EPA's PoD. One group of commenters stated 
that the studies clearly support EPA's conclusion that the post-natal 
day (PND)11 brain data on the inhibition of AChE in juvenile rats 
provide the most appropriate PoD for risk assessment. The commenters 
also claimed, however, that ``the specific PoD proposed by EPA is 0.03 
mg/kg/day, but our analysis of the best data for the risk assessment 
are found in the good laboratory practices (GLP) compliant studies and 
those studies support 0.033 as a better value for the PND11 rat.'' This 
group of commenters also described an analysis their consultant had 
conducted. According to the commenters, their consultant calculated the 
value of 0.033 mg/kg/day/day from the BMD10s and 
BMDL10s \3\ in the four FMC studies with first observation 
time equal to 0.25 hours. The BMDs and BMDLs were calculated separately 
for each of these datasets. The results for the four datasets were 
combined, but, unlike EPA's analyses, the datasets themselves were not 
combined.
---------------------------------------------------------------------------

    \3\ BMD is an abbreviation for benchmark dose. The 
BMDL10 is the lower 95% confidence limit on the 
BMD10. The BMD10 is the estimated dose (i.e., 
benchmark dose) to result in 10% AChE inhibition. EPA uses the BMDL, 
not the BMD, as the point of departure.
---------------------------------------------------------------------------

    With respect to using the PND11 rat pup data as the PoD, the Agency 
acknowledges this area of agreement with the commenters. Ultimately, 
the BMDL10 recommended by the commenters differs from the 
EPA's BMDL10 by only 6% (0.031 mg/kg/day vs. 0.033 mg/kg/
day), a difference that is not biologically significant. Moreover, when 
rounded to one significant digit, as is done by typical convention and 
consistent with the dose information provided in the comparative 
cholinesterase (ChE) studies (also called CCA studies), both values 
yield the identical PoD of 0.03 mg/kg/day.
    Moreover, the Agency notes that the value of 0.033 mg/kg/day 
recommended

[[Page 23053]]

by the commenter does not include the 0.5-hr time-point from MRID no. 
47143705 although this dataset yielded the lowest BMDL for individual 
datasets reported by the commenters. As such, the commenter's 
recommended value does not include all of the relevant data collected 
at the time of peak effect. The commenters have provided no rationale 
for why it would be appropriate to selectively exclude data from the 
time frame in this study most relevant to the risk assessment. 
Accordingly, as noted in footnote 115 of the comment, when the 
commenters included the data at 0.5-hr timepoint from MRID no. 
47143705, the BMDL10 was lowered from 0.033 to 0.030 mg/kg/
day--a value almost identical to the Agency's BMDL10 of 
0.031 mg/kg/day.
    Thus, although the commenters are critical of the Agency's 
approach, there is basic consensus between EPA and the commenters that 
the PoD is 0.03 mg/kg/day given the precision of available data in 
deriving the BMDL10.
    The Agency also notes that specific details about the commenter's 
BMD modeling were not provided to the Agency. The Agency is therefore 
unable to fully evaluate the scientific validity of the modeling 
procedure used by the commenter.
    Some commenters claimed that ``EPA's derivation of its PoD, 
however, is not transparent and is not scientifically supported. 
Equally important, based on a recent review of the raw data from the 
Moser study (obtained via a FOIA request originally filed in April 
2008), we believe that the Moser study may not meet minimum criteria 
for scientific acceptability. Critical data are simply unavailable for 
this study, including: a complete protocol, analysis of dosing 
solutions, clinical observations, standardization of brain and red 
blood cell (RBC) AChE results in terms of amount per unit of protein, 
and quality assurance records of inspections for the carbofuran portion 
of the study.'' As a result, the commenters assert that the better 
approach is to use the brain AChE inhibition values calculated from the 
GLP-compliant registrant studies, because the commenters claim that EPA 
has acknowledged them to be valid, and which the commenters claim are 
fully documented. Using EPA's BMD dose-time response model, the 
commenters claim that the correct PoD is 0.033 mg/kg/day.
    The Agency disagrees with the commenters' assertions that the 
derivation of the PoD was not transparent. The Agency's analysis, 
computer code, and data have been placed in the docket for public 
scrutiny. EPA's models have been repeatedly reviewed and approved by 
the FIFRA SAP (Refs. 42, 43, and 44), and, as part of that process, 
been made available to the public. The most recent occasion was as part 
of the February 2008 FIFRA SAP meeting on the draft carbofuran NOIC. As 
EPA has explained numerous times, the Agency has not deviated from its 
standard practice. Most recently, EPA laid out its approach at length 
in the proposed rule. While it is true that EPA may not have repeated 
in this most recent analysis all of the specifics that it has 
previously provided, it is inaccurate for the commenter to claim that 
the information is not available, or that its review has in any way 
been hampered by this so-called lack of transparency. Indeed, given 
that the commenters appear to have been able to duplicate EPA's 
analyses, it seems reasonable to assume that the information was 
available. It is further worth noting that the commenters had 
sufficient access to the Moser data to allow a complete re-analysis 
before the 2008 SAP on the draft carbofuran NOIC, which was months 
before the FOIA request was filed with the Agency. In addition, a 
complete study protocol as well as a report of the quality assurance 
(QA) technical and data reviews of the study were included in the 
documents provided in response to the FOIA request. The Agency further 
notes that although the commenters complain about their perceived lack 
of transparency in EPA's BMD calculations, they did not provide any 
detailed information about the derivation of their proposed value.
    EPA also disagrees with the claim that EPA's PoD is not 
scientifically supported. As an initial matter, EPA notes that the 
commenters' suggested PoD of 0.033 mg/kg/day is not significantly 
different than EPA's PoD of 0.03 mg/kg/day (see Unit VIII.B.). The 
criticisms of the Moser study are also incorrect. The procedures and 
documentation are in accordance with the ORD Quality Assurance 
Management Plan. Concerning standardization of brain and RBC AChE in 
terms of protein, it is interesting to note that, despite their 
complaints that EPA had failed to do this, the registrant also failed 
to do this in their own studies. However, in the Moser study, the AChE 
activity was standardized in terms of tissue weight per ml, so the 
amount of protein was consistent across samples. This is an acceptable 
and widely used practice. Further, abnormal (or ``clinical'') 
observations were recorded when they occurred; however, it is not 
technically possible to observe the animals while they are being tested 
for motor activity. Finally, the registrant is correct that the dosing 
solutions for the CCA study were not analyzed, but this was done for 
the adult studies in McDaniel et al., (2007), and the preparation and 
stability of the carbofuran samples were confirmed therein.
    If, however, the Agency elected to follow the commenters' 
recommendation to not use the ORD data in the risk assessment, there 
would be no high quality RBC AChE inhibition data available in juvenile 
rats. As such, there would be no surrogate data evaluating AChE 
inhibition in the peripheral nervous system (PNS), much less any data 
from the PNS itself. As discussed in Unit VIII.C., with the 
availability of some RBC data from ORD evaluating the effects in the 
PNS, the Agency is able to reduce the children's safety factor from 10X 
to 4X. Without the ORD data, the Agency would be required to retain the 
statutory 10X.
    Some commenters raised concern that EPA's PoD was not sufficiently 
protective. The commenters point to comments from the February SAP 
review of EPA's draft carbofuran NOIC, quoting the following language 
from the report, which indicated concern that the starting point used 
in the risk assessment was not sufficiently protective:

    Some Panel members questioned the assumption that a 10% level of 
brain AChE inhibition (i.e., BMD10) is sufficiently 
harmless to be used as a point of departure in risk assessment. It 
was noted that as more refined brain data become available, we are 
beginning to understand that not all regions of this organ show the 
same level of AChE inhibition. Thus a 10% inhibition for the whole 
brain may imply significantly greater inhibition in a more sensitive 
region.

    The FIFRA SAP report provides conflicting information on the issue 
of the benchmark dose response used by EPA in its BMD calculations. On 
page 53 of the FIFRA SAP report, the text suggests that the available 
data do not support the 10% response level used in BMD modeling and 
that a 20% response level is more appropriate. The text quoted by the 
commenters from the report argues that a 10% response level may not be 
sufficiently health protective, but that a 5% response level may be 
more appropriate. Given the lack of unanimous advice by the Panel in 
this case, and that past SAPs have previously supported the use of a 
10% level in comparable cases, the Agency has concluded that the 
overall weight of the available evidence supports a decision that use 
of a 10% response level will be protective of human health.

[[Page 23054]]

A more detailed response to this issue can be found in the Agency's 
response to the SAP (Ref. 109).
    2. Comments relating to the children's safety factor--a. Reliance 
on RBC to predict effects on the PNS. Some commenters argued that brain 
is a better surrogate for the PNS than RBC, and that therefore reliance 
on the brain data is sufficiently protective that no additional 
children's safety factor is necessary. The commenters claim that the 
carbofuran data on brain AChE inhibition and on clinical signs of 
toxicity indicate that PNS AChE inhibiton is sufficiently modeled by 
brain AChE inhibtion. They note that the available data show that brain 
AChE responds rapidly to carbofuran; it readily passes the blood-brain 
barrier and the data show maximal AChE inhibition within minutes. The 
commenters also alleged that brain and tissue AChE are more similar to 
each other than to RBC AChE. The commenters also point to the fact that 
oral time-course studies by EPA and the registrant show that brain 
cholinesterase responds quickly and recovers promptly. Carbofuran 
clearly reaches the brain quickly. They also cite to the fact that EPA 
has acknowledged that in adults, no difference in sensitivity is seen 
between brain and RBC AChE inhibition.
    The commenters repeatedly mention the rapid speed by which 
carbofuran reaches the brain and the rapid onset and recovery of AChE 
inhibition as support for the notion that reliance on the brain data 
will be adequately protective of PNS toxicity. The Agency agrees with 
the commenters on the rapid nature of carbofuran toxicity. However, 
this rapid toxicity occurs in multiple tissues, not just the brain. 
Moreover, the time course of such toxicity is not relevant to 
determining which tissue is more sensitive. Therefore, these comments 
are not relevant to a discussion of the use of brain versus RBC AChE as 
a surrogate for PNS toxicity.
    The commenters' allegation that brain and tissue AChE are more 
similar to each other than to RBC AChE is not scientifically 
supportable. Radic and Taylor (2006), for example, state, ``In humans 
and most other vertebrate species, only one gene encodes AChE'' (Ref. 
81). Accordingly, if only one gene encodes the enzyme, then the 
structure of the active site is the same throughout the body.
    Responses in adult animals are not necessarily predictive or 
relevant to responses in juveniles since the metabolic capacity of 
juveniles is less than that of adults. As such, juveniles can be more 
sensitive to some toxic agents. Specific to carbofuran, multiple 
studies have shown juvenile rats to be more sensitive than adult rats. 
Thus, comments about responses in adults are less relevant compared to 
data in pups from the carbofuran risk assessment, particularly in the 
evaluation of the children's safety factor.
    One group of commenters argue that there is evidence that RBC AChE 
activity can be inhibited to a greater degree than AChE in peripheral 
organs. For example, Marable et al., (2007), showed that chlorpyrifos 
caused much greater inhibition of AChE in RBC than in diaphragm, left 
atrium, and quadriceps, as well as in brain. Similarly, Padilla et al., 
(2005), reported a greater inhibition of AChE in RBC than in diaphragm 
or brain. Bretaud et al., (2000), showed that carbofuran caused 
significant inhibition of AChE in brain tissues but not in muscle in 
goldfish. The commenters claim that these results demonstrate that RBC 
AChE activity does not reflect AChE activity in peripheral organs.
    The commenters mention three references: Padilla et al., 2005; 
Marable et al., 2007; Bretaud et al., 2000. Two of these studies 
involve testing with chlorpyrifos in rats (Refs. 65 and 77) and the 
third involves testing fish with carbofuran (Ref. 14). Quantitative 
extrapolation of RBC and peripheral AChE inhibition differences from 
fish to mammals is highly uncertain because distribution of carbofuran 
across fish and mammalian tissues may be quite different. The Padilla 
et al., (2005) and Marable et al., (2007) references include testing 
with chlorpyrifos, an OP whose primary mode of action is also AChE 
inhibition (Refs. 65 and 77). Exposure to OP and NMC insecticides 
results in inhibition of AChE. The Agency assumes it is this similarity 
in mechanism of toxicity, which provides the basis for inclusion of 
these chlorpyrifos references by the commenters.
    The Agency believes that direct comparison between the results of 
studies with chlorpyrifos and carbofuran should be done with great 
caution. OP and NMC insecticides have different time courses of 
effects, which lead to toxicity profiles that are somewhat different. 
The studies cited by the commenters (Padilla et al., 2005, Marable et 
al., 2007) involve long-term treatment (chronic exposure) in adult 
animals where blood, brain and peripheral tissue AChE inhibition were 
at steady-state. The time course and AChE inhibition in various tissues 
at steady state is distinctly different from acute AChE inhibition at 
the time of peak effect, like that in the carbofuran studies. In the 
case of acute toxicity with NMCs, the time course of inhibition and 
reactivation of the AChE is rapid (minutes to hours). In the case of 
OPs, when steady state inhibition is achieved in adults, recovery is 
slow (days to weeks) and is influenced by synthesis of new AChE 
protein. In addition, as stated above, responses in adults are not 
adequate for drawing conclusions in the young. As such, the Agency 
views the Padilla et al., (2005) and Marable, et al., (2007) references 
as providing limited useful information for the carbofuran risk 
assessment.
    Although the Agency is cautious about direct comparisons between 
OPs and NMCs, it must be noted in this case that: (1) The commenters 
have provided an incomplete review of the literature and ignored more 
relevant studies; and (2) the chlorpyrifos literature does, in fact, 
generally support the Agency's conclusions with respect to carbofuran.
    The commenters state specifically that ``[t]here is also evidence 
that RBC AChE activity can be inhibited to a greater degree than AChE 
in peripheral organs.'' The assertion that RBC AChE activity can be 
more inhibited than peripheral tissues ignores relevant chlorpyrifos 
data. For example, Richardson and Chambers (2003) showed that lung AChE 
can be more sensitive than serum and brain AChE in rat fetuses (Ref. 
82).
    EPA's response to comments document provides a more extensive 
review of chlorpyrifos studies (those that include data in peripheral 
tissue) than that discussed by the commenters (Ref. 112). While there 
are many studies that have measured AChE inhibition with chlorpyrifos, 
the Agency has limited its discussion here only to those in pregnant 
rats and fetuses which provide peripheral AChE data (e.g., heart, lung, 
and liver) as they are the most relevant to the present issues raised 
by the commenters. Several chlorpyrifos studies in pregnant dams and/or 
their fetuses show that peripheral AChE is more sensitive than brain 
AChE. For example, a study conducted by Dow AgroSciences showed that a 
dose of 1 mg/kg results in 4-6 fold more inhibition in heart AChE than 
in brain tissues (Refs. 66 and 67). Similarly, Hunter et al., (1999) 
showed that in pregnant dams at doses of 3 mg/kg liver AChE was 
inhibited 84% when brain tissues were inhibited by only 41% (Ref. 51). 
Fetuses evaluated at or near the peak time of effect in the Hunter et 
al., (1999) study showed 2-8 fold more AChE inhibition in liver than in 
brain. (Id.). Although there is some variation among studies, the 
preponderance of data supports the

[[Page 23055]]

conclusion that peripheral tissues are more sensitive to chlorpyrifos 
exposure than brain tissues. Thus, the chlorpyrifos data in fetuses and 
pregnant rats supports the Agency's concern that sole reliance on brain 
data may not be protective of the PNS following carbofuran exposure. 
Chlorpyrifos data in post-natal pups are described in the Agency's 
Response to Comments on the proposed tolerance revocation (Ref. 112).
    Although OPs and NMCs both inhibit AChE, the chemical reaction at 
the active site differs. This difference leads to different time 
courses of toxicity and recovery. As such, comparisons, particularly 
quantitative ones, between chlorpyrifos and carbofuran should be done 
with care. However, in general, review of these data supports the 
Agency's conclusion for carbofuran that in the absence of high quality 
data that is relevant for risk assessment in either peripheral tissue 
or a surrogate (i.e., RBCs), the Agency cannot be certain that brain 
AChE inhibition is protective of potential peripheral toxicity 
following carbofuran exposure. Therefore, the chlorpyrifos data support 
the Agency's conclusion that at least a portion of the children's 
safety factor must be retained for carbofuran given the lack of 
peripheral AChE data and lack of RBC AChE (as a surrogate for 
peripheral AChE) at the low end of the dose-response curve.
    b. Comments relating to EPA's approach to deriving the 4X factor. 
One group of commenters argued that EPA's approach to calculating its 
4X Children's Safety Factor was flawed. According to the commenters, it 
would be more plausible and straightforward to compare the RBC and 
brain AChE levels at the same time in the same rat when these rats are 
exposed to carbofuran. Based on an analysis of the RBC and brain AChE 
inhibition data, the commenters' claim that the percentage reduction in 
RBC AChE in a rat is almost the same as the percentage reduction in 
brain AChE in that same rat. The commenters summarize a statistical 
evaluation of the experimental data on AChE inhibitions in RBC and 
brain in rats due to carbofuran exposure conducted by their contractor, 
and claim that this evaluation shows that the percentage inhibition of 
RBC AChE in a rat compared to the percentage inhibition of brain AChE 
in the rat is no more than 1.5X--a difference that they claim is not 
meaningful from a physiological perspective and does not warrant 
imposition of a 4X FQPA safety factor.
    EPA notes that the commenters recommended this approach of 
comparing the degree of inhibition for each animal as part of their 
presentation to the Carbofuran SAP. EPA also addressed this approach, 
comparing RBC to brain in the same animals, at the SAP and in the 
responses to the SAP report (Ref. 109). It is notable that the SAP did 
not endorse this approach.
    EPA's analyses of the commenters' approach identified several 
significant deficiencies. First, the comparison suggested by the 
commenter means that EPA would need to ignore existing data. This is 
because only EPA's study of PND11 animals contains both brain and RBC 
data, so the comparisons suggested by the commenter can only be made 
using that dataset. However, the dose levels in that study were so high 
that the lower portion of the dose-response curve was missed. At these 
higher doses, there is little difference between the levels of brain 
and RBC inhibition. This phenomenon, namely the relative sensitivity of 
RBC compared to brain appears smaller at higher doses. This phenomenom 
is also shown in multiple chlorpyrifos studies, where blood or 
peripheral measures of AChE inhibition are more sensitive than brain at 
low to mid doses but the tissues appear to be similar at higher doses.
    Second, the commenters' approach is fundamentally flawed. The 
commenters' suggested alternative relies exclusively on comparisons 
between the degree of inhibition in the treated animals without any 
regard to the doses at which the effects occurred. For example, one 
animal may have shown, on average, 10% inhibition in the brain, when it 
demonstrated 20% RBC inhibition. Under this approach, what would be 
relevant would simply be the ratio of 1:2. But the Agency believes it 
is critical to focus on the ratios of potency, which is the ratio of 
the doses in the data that cause the same level of AChE inhibition. The 
Agency's approach of comparing potencies is more directly relevant for 
regulatory purposes than comparisons of average inhibition. This is 
because dose corresponds more directly to potential exposures, which is 
what EPA regulates (i.e., how much pesticide residue does a child 
ingest). By comparison, the commenters' suggested reliance purely on 
the average degree of inhibition provides no information that 
corresponds to a practical basis for regulation.
    Finally, the range of ratios of effects that the commenters propose 
as an alternative is consistent with range of potencies that EPA has 
calculated at the higher doses in the available data, so the 
commenters' results do not ultimately contradict EPA's assessment, 
which tries to account for what occurs at lower doses. Briefly, if the 
dose-responses for RBC and brain inhibition were linear, ratios of 
inhibition would equal ratios of BMDs. However, these dose-responses 
are not at all linear, and the available data demonstrate that brain 
and blood dose-responses have somewhat different shapes. Thus, 
estimates of relative effects at particular, relatively high, doses are 
not relevant to the problem of estimating potency ratios at lower 
doses. The dose-response curves level off at about the same level of 
inhibition, so, at high doses, there is no difference between the ratio 
of inhibitions. Except at the lowest dose, where the ratio is slightly 
greater than 2, the remaining ratios are only slightly greater than 1. 
Given the inevitable statistical noise in these measures, it is clear 
that the ratios expected from EPA's modeling are substantially similar 
to what the commenter finds in its comparison between individuals. 
Accordingly, the commenter's suggested comparisons at higher doses 
provide no evidence of what occurs at lower doses; and thus provides no 
evidence that demonstrates that EPA's modeling results at lower doses 
is inaccurate.
    One group of commenters claimed that the statistical comparisons 
that support EPA's selection of a 4X children's safety factor are 
flawed. The commenters claim that, even assuming that RBC values are 
relevant, EPA's conclusion that RBC effects in the relevant studies 
were four times more sensitive than brain effects is not mathematically 
supportable. The commenters reference statistical analyses performed 
for them by a contractor, which they claim show that EPA's calculation 
of the 4X children's safety factor is simply incorrect. The commenters 
complain that the datasets EPA used for brain differ not only because 
they were from different studies, but also because the data were taken 
at different times ranging from 15 minutes to 4 hours after dosing. The 
commenters also raise the concern that EPA's decision to combine data 
for different strains of rats, sexes, experiments, laboratories, dates, 
dose preparations, rat ages, and times between dosing and AChE 
measurement, is problematic, claiming that these differences in study 
design severely limit the validity of EPA's comparisons. In addition, 
the commenters claim to have found a number of errors and 
inconsistencies in how the modeling was conducted. Correcting for these 
errors, the commenters claim, shows that the

[[Page 23056]]

BMDs for brain and RBC data are essentially the same.
    As discussed at length below, and in EPA's Response to Comments 
document, EPA disagrees that its statistical modeling was in any way 
flawed (Ref. 112).
    In general, EPA believes that consideration of all available data 
is the scientifically more defensible approach, rather than the 
selective exclusion of reliable data. The Agency's Draft BMD Guidance 
says the following: ``Data sets that are statistically and biologically 
compatible may be combined prior to dose response modeling, resulting 
in increased confidence, both statistical and biological, in the 
calculated BMD'' (Ref. 100). The Agency's carbofuran analysis has 
included all available, valid data in its analysis. Further regarding 
combining data from multiple strains, the SAP was fully aware that the 
Agency was planning to derive BMD estimates from data sets using 
different strains of rats (Ref. 43).
    By contrast, the commenters' suggested analysis ignores relevant, 
scientifically valid data. The FMC analysis left out the 30-minute data 
from MRID no. 47143705. The commenters have provided no rationale as to 
why it would be appropriate to selectively exclude data from the time 
frame in this study most relevant to the risk assessment (i.e., peak 
AChE inhibition). The commenters' analysis of the individual datasets 
from MRID no. 47143705, showed that at 30 minutes the females and males 
provide BMDL10s of 0.009 mg/kg/day and 0.014 mg/kg/day, 
respectively. When the datasets were combined, inclusion of the 30-
minute timepoint from MRID no. 47143705 decreased the BMDL10 
from 0.033 mg/kg/day to 0.030 mg/kg/day.
    EPA has used a sophisticated analysis of multiple studies and 
datasets to develop the PoD for the carbofuran risk assessment. 
However, instead of this analysis, EPA could simply have followed the 
general approach laid out in its BMD policy (Ref. 100), which is used 
in the majority of risk assessments. Under this general approach, EPA 
would regulate using the most sensitive effect, study, and/or dataset. 
If the Agency chose not to combine the data in its analyses, as the 
commenters' suggested, data collected at or near the peak time of 
effect (i.e., 30 minutes) would in fact provide the more relevant 
datasets. If this more simple approach were taken, in accordance with 
BMD guidance, EPA would select the lowest BMDL10. Assuming 
the commenters' values were used, EPA would have selected a PoD of 
0.009 mg/kg/day, instead of 0.03 mg/kg/day, which is the value EPA is 
currently using in its risk assessment.
    Further, the commenters complain that EPA's approach of combining 
data across multiple studies is scientifically inappropriate. The 
commenters have, however, combined the results of analysis from four 
datasets. It is notable that most of the issues cited by the commenters 
also apply equally to the commenter's own analysis, as described in 
more detail in EPA's Response to Comments document (Ref. 112).
    EPA has addressed all of the commenters' claimed inconsistencies in 
its Response to Comments document (Ref. 112). The majority of these 
claimed flaws and inconsistencies were either misunderstandings by the 
commenters or areas where it was the commenters who were incorrect, not 
EPA. However, in response to some of their allegations, EPA conducted 
new analyses to determine whether the suggested alternative approaches 
would make any significant difference in EPA's modeling outcomes. For 
example, in response to one of their comments, EPA used the dose-time-
response model to extrapolate BMD50s to develop a common 
point of comparison between all studies. Specifically, EPA extrapolated 
the PND11 brain analysis to estimate BMD50 for 40 minutes 
after dosing for comparison with the existing PND11 RBC 
BMD50, and extrapolated the PND11 RBC BMD50 to 15 
minutes after dosing for a range of assumed recovery half-lives, for 
comparison to the existing PND11 brain BMD50 (Refs. 30 and 
31). In either approach, the estimate of the RBC to brain potency ratio 
in PND11 animals is increased, and EPA's safety factor would 
correspondingly increase to reflect that larger difference. For 
example, when the PND11 brain BMD50 is extrapolated to 40 
minutes, the RBC to brain potency ratio grows to 4.7 (Ref. 30), and 
when the PND11 RBC BMD50 is extrapolated to 15 minutes, 
using a range of estimates for the recovery half-life of the RBC 
endpoint, the RBC to brain potency ratio ranges from 4.2 to 4.6 (Ref. 
31). The commenter's approach would therefore support a children's 
safety factor of 5X rather than 4X.
    Similarly, in response to the complaint that EPA should have 
generated a new dose-response model in order to calculate the 
BMD50s for brain and RBC, EPA conducted the suggested 
calculation (Ref. 112). The ratio of brain to RBC BMD50s in 
this new analysis is the same as that calculated by EPA using the 
mathematical expression. Both provide a ratio of brain to RBCs 
BMD50 of 4X. Specifically, the values are for PND11 brain 
BMD50 0.35 and for RBC, 0.086, resulting in a ratio of 4.09 
(Ref. 112).
    Several commenters disagreed with the Agency's decision to apply a 
4X, arguing that the high bar set by the statute for lessening the 
tenfold safety factor has not been achieved because ``important data 
gaps exist.'' These commenters raised the concern that key data on 
carbofuran toxicity and exposure for the very young are inadequate. 
Examples include: No data were presented for pre-natal sensitivity as 
would have been desirable for addressing the need to protect developing 
individuals; BMD10 estimates from the available RBC AChE 
inhibition data are not reliable due to lack of data at the low end of 
the dose response curve. The commenters also highlighted EPA's 
assumption that the RBC and brain AChE dose response curves are 
parallel, noting that there are currently no data to test this 
assumption for carbofuran. One commenter raised the concern that ``EPA 
has no substantial research on alternate mechanisms of carbofuran 
toxicity. EPA has acknowledged but failed to incorporate in its 
assessment the potential for lasting adverse effects from transient 
exposures during fetal and newborn life-stages, and EPA has 
acknowledged that there are uncertainties in the available data (as 
raised by the SAP).'' The commenters concluded that the Agency does not 
have the requisite ``completeness of data'' required by law to lessen 
the safety factor,'' and urged the Agency to reinstate the default 10X 
safety factor.
    Section 408(b)(2)(C) of the FFDCA requires that EPA consider the 
``completeness of data with respect to exposure and toxicity to infants 
and children'' when evaluating whether retention of the default 10X 
safety factor is appropriate. The Agency has concluded that available 
exposure information is sufficient for purposes of developing its human 
health risk assessment, and has adequately accounted for the lack of 
certain hazard information with the retention of a 4X children's safety 
factor. Moreover, the Agency has concluded that the exposure assessment 
does not substantially underestimate food or water exposure. The 
completeness of the hazard database and the interpretation of available 
toxicity studies were described elsewhere in this final rule preamble. 
The Agency continues to believe that a 4X children's safety factor is 
appropriate for carbofuran.
    Several commenters alleged that application of a 4X children's 
safety factor, rather than a 10X, is inconsistent with the SAP's 
advice. These

[[Page 23057]]

commenters argued that the SAP report reflected strong support, if not 
unanimity, among panel members for a safety factor of at least 
fivefold, and pointed to the statement in the report that ``some Panel 
members considered it reasonable to retain the full 10X [children's] 
safety factor (Panel Scenario 5). Given the uncertainty in the data and 
in its interpretation for risk assessment by the entire Panel, these 
Panel members believed that this standard for change had not been 
met.''
    As described in detail in the Agency's response to the SAP report 
(Ref. 109), the Agency believes there was a general consensus that a 
children's safety factor of 2X or greater was necessary. The Agency 
does note that one Panel member thought a 1X was appropriate and at 
least two believed a 2X was appropriate. Given that the Panel did not 
take a vote on the record and the report notes that the Panel did not 
endorse a particular approach, any conclusions about the possible 
``unanimity'' of the Panel is speculation. However, as described in the 
Agency's response to the SAP and in the July 2008 proposed rule, EPA 
believes that on balance, its reliance on the data derived factor of 4X 
is consistent with the SAP's advice, as a whole.
    Several commenters raised concern that EPA's application of a 4X 
children's safety factor did not adequately account for the differences 
between children and adults. The commenters raised several reasons that 
children are more vulnerable than adults to carbofuran. These include 
the following:
    (1) Children are growing. Pound for pound, children eat more food, 
drink more water and breathe more air than adults. Thus, the commenters 
conclude, they are likely to be more exposed to substances in their 
environment than are adults. Children have higher metabolic rates than 
adults and are different from adults in how their bodies absorb, 
detoxify and excrete toxicants.
    (2) Children's bodies, including their nervous, reproductive, 
digestive, respiratory and immune systems, are developing. This process 
of development creates periods of vulnerability. Exposure to toxicants 
at such times may result in irreversible damage when the same exposure 
to a mature system may result in little or no damage.
    (3) Children behave differently than adults, leading to a different 
pattern of exposures to the world around them. For example, they 
exhibit hand-to-mouth behavior, ingesting whatever substances may be on 
their hands, toys, household items, and floors. Children play and live 
in a different space than do adults. For example, very young children 
spend hours close to the ground where there may be more exposure to 
toxicants in dust, soil, and carpets as well as low-lying vapors.
    (4) The recovery time from carbofuran exposure for the very young 
is more than four times that of adults, as the SAP noted.
    Carbofuran does not have any residential uses. As such, comments 
about the breathing rate of children and hand-to-mouth behavior do not 
apply to carbofuran's risk assessment. The Agency agrees with the 
commenters that infants and children represent a potentially 
susceptible lifestage to carbofuran exposure. Accordingly, the Agency 
has taken steps to incorporate lifestage specific information in its 
risk assessment. For example, the Agency's hazard assessment has used 
data from PND11 rat pups as the PoD in extrapolating human risk. 
Although it is not possible to directly correlate ages of juvenile rats 
to humans, PND11 rats are believed to be close in development to 
newborn humans (Refs. 5, 12, and 26). The Agency's food exposure 
assessment relies on DEEM-FCID\TM\, which uses the CSFII database, 
including the 1998 supplemental survey of children. As such, the 
Agency's aggregate risk assessment accounts for the decreased metabolic 
capacity of juveniles in addition to age-specific behaviors in eating 
and drinking.
    One commenter noted that while they agreed that the use of brain 
and RBC AChE inhibition data is an appropriate endpoint for use in 
EPA's risk assessment, they did not believe that it is sufficiently 
health-protective to only rely on this endpoint without an uncertainty 
factor because it has not been established scientifically that AChE 
inhibition is the most sensitive endpoint. The commenter noted that one 
SAP member argued for retaining a 10X children's safety factor because 
of uncertainty in both the dosimetry in subtle developmental effects 
and also the available data on related pesticides suggesting effects on 
nerve outgrowth at cholinesterase inhibition levels of 20% or less, and 
some effects at less than 10%. The commenter asserted that ``this 
position is supported by published studies on the toxicity of a related 
family of pesticides, the OPs, reporting that exposures during fetal 
and newborn life-stages affect diverse cellular functions by mechanisms 
of toxicity that are independent of cholinesterase inhibition, and may 
occur at exposures that elicit less than 20% inhibition (Refs. 1, 2, 
32, and 91). This is important because while the systemic toxicity that 
results from cholinesterase inhibition is reasonably well 
characterized, it does not explain why rodents exposed pre- and post-
natally seem to recover from cholinesterase inhibition relatively 
rapidly, yet display persistent and more severe damage to the central 
nervous system'' (Ref. 90). The commenter also pointed to what they 
assert is a ``growing body of science for OPs demonstrating that non-
cholinergic mechanisms of toxicity may be acting to disrupt multiple 
brain targets'' (Ref. 80). According to the commenter, experts have 
warned that ``the fact that alterations in neurodevelopment occur with 
OPs below the threshold for cholinesterase inhibition reinforces the 
inadequacy of this biomarker [cholinesterase inhibition] for assessing 
exposure or outcome related to developmental neurotoxicity'' (Ref. 92). 
When reviewing the EPA assessment of the OPs, the commenter asserted 
that the FIFRA SAP in 2002 had raised the same concern, stating that 
``reliance on a single biochemical assay to measure brain damage may 
become problematic'' (Ref. 41).
    The Agency is aware of the available studies noted by the 
commenters on the OPs and has recently developed a draft issue paper on 
many such studies as part of its on-going review of chlorpyrifos. The 
Agency cautions the commenters against extrapolating these studies to 
the NMCs. The Agency is not aware of any studies in laboratory animals 
where long-term behavioral or other effects were noted with exposure to 
NMCs. Moreover, the Agency is not aware of any epidemiology study that 
has associated NMC exposure with adverse birth or neurodevelopmental 
outcomes in children. Although OPs and NMCs both inhibit AChE, the 
chemical reaction at the active site differs. This difference leads to 
different time courses of toxicity and recovery. Time to peak effect 
and time to recovery for the NMCs is very rapid in comparison to OPs. 
Moreover, once reactivation of the AChE occurs, the parent compound is 
no longer active. As such, NMCs may not be present in the body long 
enough to cause the types of outcomes associated with OP exposure. The 
Agency concludes that there are no data which link NMC exposure, 
including studies with carbofuran, at relatively low doses to long-term 
outcomes in juvenile animals or children. Therefore, the Agency further 
concludes that the OP studies noted by the commenters have limited 
relevance to the carbofuran human health risk assessment.
    c. Comments regarding consistency in approach. One group of 
commenters

[[Page 23058]]

claimed that the derivation of carbofuran's PoD and children's safety 
factor was inconsistent with EPA's analyses for other NMCs, including 
aldicarb and carbaryl.
    The commenters are incorrect. The Agency's recent hazard 
assessments of carbaryl and aldicarb are each consistent with OPP 
policies and practice, as well as with the Agency's approach to the 
assessment of carbofuran.
    The commenters' assertions regarding aldicarb were based on an 
earlier assessment. At the time the Agency conducted the assessment to 
which the commenters refer, the Agency was unaware of the differences 
in sensitivity between PND17 and PND11 animals. Since EPA became aware 
of the differences, EPA has required the aldicarb registrant to conduct 
a CCA study in PND11 rats; the Agency anticipates the receipt of this 
study and the companion range-finding and time course studies in 2009. 
In the absence of these data, EPA will apply the statutory default 
children's safety factor to account for the additional sensitivity of 
PND11 animals, because the Agency lacks any data that could be used to 
derive a reduced factor that EPA could determine will be ``safe for 
infants and children.''
    Carbaryl was not evaluated any differently than carbofuran. EPA's 
typical practice which was used in both the carbofuran and carbaryl 
risk assessments, is to use the central estimate on the BMD to provide 
an appropriate measure for comparing chemical potency and to use the 
lower limit on the central estimate (i.e., BMDL) to provide an 
appropriate measure for extrapolating risk. This approach is also 
consistent with the NMC cumulative risk assessment (CRA) and single 
chemical risk assessments for multiple OPs.
    In the case of carbaryl, the commenters inappropriately focused on 
the BMDL10s, instead of the BMD10s. The more 
appropriate comparison is between the BMD10s; the carbaryl 
brain BMD10 is 1.46 mg/kg/day compared with the RBC 
BMD10 of 1.11 mg/kg/day. As such, the brain to RBC ratio is 
1.3X. Therefore, for carbaryl, the brain and RBC AChE data are 
similarly sensitive, and, when the tissues are similarly sensitive, the 
Agency prefers to use data from the nervous system tissue (i.e., brain) 
over data from a surrogate tissue (i.e., RBC) (Ref. 108). Thus, for 
carbaryl, the RBC AChE inhibition (a surrogate for PNS AChE inhibition) 
and brain AChE inhibition were basically equivalent. This contrasts 
with the situation with carbofuran where a significant difference in 
AChE inhibition between the two is noted.
    With regard to the carbaryl children's safety factor, the available 
brain and RBC dose-response data in PND11 pups include data from the 
lower end of the dose-response curves. ORD's comparative AChE data with 
carbaryl show that at the lowest dose at or near 20% inhibition in 
brain and RBC AChE was observed. Although not ideal, the carbaryl data 
provide information closer to the benchmark response of 10%, which 
allows for a reasonable estimation of the BMD10 and 
BMDL10. This is distinctly different from ORD's data with 
carbofuran in PND11 and PND17 pups where 50% or greater RBC AChE 
inhibition was observed at the lowest dose.

C. Comments Relating to EPA's Exposure Assessment

    1. Food exposures. One group of commenters alleged that it is more 
appropriate to apply USDA PDP residue monitoring data from winter 
squash to pumpkins, rather than residue data from cantaloupes.
    The Agency agrees with the commenters. An appropriate residue 
assignment has been made in the latest dietary exposure assessment 
(Ref. 71). The results of this assessment are discussed below in Unit 
VIII.E.1.b.
    One group of commenters asserted that the measurable residues of 
carbofuran in milk obtained by the USDA PDP program should be 
``adjusted to a lower level because a significant proportion of the 
milk residues in the PDP database are due to carbofuran use on alfalfa, 
which is no longer permitted under the carbofuran label.'' The same 
commenters discussed the results of an exposure assessment that they 
apparently conducted, in which they have reduced the residues 
anticipated to be found in milk by some unspecified amount.
    Based on the commenters' results, their adjustments to milk 
residues appear to have about a 50% reduction on the risk estimates for 
the food only results. While the commenters appeared to have made the 
adjustments to milk residues in most of their food-only assessments, as 
well as their food+water assessment, they did not: (1) Describe the 
amount by which residues were reduced; (2) present the DEEM-FCID\TM\ 
input files detailing the residue inputs used in their assessment; or 
(3) provide to the Agency related data to support any such reduction 
factor--information that the Agency would need to accept such an 
adjustment. Because of the lack of any explanation or rationale, the 
Agency attempted to determine how the commenters made the ``adjustment 
to residues'' to account for the cancellation of use on alfalfa. As 
described in the Agency's Response to Comments, EPA was not able to 
reproduce the commenters' results, but did approximate their reported 
results after reducing milk residues by 77% (Ref. 112).
    In actuality, it is difficult to ascertain how the recent 
cancellation of carbofuran use on alfalfa may affect future residues 
found on milk (from dairy feed items associated with corn, potatoes or 
sunflowers). This is especially true for milk since it is a blended 
commodity. That is, milk may be obtained from dairy cows from multiple 
farms (i.e., a dairy cooperative). The milk in any particular PDP 
sample may have come from dairy cows that might have had a diet that 
contained substantial amounts of alfalfa, or a diet that contained 
predominately corn, or from multiple farms using various combinations 
of feed that may or may not have been treated with carbofuran. In any 
case, the aggregate pesticide use statistics do not support the 
contention that most residues in milk are (or have been) due to 
carbofuran use on alfalfa--the USDA and Proprietary use data indicate 
that field corn has historically had a greater overall amount of total 
carbofuran use than alfalfa. Potatoes and sunflowers rank 3rd and 4th.
    The Agency included a summary of dietary burdens for dairy cattle 
in the dietary exposure analysis memorandum documenting the higher 
dietary burden involved with field corn feed stuffs (Refs. 70 and 71). 
These two diets represent a corn-based diet and an alfalfa-based diet, 
accounting for appropriate amounts of roughage and protein. Based on 
these dietary burdens, milk from dairy cows having a corn-based diet 
may have higher concentrations of carbofuran than milk from cows having 
an alfalfa-based diet (Refs. 70 and 71).
    The Agency notes that 3-hydroxy carbofuran was detected in about 
7.5% of all PDP milk samples analyzed in 2004 and 2005 (7.5% = 110 
detects in 1,485 samples).
    Considering all of the various factors involved with the PDP milk 
samples-e.g., uncertainty regarding mixture of feeds, pesticide use and 
corresponding residues--the Agency finds no basis for applying 
estimated reduction factors to actual measured concentrations of 
carbofuran residues found by the PDP program in milk based on the 
cancellation of alfalfa uses. In the absence of supporting data the 
Agency has no scientific basis for making the

[[Page 23059]]

commenters' recommended changes to the dietary exposure assessment with 
regard to carbofuran residues in milk. Certainly, the commenters' have 
failed to provide any scientific justification for their position. 
Moreover, since the Agency was unable to reproduce the commenters' 
results, EPA could not make the suggested adjustment, even if they had 
provided details on the exact adjustment figure they wanted EPA to 
apply.
    One group of commenters raised concern that PCT estimates used by 
the Agency for bananas, potatoes, and milk are conservatively high.
    In response to those comments, the Agency reviewed its PCT 
estimates for the two crops and revised its PCT estimates for bananas 
from 78% to 25%. The Agency also developed a regional PCT estimate for 
potatoes of 5% based on projected limited use in the Northwest, and has 
applied these estimates in its revised dietary risk assessment (Ref. 
71). The Agency also applied a 5% CT for milk, based on the PCT for 
potatoes, which is the feed stuff with the highest PCT. Further 
discussion regarding the Agency's previous and revised PCT estimates 
can be found in References 71 and 122. As discussed below in Unit 
VIII.E.1.b., these adjustments had relatively modest effects on the 
dietary exposure assessment of those crops the registrant now seeks to 
maintain.
    Some commenters claimed that the Agency acted inconsistently in the 
way in which it conducted its ``Eating Occasion Analyses'' to account 
for the extent to which individuals recover from AChE inhibition 
between exposure events. The commenters claimed that the Agency 
analyzed aldicarb and carbofuran differently, and came to different 
conclusions concerning the effects of reversibility for these two 
compounds.
    The commenter's assertion that the Agency came to different 
conclusions concerning the effects of reversibility for aldicarb and 
carbofuran is incorrect. EPA discusses the Eating Occasion Analysis it 
conducted for carbofuran in greater detail in Unit VIII.E.3. below and 
in its Response to Comments document (Ref. 112).
    The Agency concurs with the commenter that ``there is no basis for 
treating aldicarb-treated potatoes differently from carbofuran treated 
potatoes.'' The commenters' assertions regarding what the Agency has or 
has not done with respect to the Eating Occasion Analysis (i.e., 
``reversibility'') to some extent reflects confusion resulting from the 
several assessments the Agency has produced since 2006. Since that 
period, EPA has conducted several risk assessments, based on the 
tolerances FMC has variously indicated that it wished EPA to retain. 
EPA notes, for clarity, that for the proposed rule, EPA conducted a 
risk assessment of ``all registered carbofuran uses'' that did 
incorporate the concept of reversibility (i.e., ``persisting dose''). 
The proposed rule also contained an assessment of the subset of ``6 
domestic uses'' that EPA believed the registrant primarily wished to 
retain, which did not incorporate this concept because these were not 
the only crops on which carbofuran was legally permitted to be used. 
However, now that the registrant has cancelled all but four domestic 
food uses, the Agency's risk assessment of all the remaining uses 
accounts for reversibility, performed using the same DEEM-based Eating 
Occasion Analyses previously used for both carbofuran and aldicarb.
    In support of their contention, the commenters took an observation 
in the aldicarb IRED that exposures did not pass at the per capita 
99.9th percentile, but were equal to the aPAD at a lower percentile--
out of context, and used that statement to infer that the Agency 
regulates at this lower percentile. This is incorrect. The aldicarb 
registrant agreed to a number of risk mitigation measures that brought 
the aggregate risks to below the aPAD at the 99.9th per capita 
percentile. The registrant agreed to modify the aldicarb label to 
require a 500-foot well set back for aldicarb use on peanuts (GA soil 
type), since aggregate exposure at the per capita 99.9th percentile for 
infants continued to exceed the level of concern even after 
reversibility was accounted for in the Eating Occasions Analyses under 
the 300-foot well set back scenario.
    In summary, the Agency did not analyze aldicarb exposure and risk 
any differently than it analyzed carbofuran exposure and risk; the 
``persisting dose'' concept was used in both assessments. 
Mathematically and conceptually, the calculations of the adjustment for 
reversibility are the same for both exposure assessments. Any 
differences in the conclusions EPA drew from the analyses are 
attributable purely to the factual differences between the two 
compounds. The reduction in ``persisting dose'' is slightly greater for 
aldicarb due to its quicker recovery times (2-hour half-life for 
aldicarb), but in both cases, the Agency applied the same procedure to 
account for reversibility. The qualitative results for the food only 
and food + water scenarios presented in Unit VIII.E., produce similar 
qualitative results: in both cases, accounting for reversibility 
between eating occasions for food alone results in relatively modest 
reductions in the ``persisting dose'' at the per capita 99.9th 
percentile, and a relatively large effect on exposure for water alone, 
or food+water, when water is the predominant contributor (73 FR 44864). 
These Eating Occasion Analyses support the Agency's position that 
reversibility has a relatively greater effect for drinking water 
exposures than for food exposures.
    One group of commenters claimed that the Agency should have 
calculated the effects of carbofuran exposure based on the ``persisting 
dose'' over the 1,440 person-minutes rather than on the person-days 
that are currently used by the Agency.
    In effect, the commenters suggest that the ``persisting dose'' 
should be calculated over the entire 1,440 minutes of each modeled 
person-day (1,440 minutes/day = 24 hrs x 60 minutes/hr). EPA has 
rejected this approach for a number of reasons. While the commenters' 
person-minute approach may be an attempt to capture multiple measures 
with one statistic, it does not properly capture the Agency's concern 
regarding peak inhibition, and the commenters' assertion that the 
Agency should use all person-minutes to calculate the per capita 99.9th 
percentile is misguided at best since: (1) It does not reflect a 
comparison to peak inhibition which is what the Agency believes is the 
most appropriate and relevant toxicological measure and (2) it produces 
risk estimates that are entirely dependent upon the time of day at 
which consumption occurs. Hence, this approach will obtain different 
values depending upon the reported time of consumption even if exposure 
occurs on a single eating occasion. The commenters suggested approach 
does not appear to capture peak inhibition, or other temporal aspects 
of cholinesterase inhibition (e.g., duration over which inhibtion 
exceeds 10%). EPA's Response to Comments document provides a further 
explanation of this issue and details why the Agency's approach is 
consistent with the identified endpoint (peak inhibition) and the 
corresponding point of departure (BMDL10 that serves as the 
basis for calculating a %aPAD (Ref. 112).
    2. Drinking water exposures. As part of their comments on the 
proposed tolerance revocation, FMC submitted a revised label with use 
restrictions intended to address drinking water contamination. These 
measures include eliminating a number of crop uses, prohibiting use in 
a broad swath of areas with potentially vulnerable soils, and

[[Page 23060]]

requiring application buffers in other areas. In addition to these 
label modifications, the registrant, along with two other commenters, 
submitted comments summarizing the results of risk assessments they had 
previously submitted, and the results of new risk assessments they 
claim to have conducted. The commenters did not provide to the Agency 
either the new risk assessments they claim to have conducted, or the 
underlying support documents for those assessments, including the 
``national leaching assessment'' or the ``crop-specific evaluation of 
use patterns and the registrant's proposed non-application buffers 
using the PRZM-EXAMS model.'' FMC concludes that their label revisions 
have a pronounced effect on dietary risk and result in ``exposure that 
even fit within the risk cup that EPA has proposed.''
    EPA has reviewed the September 2008 proposed label modifications, 
and a synopsis of the Agency's conclusions are summarized below in this 
Unit. More detailed analyses can be found in EPA's Response to Comments 
(Ref. 111). In addition, EPA's revised risk assessment, discussed below 
in Unit VIII.E., is based on this revised label.
    The label revisions leave two national food uses on the label, corn 
and sunflowers, and two regional food uses, potatoes in the northwest 
and pumpkins in the southeast. EPA has assessed the impact of all of 
these remaining uses, taking into consideration all label restrictions, 
and has concluded that remaining uses may result in concentrations in 
some locations that are similar in magnitude to those estimated 
previously (Refs. 57, 58, 60, and 62).
    a. Comments relating to EPA's ground water analyses. One group of 
commenters alleged that ``[g]roundwater sources are vulnerable to 
carbofuran leaching only under certain conditions, namely where 
permeable soils (e.g., areas with soils greater than 90% sand and less 
than 1% organic matter), acidic soil and water conditions, and shallow 
water tables predominate (e.g., where ground water is less than 30 
feet).'' The commenters claim that these conditions are rare in areas 
where carbofuran is used. They further assert that in ``most states 
where carbofuran is used, less than 2% of the entire surface areas 
possess sandy soil texture'' and that ``low pH conditions are not found 
in carbofuran use areas allowed under the registrant's amended label''.
    EPA disagrees that the commenter's specific criteria define 100% of 
conditions where ground water sources are vulnerable to carbofuran 
leaching. No comprehensive analysis was provided evaluating how they 
reached this conclusion. Although these criteria appear on the revised 
carbofuran label restricting use, the spatial extent of the label 
restrictions is not provided. As discussed in greater detail in EPA's 
Response to Comments, the information provided as part of FMC's 
comments (primarily maps depicting areas identified as vulnerable) is 
not sufficient to allow the Agency to evaluate their claim (Ref. 111). 
For example, water table depth can vary with the time of the year, 
depending on such factors as the amount of rainfall that has occurred 
in the recent past, and how much irrigation has been removed from the 
aquifer. It is difficult to determine how the depth to the water table 
varies throughout fields, and the definition of a ``shallow'' water 
table is indeterminate (e.g., less than 30 feet). Furthermore, the 
vulnerability associated with depth varies with location; for example, 
deeper aquifers may be more vulnerable in areas with greater 
precipitation and rapid recharge.
    While the assertion regarding percent sand is in part true, it is 
misleading. While many states have only small areas of sandy soils, 
some states have quite extensive areas. For example, according to FMC's 
own assessment of high use states (Ref. 8), Texas had 4.2% sand, 
Michigan had 21.3% and Nebraska had 26.3%. In addition, this statement 
implies that soils that are sandy textured define the universe of soil 
textures that are vulnerable to leaching. It is possible that more 
fine-textured soils, for example sandy loams or silt loams, could also 
be sufficiently permeable to result in carbofuran leaching as it has 
not been established how much of a reduction in leaching might occur as 
texture becomes finer. Furthermore, finer textured soils tend to have 
more cracks and root channels and thus are more prone to preferential 
flow.
    EPA also disagrees that the commenters have provided sufficient 
information to support their general claim that only high pH conditions 
(pH above 7) exist in all the areas in which carbofuran could be used 
under FMC's September 2008 revised label. There is considerable spatial 
variability in pH conditions for both the subsurface and surface 
environments. The pH has a large effect on the persistence of 
carbofuran as, for more acidic conditions, the hydrolysis half-life 
increases from 28 days at pH 7 to years or more at pHs less than 6. 
Further, the results of EPA's corn ground water simulations (bounded by 
the high and low pH values of the aquifer system underlying the 
scenario location) showed that a relatively small (0.5) decrease in pH 
from 7 to 6.5 resulted in an increase by 4 orders of magnitude in the 
1-in-10-year peak concentration of carbofuran. EPA has presented its 
assessment of the newly submitted label in its Response to Comments 
document and these issues are addressed in more detail there (Ref. 
111).
    Accordingly, the criteria the commenters suggest are not sufficient 
to prohibit use in all areas that could reasonably be expected to be 
vulnerable to ground water contamination from carbofuran use. EPA's 
assessment identifies an example of one area where carbofuran use would 
still be permitted on the proposed labels; an additional scenario for 
the updated ground water modeling provided in Reference 111 was based 
on this location in the south-central region of Wisconsin. This 
scenario is in no way unique; EPA expects that other similar sites 
exist in other locations where carbofuran could still be used across 
the United States.
    One group of commenters claimed that the most recent label 
modifications ``has ensured that carbofuran use will not occur in these 
vulnerable areas by removing them from the label.'' They support this 
by reference to a map of the carbofuran use areas in 2005, that 
identifies counties with DRASTIC scores as high as that of the location 
of the prospective ground water study (PGW study) conducted by FMC in 
Maryland, defining that combination as vulnerable.
    DRASTIC is a USEPA model that was developed as a screening tool to 
identify ground water resources that are ``generally vulnerable to the 
release of contaminants at the surface * * *.'' (Ref. 6). The 
commenters indicate that the map provided in their comments shows 
counties ``identified as vulnerable,'' based on DRASTIC scores that 
exceed 185, and 2005 carbofuran usage, although the map's level of 
resolution is insufficient to provide more than a general impression of 
the location of ground water classified as vulnerable. In FMC's 
September 2008 label revisions, FMC expanded the areas where carbofuran 
cannot be applied, apparently because of ground water concerns. The 
specific criteria that FMC used to determine these further locations 
were not provided to the Agency. Nevertheless, EPA does agree that 
ground water in the Atlantic Coastal Plain is vulnerable, and that FMC 
has restricted use in those areas.
    However, EPA does not agree with the premise that only locations 
with DRASTIC scores as high as that of the location of the Maryland PGW 
study are those that require mitigation. DRASTIC

[[Page 23061]]

scores as high as those identified by the commenters would indicate 
that the site is located in a generally sensitive or vulnerable area. 
The Agency agrees that the DRASTIC tool can be used to generally 
identify areas that may be vulnerable to pesticide contamination. 
However, DRASTIC is somewhat dated (1987), and better methods currently 
exist that can take advantage of geospatial data at a more refined 
level than the county level used here. FMC apparently agrees with this 
criticism since they subsequently developed the ``National Leaching 
Assessment'' as part of their comments on the proposed tolerance 
revocation, to replace their earlier DRASTIC assessment.
    Importantly, EPA believes that FMC has used an inappropriate 
criterion for determining whether a site is vulnerable-that it has the 
same or greater vulnerability (based on a DRASTIC score greater than 
185) as that of the Maryland PGW study site. The maximum concentration 
at the Maryland PGW site, adjusted to simulate an application rate of 1 
lb/acre, was 21 [mu]g/L this exceeds acceptable exposure thresholds by 
factors of 10 to 20 (Ref. 71). Thus, sites that are less vulnerable 
(e.g., deeper aquifer, high soil sand content, higher organic matter), 
with lower DRASTIC scores, could still be prone to have carbofuran 
concentrations exceeding acceptable exposures.
    Further, the commenters provide no detail on the specific data used 
to generate their DRASTIC estimates. In footnote 39 of their comments 
they indicate that ``Data to support these [DRASTIC] inputs were 
primarily collected from state-wide, statistically designed studies 
conducted by state and federal agencies (primarily the National Water 
Quality Assessment Program (``NAWQA''), but also state surveys and 
other state and federal agricultural data, where NAWQA data were not 
available.'') Given EPA's general reservations about their approach, 
EPA cannot conclude that the commenters' assessment is scientifically 
supportable or useful, without information on the sources of the data, 
the geographic scale of the data, or how that input data was prepared 
for the analysis.
    One group of commenters assert that their ``assessments revealed 
that the soils and water pHs are generally higher in those states in 
the Midwest and Northwest where most carbofuran is used, providing 
further confirmation that conditions that favor carbofuran leaching in 
those areas do not exist.''
    Since the commenters have not provided all of the assessments they 
appear to have conducted, EPA is unable to confirm whether their 
assessments do in fact support their contention. However, as a general 
matter, none of the previously submitted assessments provided a 
comprehensive analysis of the distribution of soil and water pHs for 
the Midwest, Northwest or any other region of the country where 
carbofuran use would be permitted on the September 2008 label, nor have 
the commenters provided such an analysis with their most recent 
comments. Further, the available scientific information does not 
support their contention.
    EPA examined readily available data with respect to ground water 
and soil pH in order to evaluate the spatial variability of pH. Data 
from the United States Geological Survey (USGS) and other readily 
available sources do not necessarily encompass the entire range of 
ground water pH values present within a state. This is especially true 
for shallow ground water systems, where local conditions can greatly 
affect the quality and characteristics of the water. Also, pH in a 
water body can be higher or lower than the tabulated average values. In 
addition, average ground water pH values for a given area do not truly 
characterize the area's temporal and especially spatial heterogeneity. 
This can be seen by comparing differences in pH values between counties 
within a state, and noting that even within a county individual wells 
will consistently yield ground water with either above- or below-
average pH values for that county. The ground water simulations in 
Reference 111 Appendix I reflect variability in pH by modeling 
carbofuran leaching in four different soil and subsurface pH conditions 
(pH 5.25, 6.5, 7.0, and 8.7), representing the range in the aquifer 
system in that area. This range also approximates the pH range of 
natural waters in general. The results of the ground water simulations 
for corn use showed that a relatively small (0.5) decrease in pH from 7 
to 6.5 resulted in an increase in the 1-in-10-year peak concentrations 
of carbofuran in ground water of 4 orders of magnitude.
    FMC summarized the results of their ``National Leaching 
Assessment'' which used PRZM and ``databases specifically created to 
provide access to all necessary inputs for a national scale PRZM 
modeling.'' They claim that after accounting for the use prohibitions 
on their September 2008 label, the maximum 1-in-10-year peak 
concentrations in all potential carbofuran use areas is 1.2-1.3 ppb, 
while expected concentrations in most areas covered by this assessment 
are below 1.0 ppb. They claim to have modeled a single application to 
corn at 1 lb/acre--which is the application rate on the September 2008 
labels applicable to the rescue treatment on corn--and simulated ground 
water recharge and lateral flow. They assert that their estimate that 
1-in-10-year peak carbofuran concentrations will not exceed ``~1 ppb'' 
is consistent with EPA's NMC CRA.
    Neither the ``National Leaching Assessment,'' nor the ``National 
Pesticide Assessment Tool'' upon which the assessment appears to have 
been based, were submitted to EPA for review, therefore EPA cannot 
comment further on the methodology for reaching these conclusions, or 
indeed, whether the assessment actually supports their claims. Based on 
the information provided, EPA cannot confirm or negate the assertion 
that there is no overlap between use and all potentially vulnerable 
ground water, as the information provided does not enable the Agency to 
evaluate this claim.
    EPA's assessment of the impacts of FMC's September 2008 label 
differs significantly from the commenters' summary conclusions; these 
differences are addressed more completely in EPA's Response to Comments 
document, and are based on application by FMC of unsupported factors 
(Ref. 111).
    Part of EPA's assessment of ground water exposure for the proposed 
tolerance revocation was based on simulation modeling using PRZM for 
corn grown on the Delmarva Peninsula in Maryland receiving an annual 
application of 1.0 lb/acre-1. The 1-in-10-year peak estimated drinking 
water concentration (EDWC) was 30.8 [mu]g/L. FMC's assessment of the 
same label resulted in their estimate of concentrations up to 22.7 
[mu]g/L. The September 2008 labels prohibit application at sites in the 
Atlantic Coastal Plain with similar vulnerability to the Delmarva site. 
However, EPA believes that the study and the resulting scenario derived 
from this study remain relevant for other areas with similar 
conditions, where use remains. Based on the September 2008 labels, EPA 
has concluded that there are locations in the United States where 
carbofuran could still be applied, and in which ground water 
concentrations are estimated to be high enough to cause concern. For 
example, simulations of corn grown the central sands region of 
Wisconsin had an estimated 1-in-10-year peak concentration of 16 [mu]g/
L at pH 6.5 and 284 [mu]g/L at pH 5.25, both of which are in the pH 
range for aquifers in this area (Ref. 115). For higher pH's in that 
area,

[[Page 23062]]

estimated carbofuran concentrations were generally close to zero.
    As noted the ``National Leaching Assessment'' has not been provided 
to EPA for review, and consequently, the Agency cannot determine model 
input parameters or check model algorithms. In many cases, model inputs 
cannot be directly inferred from values in the available weather and 
soil databases (e.g., NOAA SAMSON weather datasets, NRCS Soil Datamart) 
(Refs. 75 and 93). Methods used by FMC to select or calculate values 
for model input from these databases were not described. The only model 
output provided was in map format. While maps are useful for 
interpreting results, maps alone are insufficient for a thorough 
evaluation of the assessment, in part because of their spatial 
resolution. Further, the maps provided by FMC do not represent all 
carbofuran use patterns. For example, Figure IV-2 on page 42 of FMC's 
comments does not address the granular use patterns and proposed label 
prohibitions.
    FMC contends that their results are consistent with the NMC CRA, 
but this is untrue. The NMC CRA examined carbofuran at two sites, 
northeast Florida and the Delmarva Peninsula. In Florida, 
concentrations were found to be below levels of concern because of high 
pH, but in Delmarva, both in corn and in melon scenarios EPA estimated 
that 90% of daily concentrations could be as high as 20.5 and 25.6 
[mu]g/L, respectively. These values are greater than the 1 [mu]g/L that 
FMC claims is the maximum expected 1-in-10-year peak concentration. The 
claim that EPA's modeling fails to address use patterns ``changing 
naturally over time'' is ambiguous, and EPA cannot evaluate any inputs 
included by FMC to address this in their own modeling, if indeed they 
did so. Because of these deficiencies, EPA is unable to verify or 
evaluate the results of FMC's analysis and can reach no conclusion on 
its validity or utility.
    FMC asserts that ``EPA's approach is not consistent with the 
Agency's treatment of other carbamates. For example, in the aldicarb 
assessment, EPA used monitoring data to develop eight different region-
specific scenarios, `based on broad similarity in compound usage, crop 
type or soil conditions', and taking a `single maximum sample result 
detected within [each] region during the last 5 to 10 years to 
represent ground water concentrations within that entire region.' The 
Agency estimated drinking water concentrations for risk assessment 
purposes by accounting for the effect of ground water mitigation 
measures (i.e., setbacks).'' In footnote 53 of their comments, FMC 
apparently quotes from the aldicarb IRED ``[H]igher residue values that 
may have resulted from historical use if aldicarb in vulnerable areas 
were excluded.''
    EPA disagrees with FMC's assertion that the carbofuran drinking 
water exposure assessment was not consistent with other carbamates, 
particularly aldicarb. In both cases, Tier 2 modeling, using the PRZM 
and EXAMS models, was used to characterize surface water exposure and 
in both cases available monitoring data were summarized. For 
carbofuran, ground water exposure was characterized using a combination 
of targeted and non-targeted monitoring data, a PGW study, and Tier 2 
modeling, through the course of two RED chapters and several post-RED 
drinking water exposure assessments. For aldicarb, two different ground 
water exposure assessments were conducted for the initial and the final 
IRED chapters. In the comment quoted above, FMC has described the 
process used for the aldicarb risk assessment supporting the initial 
aldicarb IRED dated May 12, 2006.
    The second aldicarb ground water exposure assessment supported the 
revised dietary exposure assessment in February 2007 (Ref. 48). This is 
a more refined assessment, which relies on simulation modeling for 
ground water using PRZM in places vulnerable to ground water leaching 
where aldicarb was used. While FMC has correctly quoted ``[H]igher 
residue values that may have resulted from historical use of aldicarb 
in vulnerable areas were excluded,'' the implication that this is 
different from EPA's evaluation of carbofuran is not correct. For 
example, the carbofuran IRED describes monitoring in New York where 
carbofuran use was canceled in 1984, and where detections of carbofuran 
continue. The carbofuran IRED did not use the high concentrations of 
carbofuran measured in drinking water wells in that study, up to 178 
ppb, which resulted from historical use of carbofuran. In both cases, 
historical monitoring data were described (Refs. 10 and 47), but 
endpoints used for ground water exposure assessment were only based on 
monitoring relevant to use patterns current at the time of the 
assessment. For aldicarb, the Agency utilized retrospective monitoring 
data collected after 1990. For carbofuran, the most relevant monitoring 
data set was the Maryland PGW study. Because of the design of that 
study, results could be adjusted to represent current use patterns.
    The aldicarb assessment took into account the impact of well 
setbacks on estimated concentrations in ground water modeling conducted 
in 2007. The carbofuran modeling in EPA's most recent assessment also 
took into account the impact of well setbacks on estimated 
concentrations in ground water. Previous carbofuran assessments did not 
assess the impact of well setbacks, as setbacks were not included on a 
proposed carbofuran label until September 2008.
    In summary, both assessments for aldicarb and carbofuran used a 
combination of monitoring data and simulation modeling for the drinking 
water exposure assessments, simulating the impact of mitigation 
measures on the labels.
    b. Comments relating to EPA's surface water assessment. One group 
of commenters summarized conclusions based on a previously submitted 
surface water assessment based in Indiana. Specifically, they claim 
that: (1) EPA's standard index reservoir scenario overestimates surface 
water concentrations compared with ``expected concentrations in actual 
Indiana community water system (CWS) where carbofuran is used,'' (2) 
``Indiana CWSs bracket the Index Reservoir scenario (i.e., some 
reservoirs are more sensitive and others are less); however, in each 
instance the expected concentrations in the Indiana CWSs were 
significantly less than those estimated by the Index Reservoir 
scenario.''
    EPA has reviewed the Indiana surface water assessment submitted by 
the registrant previously, and has provided comments on that submission 
(Ref. 59). FMC's first major conclusion from this study is that ``EPA's 
standard index reservoir scenario overestimates surface water 
concentrations compared with expected concentrations in actual Indiana 
CWS where carbofuran is used.'' The Index Reservoir is designed to be 
used as a screen, and as such, represents watersheds more vulnerable 
than most of those which support a drinking water facility. It is thus 
protective of most drinking water on a national basis. That, however, 
does not mean that EPA believes this scenario overestimates 
concentrations for all drinking water reservoirs. While EPA agrees that 
it is an appropriate refinement to simulate local and regional 
watersheds, and has in fact done so (Refs. 58, 60, 61, 62, and 111), 
EPA does not believe that FMC's assessment refutes the concern for 
carbofuran occurrence in Indiana surface water source drinking water. 
Even accepting the Indiana surface water assessment at face value 
(which we do not), FMC estimated 1-in-10-

[[Page 23063]]

year peak concentrations at some facilities as high as 6.88 [mu]g/L, 
and these concentrations substantially exceed the concentration they 
now claim represent reasonable estimates.
    FMC's second major conclusion has two parts: (1) That the 
vulnerability of the Indiana CWSs ``bracket'' the Index Reservoir, and 
(2) that the concentrations they estimated for these locations are 
significantly less than EPA estimates. Regarding the vulnerability of 
the CWS, FMC's assessment describes their approach for modifying the 
parameters of the Index Reservoir scenario to represent 15 reservoir-
based watersheds in Indiana cropped in corn. FMC indicates they have 
included data that, based on our review of these submissions, are not 
available at the appropriate scale to determine all site-specific 
parameters. FMC modified some of the parameters based on available data 
to represent more localized conditions that are more or less vulnerable 
than for the Index Reservoir. From FMC's description, their approach is 
similar to the methods that EPA uses to develop new scenarios, in that 
soil and weather data are varied in order to represent different 
locations. However, for other parameters, EPA believes FMC's 
modifications are inconsistent with fundamental assumptions upon which 
the modeling is based. In submissions made to the Agency, FMC has 
described that they have made modifications to scenarios to reflect 
local conditions of each CWS in Indiana by modifying the soil, and 
weather data and altering the ratio of watershed drainage area to the 
reservoir capacity (Ref. 120). EPA agrees that soils and weather data 
can be modified to reflect conditions at local watersheds. However, 
other modifications FMC made cannot reasonably be justified for all 
scales without contradicting the assumptions upon which the modeling 
relies (uniformity of soils, equal and simultaneous movement of runoff 
to the reservoir, and uniform weather across the watershed).
    FMC also calculated their own PCAs for this assessment. The PCA is 
the fraction of the drinking water watershed that is used to grow a 
particular crop. EPA uses the maximum PCA calculated for any HUC8 (8-
digit hydrologic unit code) watershed in exposure estimates. HUC8s are 
cataloging units for a watershed developed by the USGS and are used as 
surrogates for drinking water watersheds. The process by which PCAs 
were developed and how they are used by the Agency has been vetted with 
the FIFRA SAP (Refs. 37 and 38). The Agency has developed PCAs for four 
major crops, corn, soybeans, wheat, and cotton, and uses a default PCA 
based on all agricultural land for characterizing other crops. The 
Agency has also calculated regional default PCAs for use in 
charactering regional differences in drinking water exposure. EPA 
limited further development of PCAs for additional crops, as a result 
of FIFRA SAP peer review comments, which concluded that data were not 
available at the appropriate scale to do so. In their assessment, FMC 
estimated PCAs for specific watersheds in Indiana. FMC did not provide 
sufficient detail in their descriptions of how they calculated PCAs to 
enable EPA to assess their validity.
    Regarding FMC's statement that the concentrations they estimated 
for these locations in Indiana are significantly less than EPA 
estimates, EPA has determined that FMC has included an adjustment 
factor to account for the percent of a crop that is treated with 
carbofuran. As discussed in more detail below, although EPA does 
evaluate such factors in conducting ``sensitivity analyses'' to 
understand the impact that various PCT assumptions may have, EPA does 
not believe that it is appropriate to base its aggregate risk estimates 
on PCT within watersheds. This is because data and/or methods are not 
available that would allow EPA to develop PCT at the watershed scale 
with the necessary level of confidence to allow EPA to make a safety 
finding. The PCT factors that FMC generated would lead to significantly 
lower concentrations than those estimated by EPA.
    One group of commenters reiterated conclusions from a previously 
submitted surface water assessment, the ``Nationwide CWS Assessment.'' 
Based on this assessment, the commenters allege that: ``use intensity 
in the majority (~ 75%) of carbofuran use areas is less than 2.1 lbs 
a.i./sq. mi,'' and that based on this use intensity, the commenters' 
modeling results in surface water concentrations ``that are not above 
the applicable level of concern.'' The commenters also claim that, 
because areas with historical use intensities greater than 2.1 lbs. 
a.i./sq. mi may be more sensitive to carbofuran, the registrant 
proposed no-application buffers which effectively mitigate the risks in 
these areas.
    EPA has reviewed FMC's ``Nationwide CWS Assessment'' previously and 
has provided a response to the submission (Ref. 59). It is worth noting 
that FMC only assessed use intensity for reservoir-based systems and 
excluded use intensity for all stream- or river-based systems from 
their assessment.
    Similar to the Indiana CWS study discussed in the previous 
response, this study relied on county-level usage estimates to estimate 
use intensity. This value was subsequently used in modeling to draw 
their second major conclusion, which FMC states formed the basis for 
their decisions to propose no-application buffers to mitigate risks in 
those areas, their third conclusion. To respond to this comment, 
therefore, it is important to understand how FMC arrived at these use 
intensities. Their methods have been poorly described in statements, 
but EPA was able to piece together a general sense of the methods from 
the various reports FMC provided to EPA.
    To summarize, for FMC's National CWS Assessment, the registrant 
relied on sales data to generate its use intensity estimates, but these 
data were not provided to EPA. The method FMC used to generate the 
county-level use estimates from the sales data is not described. The 
actual county level use estimates used in the use intensity 
calculations were not provided. There is a limited description 
indicating only that the county level use estimates were apportioned to 
different crops, but the method FMC used to do this was not provided. 
FMC used an objective method to group the county-level use estimates 
into 5 classes, but the method is only briefly described. Thus, because 
EPA cannot determine how use intensity was estimated, the Agency cannot 
determine if the conclusions made in the National CWS Assessment are 
justified by the underlying data.
    Since carbofuran sales data used for FMC's assessment were not 
provided in the document submitted to EPA, or with the comments to the 
SAP (Ref. 33), or with the comments on the proposed tolerance 
revocation, it was not possible for EPA to determine if FMC's claim 
that 75% of the use areas have a carbofuran use intensity of less than 
2.1 lbs a.i./sq. mi., is accurate. Use intensity data in maps provided 
in their comments appear to indicate that carbofuran use varies year by 
year, however, it is also not clear for which year or years FMC is 
making this conclusion.
    EPA agrees that using lower rates of carbofuran will result in 
lower exposure. But EPA does not agree that it has been demonstrated 
that a use intensity below 2.1 lbs a.i./sq. mile will assure that 
surface water concentrations will be below the applicable level of 
concern. The National CWS Assessment does not justify such a finding, 
nor has any other assessment that has been submitted to date. The 
Agency modeled use rates for carbofuran on corn based

[[Page 23064]]

on the label proposed in September 2008 and results are described in 
Unit VIII. and in Reference 111.
    EPA is equally unable to confirm the claims that the no-application 
buffers on the September 2008 labels will adequately mitigate the risks 
``in areas with historical use intensities greater than 2.1 lbs a.i./
sq. mi.'' On the September 2008 labels, FMC included buffers of 300 
feet on water bodies in Kansas, and 66 feet around water bodies in 
other places, but EPA cannot evaluate how these buffers relate to areas 
where carbofuran use intensities exceeded a specific value, for all of 
the reasons stated above. EPA did, however, model the effects from the 
buffers proposed on the September 2008 labels and found that these 
buffers reduce exposure by 5.1% (33.5 to 31.8 [mu]g/L) for corn in 
Kansas with a 300 foot spray drift buffer and 4.7% (29.9 to 28.5 [mu]g/
L) for corn in Texas with a 66 foot spray drift buffer. These results 
are described in more detail in Reference 111, Appendix I.
    One group of commenters claimed that EPA's modeling assumptions are 
``implausible for most surface water systems across the country.'' They 
specifically criticize the following assumptions: (i) ``a lack of 
inflow to or meaningful outflow from the CWS; (ii) instantaneous and 
homogeneous mixing throughout the entire CWS; (iii) all receiving water 
directly abut the treated field and there are no buffers; and (iv) a 
lack of variation in pH across water bodies in the United States.''
    All of the commenters' claims are incorrect. Their first 
contention, that EPA assumes that there is a lack of inflow to or 
meaningful outflow from the CWS, is incorrect. EPA's modeling assumes 
the inflow to the reservoir is equivalent to the mean annual runoff 
into the reservoir. Since the EXAMS model is a steady state model, 
outflow will equal inflow to the reservoir. Assuming that outflow 
equals inflow and that mixing occurs instantaneously throughout the 
reservoir are reasonable assumptions; the commenters made the same 
assumptions in their modeling. Secondly, the commenters believe the 
assumption that there is instantaneous and homogeneous mixing 
throughout the entire reservoir supporting the community water supply 
is implausible. This is a reasonable assumption for small, un-
stratified reservoirs like the Index Reservoir. Also, the commenters 
made the same modeling assumption in their modeling in the Indiana CWS 
study, and apparently in the modeling done in support of their 
submitted comments on the proposed tolerance revocation. Thirdly, the 
commenters believe it is implausible to assume that all receiving water 
directly abuts the treated field, and there are no buffers. This claim 
is also not accurate. Until the September 2008 label, carbofuran labels 
did not require buffers, thus, EPA did not have reason to assess the 
impact of buffers. EPA's assessment of FMC's September 2008 labels 
considered the impact of the buffers (see Ref. 111, Appendix I). 
Finally, FMC contends that EPA's assumption of pH was implausible. EPA 
disagrees; EPA's assessment was based on the middle of the range of pH 
occurring in natural waters. In addition, as a sensitivity analysis, 
EPA assessed exposure assuming a high pH, representative of a high end 
pH of waters in Western Kansas, as well as the high end of natural 
waters in general.
    One group of commenters summarizes conclusions from a previously 
submitted assessment based on the Watershed Regression for Pesticides 
(WARP) (Ref. 117) model. They claim, based on this assessment that 
``[t]he maximum 1-in-10 day estimated concentrations of carbofuran at 
the 90th percentile level in Illinois, Indiana. Iowa, and Nebraska 
(where a majority of current carbofuran is located) will be less than 
or equal to 0.3687 ppb.'' They claim that WARP's 1-in-10-day estimates 
are a reasonable surrogate for the 1-in-10-year peak concentrations 
typically relied on by the Agency because ``the extreme nature of a 1-
in-10-year event (i.e., severe rain) would result in dilution effects 
that cancel out any increased loading.'' They also allege that the 
differences in surface water concentrations estimates in their 
assessment and EPA's modeling are due to their use of ``actual county-
level usage data.''
    EPA has reviewed the WARP assessment previously and has provided 
comments on the submission (Refs. 59 and 117). The WARP model has not 
been fully evaluated for quantitative use in exposure estimation by the 
Agency, although it has been preliminarily reviewed by the SAP (Ref. 
39). EPA used WARP to select monitoring sites for the herbicide 
atrazine, based on predicted vulnerability of watersheds to atrazine 
runoff within the corn/sorghum growing regions. EPA presented its 
approach to the FIFRA SAP in December 2007. The SAP report concluded 
that ``WARP appears to be a logical approach to identify the areas of 
high vulnerability to atrazine exposure,'' endorsing EPA's use of this 
tool only for atrazine, and for the limited purpose of designing a 
monitoring program. The SAP noted that the most important explanatory 
value with WARP was use intensity, and underscored the importance of 
having the most accurate data for this parameter.
    WARP is a regression model developed by the USGS to estimate 
concentrations of the pesticide atrazine in rivers and streams. As a 
regression model, it is based on monitoring data, in this case from 112 
USGS National Ambient Water Quality Assessment (NAWQA) monitoring 
locations. WARP does not directly estimate daily concentrations, but 
predicts the percent of the time in a randomly selected year that 
concentrations of the pesticide are less than a specified value, with a 
specified level of confidence. USGS attempted to develop an approach to 
estimate annual time series for other pesticides, and concluded that 
``further data collection and model development may be necessary to 
determine whether the model should be used for areas for which fewer 
historical data are available * * * Because of the relative simplicity 
of the time-series model and because of the inherent noise and 
unpredictability of pesticide concentrations, many limitations of the 
model need to be considered before the model can be used to assess 
long-term pesticide exposure risks.'' (Ref. 126).
    The commenter's conclusion that the ``maximum 1-in-10-day estimated 
concentrations of carbofuran at the 90th percentile level in Illinois, 
Indiana, Iowa, and Nebraska [* * *] will be less than or equal to 
0.3687 ppb,'' is erroneous. WARP does not provide direct estimates of 
return frequency, i.e., 1-in-10 days, but rather percentiles of the 
expected distribution of measurements. This may be similar but not 
identical to the return frequency expressed as a percentile, depending 
on the number of measurements used to support the regression. EPA 
lacked the information necessary to determine whether FMC's contractor 
calibrated the model correctly. However, taking the conclusion at face 
value, the value FMC predicted using WARP, 0.3687 ppb, appears to 
represent the maximum of the estimated values of the annual 90th 
percentile among all the sites evaluated. Such a site would be expected 
to have higher concentrations than 0.3687 ppb about 37 days a year (10% 
of the year). Generally, the 90% prediction intervals tend to be about 
plus or minus an order of magnitude. Thus, roughly 5% of such sites 
could have about 37 days a year greater than about 3.7 ppb.
    The Agency also disagrees that the differences between FMC and EPA 
estimates are only due to FMC's use of county-level usage data. Most 
importantly, the Agency does not concur that 1-in-10-day estimates are 
a reasonable surrogate the for the 1-in-

[[Page 23065]]

10-year peak concentrations estimates used routinely by EPA. 1-in-10-
day concentrations are not the measurement endpoint EPA uses for human 
health risk assessment and are not appropriate for estimating drinking 
water exposure. The Agency uses 1-in-10-year peak concentrations for 
screening level assessments, and the full time series (typically 30 
years) of daily concentration values for refined assessments. For 
example, EPA's estimate of the 1-in-10-year peak concentration from the 
simulation of corn in Kansas with a 300 ft buffer was 31.8 [mu]g/L. 
EPA's estimate of the 1-in-10-day concentration from the same 
simulation was 4.5 [mu]g/L. The measurement endpoint used by EPA, which 
has been subject to peer review by the FIFRA SAP, is the 1-in-10-year, 
peak concentration. A concentration that occurs 1-in-10 days occurs 350 
times as often as a 1-in-10-year event. Assuming this statistic instead 
of the one EPA used would result in a significantly lower estimates of 
pesticide water concentration and human exposure. Such an approach 
would be inconsistent with the SAP's advice and EPA's typical practice, 
as well as with EPA's statutory requirement to protect human health. 
EPA disagrees with FMC's claim that ``the extreme nature of a 1-in-10-
year event would result in dilution effects that cancel out any 
increased loading.'' The Index Reservoir scenario has been validated 
against monitoring collected at the site it was designed to represent, 
Shipman City Lake in Illinois (Ref. 56). This assessment showed that 
the 1-in-10-year event EPA modeled was similar in magnitude to the peak 
value of the pesticide concentrations shown in 5 years of monitoring 
data collected at that site. The 1-in-10-year peak concentration 
calculated for that pesticide (not carbofuran), using the Index 
Reservoir was 33 [mu]g/L, while the peak value from 5 years of 
monitoring was 34 [mu]g/L.
    EPA cannot comment on the use intensities assumed for FMC's 
assessment. The source of county level use data was not described. 
Based on the comments submitted to the SAP by FMC (Ref. 33) the source 
is likely to be sales data at the distributor level. However, the 
method chosen to estimate county level use estimates from the sales 
data was not provided. The county level estimates used in the 
assessment for 2002 to 2004 for Illinois were provided in a table. 
These estimates for each county were averaged over the 3 years for 
input to the model. A summary description of how watershed-scale use 
estimated from county level use data was provided, but because the 
sales data and method that was used to generate county level estimates 
were not available, this validity of this assessment cannot be 
evaluated.
    Several commenters criticize the Agency for the assumption that 
100% of the cropped area in a watershed is treated. These commenters 
claim that actual carbofuran sales data on a county basis confirm that 
the actual carbofuran PCT is less that 5%, with most PCTs less than 1%. 
The commenters claim that these county level sales data either were 
provided to EPA as part of reports prepared by their consultants, or 
would be provided to EPA. They further claim that ``how these data were 
analyzed, interpreted, and applied'' was provided to EPA in a report on 
best management practices.
    While the Agency typically uses PCT in developing estimates of 
pesticide residues in food, this is entirely different than developing 
estimates of the percent of a watershed that is treated for purposes of 
estimating drinking water exposures. Food is generally randomly 
distributed across the nation without regard to where it is grown. This 
tends to even out any PCT variations that may arise on local levels. By 
contrast, the source of water consumption (and consequently exposure) 
is localized, either in a private well or a community water system. The 
PCT in any watershed will therefore directly impact the residues to 
which people living in that watershed will be exposed.
    For this reason, among others, for drinking water exposure 
estimation, the Agency assumes that 100% of the cropped area (or 100% 
PCT) is treated. EPA also makes this assumption due to the large 
uncertainties in the actual PCT on a watershed-by-watershed basis. EPA 
developed an extensive discussion of the uncertainties in PCT and how 
they impact drinking water exposure assessment in its proposed rule (73 
FR 44834) and in a background document provided to the SAP considering 
the draft carbofuran NOIC (Ref. 59). Because usage is often not evenly 
distributed across the landscape, due to differences in factors like 
pest pressure, local consultant recommendations and weather, it may be 
much higher in some areas. Further, temporal uncertainties can result 
in changes in use that might be driven by weather, changes in insect 
resistance over time, and changes in agronomic practices. To date, 
methods that account for this uncertainty, given the nature of the 
available data, have not been developed. Consequently, EPA cannot 
accurately estimate a drinking-water watershed scale PCT that, when 
used in a quantitative risk assessment on a national or regional basis, 
standing alone, provides the necessary level of certainty to allow the 
Agency to confidently conclude that exposures will meet the FFDCA 408 
safety standard.
    In most cases, EPA agrees that it is unlikely that 100% of the crop 
will be treated in most watersheds, particularly in larger watersheds. 
However, for small watersheds, it is reasonable to assume that an 
extremely high percentage of the crops in the watershed may be treated.
    Moreover, EPA has an obligation to evaluate all legally permitted 
use practices under the label, and to ensure that all such use meets 
the requisite statutory standards, not simply to base its decisions on 
the practices the majority might typically use. The September 2008 
proposed label imposes no restriction on the application of carbofuran 
related to whether a particular percent of the watershed has been 
treated. Thus, even with the restrictions on FMC's September 2008 
labels, it remains legally permissible for 100% of the watershed to be 
treated with carbofuran.
    Nor is EPA aware of an enforceable mechanism to ensure that farmers 
applying pesticide to their individual fields will have the ability to 
determine whether a particular percentage of the watershed has been 
treated. There are significant practical difficulties inherent in 
implementing such label directions, as they force individual growers to 
have continual knowledge of the variances of the behavior of other 
farmers across the entire watershed. While for small watersheds that 
involve only one or two farms it might be feasible for neighbors to 
coordinate applications with respect to adjacent fields, for larger 
watersheds, the practical difficulties increase significantly.
    However, in the proposed rule, EPA conducted a sensitivity analysis 
to explore the impact of PCT assumption on dietary risk using an 
assumed 10% PCT, a figure proposed previously by FMC (73 FR 48864). The 
results of that analysis demonstrated that even at these low 
percentages, which may significantly underestimate exposures, 
particularly in small watersheds, carbofuran exposures from drinking 
water contribute significantly to children's dietary risks. EPA 
conducted a similar sensitivity analysis for this final rule, discussed 
below in Unit VIII.E.3., which demonstrates that even assuming that a 
low percentage of a watershed is treated, exposures will be unsafe for 
infants.

[[Page 23066]]

    FMC has submitted three assessments that relied in part on what 
they refer to as ``county-level usage data'' (Refs. 36, 96, and 120). 
The description that EPA has been able to piece together from the 
registrant's various submissions indicates that the original source of 
the ``county-level usage data'' is sales data, apparently collected at 
the distributor level. FMC claims to have augmented these sales data in 
an unspecified manner, by incorporating information from the 
distributor, which FMC used to allocate carbofuran usage at the county 
level. FMC has provided maps representing county level and watershed-
scale use estimates, but has not provided the actual usage estimates in 
any clearly understandable format. Nor, as of the close of the comment 
period, has any commenter provided either the ``actual sales data'' FMC 
used to develop these estimates, or the methods used to estimate county 
level usage from the sales data. FMC has provided only a limited 
description of how these data were collected and no description of how 
they were actually analyzed or validated; what FMC characterizes as 
``careful and proven techniques to capture this data'' were not 
described. The method FMC used to attribute carbofuran sales to 
counties was not described. In the absence of the data or analyses 
described above, EPA is unable to verify or evaluate the results of any 
analyses that rely on these data and can reach no conclusion on its 
validity or utility.
    The Agency agrees that county-level use data would be useful in 
generating reasonable estimates of PCT that could be used in drinking 
water assessments. However, as discussed in the previous responses, FMC 
has only provided county-level use estimates (not the underlying data 
nor the analyses that presumably are the basis for the estimates) for 
Illinois; county-level estimates to support other risk assessments have 
not been submitted by FMC as of the end of the comment period. The 
underlying sales data (i.e., measurements) used to make the county-
level estimates and the methods FMC used to estimate county level use 
from them have also not been submitted. FMC has provided limited 
characterization of the source data, noting that these data were 
derived from FMC billings and ``EDI data'', which they did not define, 
and that the sales data had been adjusted to reflect different use 
patterns and by removing use for patterns which they no longer support 
(e.g., alfalfa). However, FMC did not provide adequate details on the 
methodology they used to make these adjustments.
    A major problem with the method FMC seemingly used is that it does 
not appear to account for uncertainties due to variation in time and 
space and the potential for use to be locally concentrated due to pest 
pressures. The method FMC summarily describes as having been used to 
allocate county-level usage estimates to watersheds appears to be 
similar to a method that has been used by others for calculating 
``best-estimate'' county-level PCT (Ref. 95) to map nation-scale 
pesticide usage. However, these methods are not appropriate for 
calculating PCTs for surface drinking water sources or watersheds that 
drain to CWSs, because they do not adequately account for the 
uncertainty in the data at the appropriate spatial scale. This 
methodology produces an estimate that is a measure of central tendency 
and, as such, roughly half the estimated values will underestimate the 
PCT. Furthermore, because, pesticide use varies from year to year, and 
can in some cases be patchy, with high levels of use in small areas and 
little use in most areas, the underestimates of PCT can be substantial 
in small watersheds. As previously noted, methods for calculating PCT 
that account for these uncertainties have not been developed.
    Several commenters allege that carbofuran use will not concentrate 
in areas due to pest pressure. One commenter criticizes EPA for failing 
to support its conclusion that the pest pressure and infestation 
patterns could result in concentrated usage that could occur within 
vulnerable watersheds, and claims that EPA ignored the county-level 
sales data provided by the registrant which can be used both to 
determine whether carbofuran usage is evenly dispersed or locally 
clustered (an assessment [FMC's contractor] expressly undertook) and 
the probability of concentrated usage within vulnerable watersheds.
    Two commenters claim that, because ``more than 60% of the total 
corn acreage is made up of rootworm resistant GMO corn, which vary 
rarely requires treatment,'' and the remaining acreage ``is refugia 
acreage for GMO fields which is widely distributed geographically,'' it 
is a ``virtual impossibility'' that all corn acreage in a particular 
watershed will require a rescue treatment in any given year. Another 
commenter made similar allegations for sunflower acreage. The commenter 
claims that ``[s]unflowers are a specialty crop that is only grown on a 
small proportion of agricultural acreage generally, particularly in 
states where carbofuran is used (i.e., Nebraska, Colorado, Kansas, and 
Texas).'' According to the commenter, the available data suggests that 
sunflowers are only used on 25% of total cropped area, and that 
carbofuran is not used on all of these acres. As further support for 
this point, another commenter cites to the sunflower PCAs they 
calculated for Nebraska, Kansas, Colorado, and Texas,'' which they 
claim is 2.12%.
    The Agency agrees that the true PCT is not likely to be 100%. 
However, as discussed in several places throughout this preamble, the 
Agency is certain that PCT is higher in some cases than values 
calculated by the commenter. The degree of spatial correlation, 
however, is unknown, and thus is a major uncertainty. FMC's own 
analysis of carbofuran use in watersheds in Indiana suggests that 
carbofuran use is indeed localized, as carbofuran use was found in 
watersheds of only 12 of the 35 community water supplies that they 
considered in the state (Ref. 120). This suggests that when pest 
pressure occurs it is not unreasonable to assume it will be localized. 
Other factors, such as market pressures, consultant recommendations, or 
local availability may also be driving disparate levels of use in 
different locations. Since there is no method to account for this 
uncertainty in estimating PCT, it cannot be estimated in this 
assessment with the degree of confidence consistent with the statutory 
requirement of a reasonable certainty of no harm.
    The commenters raise several valid points that, taken together, 
reduce the probability that carbofuran usage will be concentrated over 
large geographical areas. However, the commenters failed to rebut EPA's 
conclusion that carbofuran's use patterns could be concentrated in 
certain locations, such that a large percentage of a small watershed is 
treated. Their first observation that carbofuran is applied as a rescue 
treatment on 0.27% of all U.S. corn acreage is true at the national 
level. However, the commenters failed to note that there are regional 
differences in carbofuran use, and as the scale becomes smaller, one 
would expect these differences to become even greater, precisely 
because use of carbofuran is sporadic in both time and space. Large 
areas would not be treated, but smaller areas, such as some drinking 
water watersheds considered by EPA may have a significantly higher 
proportion of their acreage treated than compared to national 
estimates.
    The commenters' point that control failures are more likely to 
occur on biotech corn refugia is valid and will tend to prevent 
treatment of large

[[Page 23067]]

contiguous areas of corn. However, not all farmers plant biotech corn. 
Further, farmers who do grow biotech corn do not locate their refugia 
universally in one part of the field, and there is no requirement that 
farmers in contiguous fields coordinate the location of their 
respective refugia. Consequently, the possibility that several 
contiguous corn fields could be simultaneously treated in any given 
year is not precluded. It is worth noting in this context that the 
September 2008 labels do not restrict application to the refugia. 
Moreover, in those areas where carbofuran is applied aerially, such as 
Nebraska, it is frequently easier for applicators to treat an entire 
field, rather than restricting their application to only select 
portions of the field. This is particularly true in smaller fields. 
Finally, because usage is often not evenly distributed across the 
landscape due to differences in factors like pest pressure, local 
consultant recommendations and weather, it may be much higher in some 
areas, and methods that account for this uncertainty, given the nature 
of the data, have not been developed.
    EPA agrees that the 87% default PCA that has been used for EPA's 
drinking water exposure assessments is likely a conservative estimate 
of sunflower acreage in a watershed. However, EPA has not developed 
PCAs for specific crops other than for corn, wheat, and cotton, 
consistent with guidance provided by the FIFRA SAP (Ref. 38). 
Nevertheless, the sunflower growers' own estimate of sunflower PCAs 
range as high as 25%, which certainly cannot support a PCA of 2.12% as 
one of the commenters suggested.
    One commenter complained that as part of the NMC CRA, EPA relied on 
actual ``county-or multi-county level pesticide use information, based 
on agricultural chemical use surveys'' to develop its estimates of 
potential exposure, rather than assuming 100% PCT.'' The commenter 
compares their surface water estimations to those developed by EPA for 
the NMC cumulative assessment, and claims that the two are consistent.
    While it is true that in the NMC assessment, EPA used PCT numbers 
to estimate the cumulative exposure from the contamination of such 
pesticides in surface water, this was done in order to more accurately 
account for the likelihood of pesticide co-occurrence at a single 
drinking water facility. But this does not mean that use of PCT is 
appropriate in conducting an assessment of aggregate exposure from 
carbofuran residues in surface water. This difference in approach 
between the assessment of a single chemical's aggregate exposure, and 
the assessment of the cumulative exposures from several chemicals, 
stems from the differences in the purpose and scope of the two 
assessments. These differences inevitably require the application of 
different methodologies.
    In evaluating the acute risks associated with a single chemical's 
contamination of drinking water, EPA must consider all of the 
variations permitted under the label. Drinking water exposures are 
driven by uniquely local factors; not only is the source of drinking 
water local (i.e. a person drinks water from his or her local water 
system not from a combination of water systems from across the United 
States), but the likelihood and degree of contamination of any 
particular, local drinking water source, whether it is a reservoir or 
well, varies widely based on local conditions (e.g, from local pest 
pressures, weather). Given this local variability, EPA must evaluate 
how all of the practices permitted under the label will affect drinking 
water exposures, because all are legally allowed, and farmers may 
choose any of them based on their particular individual local 
conditions. This means that even if typically growers, on a national or 
regional basis, do not frequently use a particular practice, EPA must 
still evaluate whether aggregate exposures from that practice would be 
safe because the practice is legally permissible and may be used due to 
local conditions. Thus, for example, even if most growers tend to apply 
the chemical only to a portion of the field, or typically only apply 
one-half of the maximum application rate, EPA must determine whether 
use by all or some growers to the entire field or at the maximum rate 
in a local watershed would result in unsafe drinking water 
concentrations.
    By contrast, it is not feasible to conduct the identical analysis 
for a cumulative assessment of related chemicals. Since the potential 
combinations of variations in pesticide use practices for the group of 
pesticides to be assessed are essentially infinite, even with computer 
modeling it would be impossible to model or evaluate all of the 
combinations allowed under the labels. EPA therefore needed to narrow 
its evaluation of the possible combinations to those deemed ``likely'' 
to occur. In contrast to the single chemical assessment, a cumulative 
assessment is intended to develop a snapshot in time of what is likely 
occurring at the moment. Moreover, the purpose of a cumulative 
assessment is to identify major sources of risk that could potentially 
accrue due to the concurrent use of several pesticides that act through 
a common mechanism of toxicity. Thus, EPA is primarily interested in 
the subset of circumstances in which residues from such pesticides 
occur concurrently (or co-occur).
    In addition, one of the important attributes of a cumulative risk 
assessment is that its scope and complexity can potentially lead to 
inflated estimates of risk due to compounding conservatisms, which 
would reduce the interpretability and ultimately the utility of the 
assessments. Because many data sets need to be combined, reducing the 
impact and likelihood of compounding conservative assumptions and over-
estimation bias becomes very important in constructing a reasonable 
cumulative risk assessment.
    When little or no information is available to inform potential 
sources of exposure, such as a reasonable or maximum watershed scale 
PCT, it is both scientifically and legally reasonable for a single 
chemical assessment to incorporate conservative assumptions to reflect 
reasonable worst-case exposure estimates. But in a cumulative risk 
assessment, the incorporation of such conservative assumptions would 
imply multiple simultaneous reasonable worst-case exposure estimates 
for each individual chemical. This is so unlikely that the results 
would no longer represent even a reasonable worst-case estimate of the 
likely risks. Consequently, some of the conservative assumptions 
appropriately used in the single chemical risk assessments are not 
appropriate or reasonable for use in a cumulative risk assessment, and 
vice versa.
    As a result, EPA chose in the NMC to work with those data that most 
closely reflect ``representative'' exposures, and developed 
``representative'' estimates of PCT in regional watersheds. However, to 
be clear, the PCT values used in the NMC assessment do not represent 
estimates of 50% of watersheds, or even the ``average'' watershed; 
rather, they represent values that are expected to be as likely to be 
accurate as not, based on a random selection of watersheds. A 
comparable example is the statistic that the average American family 
has approximately 2 children; this may or may not be true for any 
individual family, but there is an equally good chance that it will be 
accurate for any randomly selected family, as that it will not be 
accurate. For the cumulative assessment, EPA is able accept this level 
of uncertainty in these estimates, precisely because it has confidence 
that aggregate exposures from the individual chemicals will be safe, 
based on the level of conservatism in the single

[[Page 23068]]

chemical assessments. But given the statute's mandate to ensure a 
``reasonable certainty of no harm,'' EPA could not rely on the approach 
used under the cumulative assessment in the absence of the more 
conservative single-chemical assessment that evaluates the full range 
of exposures permitted by the registration.
    Nevertheless, as discussed in Unit VIII.E.3., in response to FMC's 
concerns EPA performed a sensitivity analysis of an exposure assessment 
using a PCT in the watershed to determine the extent to which some 
consideration of this factor could meaningfully affect the outcome of 
the risk assessment. The results suggest that, even at levels below 10% 
CT, exposures from drinking water derived from surface waters can 
contribute significantly to the aggregate dietary risks, particularly 
for infants and children. Accordingly, these assessments suggest that 
use of a reasonably conservative PCT estimate, even if one could be 
developed, would not meaningfully affect the carbofuran risk 
assessment, as aggregate exposures would still exceed 100% of the aPAD.
    One commenter raised the concern that USGS monitoring found that 
concentrations of carbofuran in agricultural streams ranged from non-
detect to 7 ppb (with a 95th percentile concentration of 0.044 ppb), 
noting that the monitoring strategy used by USGS for this program is 
likely to underestimate peak contamination levels (Ref. 114). The 
commenter argued that the USGS monitoring program is not designed to 
target waterways where carbofuran is in high use, or timed to coincide 
with predicted peak levels of pesticide runoff into waterways. 
Moreover, the frequency of sampling is normally weekly or bi-weekly, 
not enough to reliably sample the sporadic peaks that are predicted to 
be associated with pesticide application days or heavy runoff following 
rains. This monitoring strategy is more likely to capture the trends in 
chronic pollutants, but miss peak events such as pesticide runoff 
following rain. The sampling strategy biases towards the null; that is, 
it is likely to underestimate contamination by missing peak events when 
they occur, but will not over-represent non-detects. The commenter 
alleged that the fact that these data show routine detections of 
carbofuran in streams from agricultural land use areas suggests that 
there are likely to be peak events that go undetected. These data 
further support EPA's decision to cancel carbofuran and support 
rejecting FMC's proposal to restrict its use only in a limited number 
of watersheds. Because carbofuran is detected in streams across the 
nation, FMC's spatially limited mitigation plan would fail to protect 
many waterways from contamination.
    One commenter argued that FMC's proposal to restrict uses of 
carbofuran in the most vulnerable watersheds, to limit ground water 
contamination, would fail to provide adequate protection. The commenter 
noted ``substantial monitoring data showing that carbofuran has been 
detected by the USGS in 10.4% of over 2,000 stream-water samples taken 
from 83 agricultural streams monitored from 1992-2001, demonstrating 
that it is a widespread water pollutant and that geographically limited 
mitigation measures are not likely to be adequately protective.'' (Ref. 
114).
    EPA agrees with the commenters that the risks of surface water 
contamination from carbofuran are significant, and that FMC's September 
2008 labels do not mitigate the risks sufficiently.
    3. Aggregate exposures. One group of commenters presented a summary 
of some of the results of their own aggregate exposure assessment. 
According to these commenters, the results of their risk assessment 
demonstrate that carbofuran residues from the four domestic food uses, 
imports, and drinking water are ``safe.''
    EPA notes that the commenters merely provided summaries of the 
results of this assessment, and describe their methodology in only the 
most general terms, but chose not to provide the actual risk assessment 
to the Agency. Nor did the commenters provide any of their input files. 
Consequently, EPA was unable to fully evaluate the scientific adequacy 
of this assessment.
    The Agency's analyses result in food only exposures comparable to 
some of those reported by the commenters (e.g., exposures from the four 
import tolerances). But the remaining scenarios could not be verified 
since the commenters did not elaborate on the methods by which the 
detected concentrations found in the PDP milk samples were adjusted. 
Nor could EPA replicate the commenters' reported results. As discussed 
in more detail in Unit VIII.E.1., the Agency's assessment for this 
subset of foods differs slightly from the commenters due to PCT 
estimates (bananas), and more significantly, in the treatment of milk 
residues detected by the PDP program. Those differences cause the 
commenters' food only scenario (without accounting for any 
reversibility of AChE inhibition) to be slightly lower than the 
Agency's revised estimates (67% vs 78%).
    EPA was also unable to replicate the commenters' results for 
drinking water exposures, or for aggregated exposures from food and 
drinking water. The commenters report that in their water only 
scenario, the DEEM results were 350% aPAD, assuming a 5% crop treated 
value. However, as discussed previously VII.C.2.b., EPA believes that 
it lacks sufficient basis to assume that only 5% of the crop in a 
watershed will be treated.
    The commenters presented the results of their ``Eating Occasions 
Analyses'' for only one aggregate scenario, which was based on a Kansas 
corn drinking water scenario, and only for the infant subpopulation. It 
is based on this scenario that the commenters claim that aggregate 
exposure to carbofuran residues will be safe. The commenters appear to 
have also developed some other scenarios for corn, sunflowers, and 
potatoes that produce similar predicted drinking water concentrations; 
some of which have slightly higher peak concentrations. However, they 
did not present any results for those scenarios, nor provide any of the 
analyses to the Agency as part of their comments. As noted, EPA was 
unable to replicate these results. But as discussed below in Unit 
VIII.E., EPA disagrees that aggregate exposures to carbofuran residues 
are safe.
    One commenter raised the concern about the numbers of people 
exposed to unsafe levels of carbofuran. The commenter stated that EPA 
has determined that the aggregate exposures to carbofuran from food and 
water at doses greater than 0.000075 mg/kg/day/day, the aPAD, will not 
meet the safety standard of FFDCA section 408(b)(2). At the 99.9th 
percentile of exposure, aggregate dietary exposure from food alone 
exceeds the aPAD by 160% for children 6-12 years (approximately 36,000 
kids), and 210% for children 3-5 years old. The commenter stated that 
when these estimates are aggregated with ground water sources of 
drinking water from vulnerable areas, the predicted exposure exceeds 
the aPAD by 1,100% for adults over 50 years (approximately 71,000 
people) and over 10,000% for infants at the 99.9th percentile 
(approximately 4,000 infants). According to the commenter there are 
approximately 24,000,000 children under 5 years old in the United 
States, so 0.1% of this age group would mean leaving approximately 
24,000 children at risk, using the 99.9th percentile exposure 
estimates. According to the commenter, no reading of the statute will 
support any approach that allows thousands of children to be

[[Page 23069]]

exposed to a pesticide at levels that exceed the aPAD.
    EPA agrees that aggregate exposures to carbofuran do not meet the 
FFDCA's safety standard. The precise figures calculated by the 
commenter were based on exposures from all of the registered uses 
assessed in EPA's proposed rule; as many of those uses have been 
canceled, the number of affected children is expected to be lower. 
However, EPA agrees that based on its revised estimates, allowing 
children to continue to be exposed to carbofuran would not be 
consistent with the statute.

D. Comments Relating to Legal or Policy Issues

    A number of commenters raised concern that EPA had proposed to 
revoke all carbofuran tolerances before taking action against the 
pesticide registrations under FIFRA ``in the absence of an imminent 
health hazard.'' Several of these commenters raised concern that EPA 
had failed to comply with FFDCA section 408(l)'s requirement to 
``coordinate action [under the FFDCA] with any related necessary action 
under the [FIFRA].
    EPA has determined with respect to carbofuran both that the 
tolerances established for that chemical fail to meet the safety 
standard set forth in section 408 of the FFDCA and must therefore be 
revoked under that statute, and that the pesticide registrations fail 
to meet the relevant standard under FIFRA, and must therefore be 
canceled under that statute. Section 408(l)(1) of the FFDCA provides 
that ``[t]o the extent practicable and consistent with the review 
deadlines in subsection (q), in issuing a final rule that suspends or 
revokes a tolerance or exemption for a pesticide chemical residue in or 
on food, the Administrator shall coordinate such action with any 
related necessary action under [FIFRA].'' 21 U.S.C. 346a(l)(1). Nothing 
in this provision establishes a predetermined order for how the Agency 
is to proceed to resolve dietary risks. Nor does FIFRA include any 
provision that imposes a requirement that the Agency act first under 
FIFRA before it may act under the FFDCA in a situation such as 
carbofuran, where pesticide registrations and tolerances fail to meet 
the relevant legal standards of FIFRA and the FFDCA. Accordingly, there 
is no support for the notion that, as a matter of law, the Agency lacks 
the legal authority to revoke pesticide tolerances under the FFDCA that 
do not meet the safety standard of that statute unless the Agency has 
first canceled associated pesticide registrations under FIFRA.
    Coordination is defined as ``to place or arrange in proper order or 
position, to combine in harmonious relation or action.'' Thus, the 
requirement to ``coordinate'' is a direction to ensure that the 
substance of actions taken under the two statutes are consistent, and 
that the Agency make a determination as to the proper order of action 
under the two statutes. This cannot be read as a requirement that 
actions under FIFRA precede actions under the FFDCA, or that any 
particular order is necessarily required. Indeed, to the extent that 
this provision offers any direction with respect to the order of 
preference, the language actually suggests that the order in which EPA 
has proceeded is entirely appropriate. Section 408(l)(1) requires EPA 
to proceed ``consistent with the review deadlines in subsection (q).'' 
21 U.S.C. 346a(l)(1).
    One commenter raised concern that the FFDCA requires EPA to 
harmonize actions under FFDCA and FIFRA ``to the extent practicable.'' 
The commenter alleges that there is no excuse for not ``harmonizing 
action under both statutes'' in the absence of an ``imminent hazard.'' 
According to the commenter, ``harmonization would allow the key science 
issues to be resolved in an orderly manner before hasty action is 
taken, would avoid needless disruption and confusion of agriculture and 
the channels of trade, and would allow the benefits of the pesticide to 
be properly taken into account.''
    As explained in the previous response, the comment is based on a 
misconstruction of FFDCA section 408(l)(1). As a preliminary matter, 
EPA interprets the commenter's phrase ``harmonizing action under both 
statutes'' to mean either: (1) Pursuing action to cancel registrations 
under FIFRA prior to revoking tolerances or (2) holding a hearing 
pursuant to FIFRA and the FFDCA simultaneously. Section 408(l)(1) does 
not require EPA to do this; as discussed previously EPA is merely 
required to ``coordinate'' action under the two statutes, ``to the 
extent practicable and consistent with the review deadlines.'' Nor is 
there any basis in either FIFRA or the FFDCA for the commenter's 
alleged requirement that EPA determine that a pesticide presents an 
``imminent hazard,'' as that term is defined in FIFRA, prior to taking 
action to resolve dietary risks under the FFDCA.
    EPA chose to initially take action exclusively under the FFDCA to 
resolve carbofuran's dietary risks for a number of reasons. First and 
foremost, this was determined to be the quickest way to resolve acute 
dietary risks to children. In addition, the fact that this would 
resolve the issues most quickly would be beneficial to all parties, 
including the registrant and growers, since it would reduce costs and 
uncertainty for all by resolving the question of carbofuran's dietary 
risks.
    An additional consideration was the belief that this route would be 
more transparent, and would ensure that there would be no confusion as 
to the appropriate standard that would be used to resolve dietary risk 
concerns. The Agency was concerned that holding a hearing under FIFRA 
would lead growers to misunderstand the role that benefits could play 
in the ultimate decision. Indeed, the commenter's claim that 
``harmonization would allow the benefits of the pesticide to be 
properly taken into account'' confirms that EPA's concern was 
justified.
    Whether under FIFRA or the FFDCA, a pesticide's benefits are 
irrelevant in determining whether a pesticide presents an unacceptable 
dietary risk. Section 408(b)(2) clearly provides that the only standard 
is whether the pesticide chemical residues will be ``safe.'' 21 U.S.C. 
346a (b)(2). Nor is the evaluation of a pesticide's ``benefits'' 
included among the factors to be considered in determining whether 
residues will be ``safe.'' 21 U.S.C. 346a (b)(2)(B). FIFRA section 
2(bb) incorporates the FFDCA's standard explicitly and without 
modification, clearly distinct from the provisions that relate to 
consideration of the benefits of the pesticide. Thus, in any FIFRA 
hearing, if it is determined that use of a pesticide fails to meet the 
FFDCA section 408 safety standard, the pesticide must be canceled, 
irrespective of whether the benefits outweigh the ecological and 
occupational risks. But since under FIFRA, all issues are addressed in 
one hearing, the potential existed for confusion on the part of the 
members of the public, who might have an interest in the proceedings.
    Finally, EPA disagrees that it has failed to proceed in an orderly 
manner or that it has taken hasty action. By the time these tolerance 
revocations will be effective, EPA will have provided numerous 
opportunities for public comment, obtained peer review of the key 
science issues from the SAP, and will, if appropriate, hold a hearing 
on remaining issues of material fact. Further, notwithstanding the 
statutory deadlines in section 408(q) for identifying and resolving 
dietary risks, the registrant had 8 additional months to generate data 
to rebut the Agency's conclusions in the IRED. In total, the registrant 
and the public will have been

[[Page 23070]]

granted numerous opportunities and well over 2 years to comment on the 
key science issues. Given that carbofuran presents acute dietary risks 
to children, and the clear statutory deadline in FFDCA section 408(q), 
EPA believes it would be difficult to characterize its action as 
``hasty.''
    Some commenters objected to EPA's revocation of tolerances on the 
grounds that it was poor public policy because the action ``sets up 
farmers and food producers for unanticipated, unwarranted, and unfair 
enforcement action and penalties for presence of residues in food from 
otherwise legally treated crops.''
    EPA shares the concerns that farmers' crops not be subject to 
unfair or unwarranted penalties based on the Agency's choice to resolve 
carbofuran's dietary risks before proceeding with a cancellation. EPA 
has taken a number of measures in response to these concerns, to ensure 
that growers will not be unfairly penalized by the Agency's action.
    First, EPA has established delayed effective dates for all of the 
tolerance revocations, to provide growers with sufficient time to use 
up stocks of carbofuran that they currently have on hand. These dates 
are well after the end of the current growing season. These delayed 
effective dates also ensure that growers have sufficient notice of when 
these requirements will be applicable to allow them to factor this into 
their purchasing and application decisions. By the time the rule is 
scheduled to become effective, growers will have been informed of EPA's 
intentions well over a year in advance; this should be more than 
sufficient time to allow growers to plan around the final revocation 
dates. Finally, EPA has initiated discussions with FDA, and will 
continue to coordinate with FDA, to ensure that food that was treated 
before the effective date of the tolerance revocations will continue to 
be allowed to be sold.
     Late comments. EPA received a number of submissions after the 
close of the comment period. The majority of these were from FMC, the 
registrant of carbofuran. These submissions included a request to stay 
the effective date of the tolerance revocation, as well as requests 
that EPA consider additional issues and factual information in this 
final rule. In addition, one timely submitted comment questioned the 
legal basis for the statement in the proposed rule that failure to 
raise issues during the comment period would constitute a waiver of 
those issues, asserting that ``EPA's requirement. . .does not appear to 
be legally binding.''
    Sections 408(e)-(g) of the FFDCA provides a multi-step process for 
the establishment and revocation of tolerances, that provides ample 
opportunities for those with an interest in the tolerance to protect 
those interests. The process essentially consists of informal 
rulemaking, supplemented as appropriate with an administrative hearing. 
See, 21 U.S.C. 321a(e)-(g). As an informal rulemaking, the process is 
governed by section 553 of the Administrative Procedures Act, (APA) 
except to the extent section 408 provides otherwise, or to the extent 
the FFDCA falls within one of the APA's exceptions. Accordingly, the 
legal basis for the Agency's statement that issues not raised during 
the comment period on the proposed tolerance revocation may not be 
raised as objections or in any future proceeding, stems directly from 
the requirements of section 553 of the APA, and the case law 
interpreting these requirements. In this regard, it is well established 
that the failure to raise factual or legal issues during the comment 
period of a rulemaking, constitutes waiver of the issues in futher 
proceedings, [e.g., Forest Guardians v US Forest Service, 495 F.3d 
1162, 1170-1172 (10th Cir. 2007)] (Claim held waived where comments 
``failed to present its claims in sufficient detail to allow the agency 
to rectify the alleged violation''); Nuclear Energy Institute v EPA, 
373 F.3d 1251, 1290-1291 (D.C. Cir. 2004) (``To preserve a legal or 
factual argument, we require its proponent to have given the agency a 
`fair opportunity' to entertain it in the administrative forum before 
raising it in the judicial forum.'') Native Ecosystems Council v 
Dombeck, 304 F.3d 886, 889-900 (9th Cir. 2002) (Purpose of requirement 
that issues not presented at administrative level are deemed waived is 
to avoid premature claims and ensure that agency be given a chance to 
bring its expertise to bear to resolve a claim); Kleissler v. U.S. 
Forest Service, 183 F.3d 196, 202 (3d Cir. 1999) (Policy underlying 
exhaustion requirement is that ``objections and issues should first be 
reviewed by those with expertise in the contested subject area''); 
National Association of Manufacturers v US DOI, 134 F.3d 1095, 1111 
(D.C. Cir. 1998) (``We decline to find that scattered references to the 
services concept in a voluminous record addressing myriad complex 
technical and policy matters suffices to provide an agency like DOI 
with a `fair opportunity' to pass on the issue.'') Linemaster Switch 
Corporation v EPA, 938 F.2d 1299, (D.C.Cir. 1991) (declining to 
consider in challenge to final rule, data alluded to in comments, but 
not submitted during the comment period, and information submitted to 
EPA office that was not developing the rule). And nothing in the 
language or structure of the FFDCA alters this. As such, this is 
indisputably a binding legal requirement.
    The fact that section 408 of the FFDCA in certain limited 
circumstances supplements the informal rulemaking with a hearing, does 
not change the fundamental nature of the process. In other words, the 
addition of further process, through the availability of an 
administrative hearing to resolve certain factual disputes, does not 
fundamentally alter the requirements applicable to informal 
rulemakings. To this end, EPA interprets the notice and comment 
rulemaking portion of the process as inextricably linked to the 
administrative hearing. The point of the rulemaking is to resolve the 
issues that can be resolved, and to identify and narrow any remaining 
issues for adjudication. Accordingly the administrative hearing does 
not represent an unlimited opportunity to supplement the record, 
particularly with information that was available during the comment 
period, but that commenters have chosen to withhold. To read the 
statute otherwise would be to render the rulemaking portion of the 
process entirely duplicative of the hearing, and thus, ultimately 
meaningless. See, e.g., FDA v. Brown & Williamson Tobacco, 529 U.S. 
120, 132-133 (2000) (Court must interpret statute as a symmetrical and 
coherent regulatory scheme, and fit, if possible, all parts into an 
harmonious whole.) APW, AFL-CIO v Potter, 343 F.3d 619, 626 (2nd Cir. 
2003) (``A basic tenet of statutory construction. . .[is] that a text 
should be construed so that effect is given to all its provisions, so 
that no part will be inoperative or superfluous, void or insignificant, 
and so that one section will not destroy another...''), quoting, 
Silverman v Eastrich Mulitple Investor Fund, 51 F.3d 28, 31 (3rd Cir. 
1995). The equities of this construction are particularly strong, 
where, as here, the information was (or should have been) available 
during the comment period. See, Kleissler, 183 F.3d at 202 
(``[A]dministrative proceedings should not be a game or a forum to 
engage in unjustified obstructionism by making cryptic and obscure 
reference to matters that ``ought to be'' considered and then, after 
failing to do more to bring the matter to the agency's attention, 
seeking to have that agency determination vacated'') citing Vermont 
Yankee Nuclear Power Corp. v. N RDC, 435 U.S. 519, 553-54 (1978).

[[Page 23071]]

    Accordingly, in this final rule, EPA has not considered any of the 
information submitted after the close of the comment period.

VIII. Aggregate Risk Assessment and Conclusions Regarding Safety

    Consistent with section 408(b)(2)(D) of FFDCA, EPA has reviewed the 
available scientific data and other relevant information in support of 
this action. EPA's assessment of exposures and risks associated with 
carbofuran use follows:

A. Toxicological Profile

    Carbofuran is an NMC pesticide. Like other pesticides in this 
class, the primary toxic effect seen following carbofuran exposure is 
neurotoxicity resulting from inhibition of the enzyme AChE. AChE breaks 
down acetylcholine (ACh), a compound that assists in transmitting 
signals through the nervous system. Carbofuran inhibits the AChE 
activity in the body. When AChE is inhibited at nerve endings, the 
inhibition prevents the ACh from being degraded and results in 
prolonged stimulation of nerves and muscles. Physical signs and 
symptoms of carbofuran poisoning include headache, nausea, dizziness, 
blurred vision, excessive perspiration, salivation, lacrimation 
(tearing), vomiting, diarrhea, aching muscles, and a general feeling of 
severe malaise. Uncontrollable muscle twitching and bradycardia 
(abnormally slow heart rate) can occur. Severe poisoning can lead to 
convulsions, coma, pulmonary edema, muscle paralysis, and death by 
asphyxiation. Carbofuran poisoning also may cause various 
psychological, neurological and cognitive effects, including confusion, 
anxiety, depression, irritability, mood swings, difficulty 
concentrating, short-term memory loss, persistent fatigue, and blurred 
vision (Refs. 19 and 20).
    The most sensitive and appropriate effect associated with the use 
of carbofuran is its toxicity following acute exposure. Acute exposure 
is defined as an exposure of short duration, usually characterized as 
lasting no longer than a day. EPA classifies carbofuran as Toxicity 
Category I, the most toxic category, based on its potency by the oral 
and inhalation exposure routes. The lethal potencies of chemicals are 
usually described in terms of the ``dose'' given orally or the 
``concentration'' in air that is estimated to cause the death of 50 
percent of the animals exposed (abbreviated as LD50 or 
LC50). Carbofuran has an oral LD50 of 7.8-6.0 mg/
kg, and an inhalation LC50 of 0.08 mg/l (Refs. 16 and 20). 
The lethal dose and lethal concentration levels for the oral and 
inhalation routes fall well below the limits for the Toxicity Category 
I, <= 50 mg/kg and <= 0.2 mg/l, respectively (40 CFR 156.62).
    Carbofuran has a steep dose-response curve. In other words, a 
marginal increase in administered doses of carbofuran can result in a 
significant change in the toxic effect. For example, carbofuran data in 
juvenile rats (PND11 and 17) demonstrate that small differences in 
carbofuran doses (0.1 mg/kg to 0.3 mg/kg) can change the measured 
effect from significant brain and RBC AChE inhibition without clinical 
signs (0.1 mg/kg) to significant AChE inhibition, and resultant 
tremors, and decreased motor activity (0.3 mg/kg) (Refs. 45 and 83). In 
other words there is a slight difference in exposure levels that 
produce no noticeable outward effects and the level that causes adverse 
effects. This means that small differences in human exposure levels can 
have significant adverse consequences for large numbers of individuals.

B. Deriving Carbofuran's Point of Departure

    There are laboratory data on carbofuran for ChE activity in plasma, 
RBC, and brain from studies in multiple laboratory animals (rat, mouse, 
and dog). These studies have been submitted to EPA as part of pesticide 
registration and include a variety of durations of exposure and types 
of toxic effects (neurotoxicity, developmental toxicity, cancer, etc). 
Consistent with its mode of action, data on AChE inhibition provide the 
most sensitive effects for purposes of deriving a RfD or PAD.
    EPA uses a weight-of-evidence approach to determine the toxic 
effect that will serve as the appropriate PoD for a risk assessment for 
AChE inhibiting pesticides, such as carbofuran (Ref. 102). 
Neurotoxicity resulting from carbofuran exposures can occur in both the 
central (brain) and PNS. In its weight-of-the-evidence analysis, EPA 
reviews data, such as AChE inhibition data from the brain, peripheral 
tissues and blood (e.g., RBC or plasma), in addition to data on 
clinical signs and other functional effects related to AChE inhibition. 
Based on these data, EPA selects the most appropriate effect on which 
to regulate; such effects can include clinical signs of AChE 
inhibition, central or peripheral nervous tissue measurements of AChE 
inhibition or RBC AChE measures (Id). Due to the rapid nature of NMC 
pesticide toxicity, measures of AChE inhibition in the PNS are very 
rare for NMC pesticides. Although RBC AChE inhibition is not adverse in 
itself, it is a surrogate for inhibition in peripheral tissues when 
peripheral data are not available. As such, RBC AChE inhibition 
provides an indirect indication of adverse effects on the nervous 
system (Id). EPA and other state and national agencies such as 
California, Washington, Canada, the European Union, as well as the 
World Health Organization (WHO), across the world use blood measures in 
human health risk assessment and/or worker safety monitoring programs 
as surrogates for peripheral AChE inhibition.
    AChE inhibition in brain and the PNS is the initial adverse 
biological event which results from exposure to carbofuran, and with 
sufficient levels of inhibition leads to other effects such as tremors, 
dizziness, as well as gastrointestinal and cardiovascular effects, 
including bradycardia (Ref. 20). Thus, AChE inhibition provides the 
most appropriate effect to use in risk extrapolation for derivation of 
RfDs and PADs. Protecting against AChE inhibition ensures that the 
other adverse effects associated with cholinergic toxicity, mentioned 
above, do not occur.
    There are three studies available which compare the effects of 
carbofuran on PND11 rats with those in young adult rats (herein called 
comparative AChE studies) (Refs. 3, 4, 5, and 83). Two of these studies 
were submitted by FMC, the registrant, and one was performed by EPA-
ORD. An additional study conducted by EPA-ORD involved PND17 rats (Ref. 
79). Although it is not possible to directly correlate ages of juvenile 
rats to humans, PND11 rats are believed to be close in development to 
newborn humans. PND17 rats are believed to be closer developmentally to 
human toddlers (Refs. 12, 26, and 27). Other studies in adult rats used 
in the Agency's analysis included additional data from EPA-ORD (Refs. 
69, 78, and 83).
    The studies in juvenile rats show a consistent pattern that 
juvenile rats are more sensitive than adult rats to the effects of 
carbofuran. These effects include inhibition in AChE in addition to 
incidence of clinical signs of neurotoxicity such as tremors. This 
pattern has also been observed for other NMC pesticides, which exhibit 
the same mechanism of toxicity as carbofuran (Ref. 107). It is not 
unusual for juvenile rats, or indeed, for infants or young children, to 
be more sensitive to chemical exposures as metabolic detoxification 
processes in the young are still developing. Because juvenile rats, 
called `pups' herein, are more sensitive than adult rats, data from 
pups provide the most relevant information

[[Page 23072]]

for evaluating risk to infants and young children and are thus used to 
derive the PoD. In addition, typically (and this is the case for 
carbofuran) young children (ages 0-5 years) tend to be the most exposed 
age groups because they tend to eat larger amounts of food per their 
body weight than do teenagers or adults. As such, the focus of EPA's 
analysis of carbofuran's dietary risk from residues in food and water 
is on young children (ages 0 to 5 years). Since these age groups 
experience the highest levels of dietary risk, protecting these groups 
against the effects of carbofuran will, in turn, also protect other age 
groups.
    EPA evaluated the quality of the AChE data in all the available 
studies. In this review, particular attention was paid to the methods 
used to assay AChE inhibition in the laboratory conducting the study. 
Because of the nature of carbofuran inhibition of AChE, care must be 
taken in the laboratory such that experimental conditions do not 
promote enzyme reactivation (i.e., recovery) while samples of blood and 
brain are being processed and analyzed. If this reactivation occurs 
during the assay, the results of the experiment will underestimate the 
toxic potential of carbofuran (Refs. 50, 55, 76, 119, and 123). Through 
its review of available studies, the Agency identified problems and 
irregularities with the RBC AChE data from both FMC supported 
comparative ChE studies. These problems are described in detail in the 
Agency's study review (Refs. 24 and 25). As such, the Agency determined 
that the RBC AChE inhibition data from the two FMC comparative ChE 
studies were unreliable and not useable in extrapolating human health 
risk. In addition, RBC data from a study performed at EPA ORD did not 
provide doses low enough to adequately characterize the full dose-
response in PND11 rats. In the recent SAP review of the draft 
carbofuran NOIC, the Panel unanimously agreed with the Agency's 
conclusion, remarking that ``[t]he Agency is well-justified in taking 
the position that the data on AChE inhibition in rat RBC, particularly 
with regard to the PND11 pups, are not acceptable for the purpose of 
predicting health risk from carbofuran'' (Ref. 44). By contrast, the 
brain AChE data from the FMC and EPA-ORD studies are acceptable and 
have been used in the Agency's dose-response analysis.
    EPA has relied on a BMD approach for deriving the PoD from the 
available rat toxicity studies. A BMD is a point estimate along a dose-
response curve that corresponds to a specific response level. For 
example, a BMD10 represents a 10% change from the 
background; 10% is often used as a typical value for the response of 
concern (Ref. 100). Generically, the direction of change from 
background can be an increase or a decrease depending on the biological 
parameter and the chemical of interest. In the case of carbofuran, 
inhibition of AChE is the toxic effect of concern. Following exposure 
to carbofuran, the normal biological activity of the AChE enzyme is 
decreased (i.e., the enzyme is inhibited). Thus, when evaluating BMDs 
for carbofuran, the Agency is interested in a decrease in AChE activity 
compared to normal activity levels, which are also termed 
``background'' levels. Measurements of ``background'' AChE activity 
levels are usually obtained from animals in experimental studies that 
are not treated with the pesticide of interest (i.e., ``negative 
control'' animals).
    In addition to the BMD, a confidence limit was also calculated. 
Confidence limits express the uncertainty in a BMD that may be due to 
sampling and/or experimental error. The lower confidence limit on the 
dose used as the BMD is termed the BMDL, which the Agency uses as the 
PoD. Use of the BMDL for deriving the PoD rewards better experimental 
design and procedures that provide more precise estimates of the BMD, 
resulting in tighter confidence intervals. Use of the BMDL also helps 
ensure with high confidence (e.g., 95% confidence) that the selected 
percentage of AChE inhibition is not exceeded. From the PoD, EPA 
calculates the RfD and aPAD.
    Numerous scientific peer review panels over the last decade have 
supported the Agency's application of the BMD approach as a 
scientifically supportable method for deriving PoDs in human health 
risk assessment, and as an improvement over the historically applied 
approach of using no-observed-adverse-effect levels (NOAELs) or lowest-
observed-adverse-effect-levels (LOAELs). The NOAEL/LOAEL approach does 
not account for the variability and uncertainty in the experimental 
results, which are due to characteristics of the study design, such as 
dose selection, dose spacing, and sample size. With the BMD approach, 
all the dose response data are used to derive a PoD. Moreover, the 
response level used for setting regulatory limits can vary based on the 
chemical and/or type of toxic effect (Refs. 40, 42, 43, and 100). 
Specific to carbofuran and other NMCs, the FIFRA SAP has reviewed and 
supported the statistical methods used by the Agency to derive BMDs and 
BMDLs on two occasions, February 2005 and August 2005 (Refs. 42 and 
43). Recently, in reviewing EPA's draft NOIC, the SAP again unanimously 
concluded that the Agency's approach in using a benchmark dose to 
derive the PoD from carbofuran brain AChE data in juvenile rats is 
``state of the art science and the Panel strongly encouraged the Agency 
to follow this approach for all studies where possible'' (Ref. 44).
    In EPA's BMD dose analysis to derive PoDs for carbofuran, the 
Agency used a response level of 10% brain AChE inhibition and thus 
calculated BMD10s and BMDL10s based on the 
available carbofuran brain data. These values (the central estimate and 
lower confidence bound, respectively) represent the estimated dose 
where AChE is inhibited by 10% compared to untreated animals. In the 
last few years EPA has used this 10% value to regulate AChE inhibiting 
pesticides, including OPs and NMCs including carbofuran. For a variety 
of toxicological and statistical reasons, EPA chose 10% brain AChE 
inhibition as the response level for use in BMD and BMDL calculations. 
EPA analyses have demonstrated that 10% is a level that can be reliably 
measured in the majority of rat toxicity studies; is generally at or 
near the limit of sensitivity for discerning a statistically 
significant decrease in AChE activity across the brain compartment; and 
is a response level close to the background AChE level (Ref. 107)
    The Agency used a meta-analysis to calculate the BMD10 
and BMDL10 for pups and adults; this analysis includes brain 
data from studies where either adult or juvenile rats or both were 
exposed to a single oral dose of carbofuran. The Agency used a dose-
time-response exponential model where benchmark dose and half-life to 
recovery can be estimated together. This model and the statistical 
approach to deriving the BMD10s, BMDL10s, and 
half-life to recovery have been reviewed and supported by the FIFRA SAP 
(Refs. 42, 43, and 44). The meta-analysis approach offers the advantage 
over using single studies by combining information across multiple 
studies and thus provides a robust PoD.
    Using quality brain AChE data from the three studies (two FMC, one 
EPA-ORD) conducted with PND11 rats, in combination, provides data to 
describe both low and high doses. By combining the three studies in 
PND11 animals together in a meta-analysis, the entire dose-response 
range is covered. The Agency believes the BMD analysis for the PND11 
brain AChE data is the most robust analysis for purposes of PoD 
selection.
    The results of the BMD analysis for PND11 pup brain AChE data 
provide a BMD10 of 0.04 mg/kg/day and BMDL10

[[Page 23073]]

of 0.03 mg/kg/day--this BMDL10 of 0.03 mg/kg/day provides 
the PoD (Ref. 89).
    Some commenters provided extensive critique with regard to the BMD 
modeling conducted by the Agency. However, ultimately, the 
BMDL10 recommended by the commenters differs from the EPA's 
BMDL10 by only 6% (0.031 mg/kg/day vs. 0.033 mg/kg/day) -- a 
difference that is not biologically significant. Moreover, when rounded 
to one significant digit, both approaches yield the identical PoD of 
0.03 mg/kg/day. Thus, although the commenters are critical of the 
Agency's approach, there is basic consensus that the PoD is 
approximately 0.03 mg/kg/day.
    As noted, although EPA does not consider RBC AChE inhibition as an 
adverse effect in its own right, in the absence of data from peripheral 
tissues, RBC AChE inhibition data are a critical component to 
determining that a selected PoD will be sufficiently protective of PNS 
effects. Because of the problems discussed previously with the 
available RBC AChE inhibition data, there remains uncertainty 
surrounding the dose-response relationship for RBC AChE inhibition in 
pups, which the EPA-ORD data clearly show to be a more sensitive 
endpoint than brain AChE inhibition. Consequently, EPA cannot reliably 
estimate the BMD10 and BMDL10 for RBC AChE data 
in pups. Furthermore, given that the EPA-ORD data clearly show pup RBC 
AChE to be more sensitive than pup brain AChE, EPA cannot conclude that 
reliance on the pup brain data as the PoD would be sufficiently 
protective of PNS effects in pups. As a result of this uncertainty EPA 
must retain some portion of the children's safety factor as described 
below.

C. Safety Factor for Infants and Children

    1. In general. Section 408 of FFDCA provides that EPA shall apply 
an additional tenfold margin of safety for infants and children in the 
case of threshold effects to account for prenatal and postnatal 
toxicity and the completeness of the data base on toxicity and exposure 
unless EPA determines, based on reliable data, that a different margin 
of safety will be safe for infants and children. Margins of safety are 
incorporated into EPA assessments either directly through use of a 
margin of exposure analysis or through using uncertainty (safety) 
factors in calculating a dose level that poses acceptable risk to 
humans.
    In applying the children's safety factor provision, EPA has 
interpreted the statutory language as imposing a presumption in favor 
of applying an additional 10X safety factor (Ref. 105). Thus, EPA 
generally refers to the additional 10X factor as a presumptive or 
default 10X factor. EPA has also made clear, however, that 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.). 
The Agency's approach to evaluating whether sufficient ``reliable'' 
data exist to support the reduction or removal of the statutory default 
10X is described below in Figure 1.

[[Page 23074]]

[GRAPHIC] [TIFF OMITTED] TR15MY09.000

    2. Prenatal and postnatal sensitivity. Prenatal developmental 
toxicity studies with carbofuran in rat and rabbit, in addition to the 
reproductive toxicity and developmental neurotoxicity (DNT) studies do 
not provide evidence for developmental or reproductive effects from in 
utero exposure. Moreover, effects noted in these studies are less 
sensitive than AChE inhibition. Post-natal exposure to juvenile rat 
pups provides the most sensitive lifestage in available animal 
toxicology studies with NMCs, including carbofuran (Refs. 19, 107, 108, 
and 124).
    As noted in the previous section, there are several studies in 
juvenile rats that show they are more sensitive than adult rats to the 
effects of carbofuran. These effects include inhibition of brain AChE 
in addition to the incidence of clinical signs of neurotoxicity (such 
as tremors) at lower doses in the young rats. The SAP concurred with 
EPA that the data clearly indicate that the juvenile rat is more 
sensitive than the adult rat with regard to brain AChE (Ref. 44). 
However, the Agency does not have AChE data for carbofuran in the 
peripheral tissue of adult or juvenile animals; nor does the Agency 
have adequate RBC AChE inhibition data at low doses relevant to risk 
assessment to serve as a surrogate in pups. As previously noted the RBC 
AChE data from both FMC supported studies are not reliable and thus are 
not appropriate for use in risk assessment. Although the EPA studies 
did provide reliable RBC data, they did not include data at the low end 
of the dose-response curve, which is the area on the dose-response 
curve most relevant for risk assessment.
    There is indication in a toxicity study where pregnant rats were 
exposed to carbofuran that effects on the PNS are of concern; 
specifically, chewing motions

[[Page 23075]]

or mouth smacking was observed in a clear dose-response pattern 
immediately following dosing each day (Ref. 116). Based on this study, 
the California Department of Pesticide Regulation calculated a 
BMD05 and BMDL05 of 0.02 and 0.01 mg/kg/day, and 
established the acute PoD (Refs. 15 and 44). These BMD estimates are 
notable as they are close to the values EPA has calculated for brain 
AChE inhibition and which are being used as the PoD for extrapolating 
risk to children. It is important to note that these clinical signs 
have been reported for at least one other cholinesterase inhibiting 
pesticide at doses producing only blood, not brain, AChE inhibition 
(Ref. 68). Thus, although RBC AChE inhibition is not an adverse effect, 
per se, blood measures are used as surrogates in the absence of 
peripheral tissue data. Assessment of potential for neurotoxicity in 
peripheral tissues is a critical element of hazard characterization for 
NMCs like carbofuran. The lack of an appropriate surrogate to assess 
the potential for RBC AChE inhibition at low doses is a key uncertainty 
in the carbofuran toxicity database. Thus, EPA cannot conclude that 
reliance on the pup brain data solely as the PoD will be protective of 
PNS effects in pups.
    To account for the lack of data in the PNS and/or a surrogate 
(i.e., RBC AChE inhibition data) in pups at the low end of the response 
curve, and for the fact that RBC AChE inhibition appears to be a more 
sensitive point of departure compared to brain AChE inhibition (and is 
considered an appropriate surrogate for the PNS), EPA is retaining a 
portion of the children's safety factor. On the other hand, there are 
data available, albeit incomplete, which characterize the toxicity of 
carbofuran in juvenile animals, and the Agency believes the weight-of-
the-evidence supports reducing the statutory factor of 10X to a value 
lower than 10X. This results in a children's safety factor that is less 
than 10 but more than 1.
    This modified children's safety factor should take into account the 
greater sensitivity of the RBC AChE. The preferred approach to 
comparing the relative sensitivity of brain and RBC AChE inhibition 
would be to compare the BMD10 estimates. However, as 
described above, BMD10 estimates from the available RBC AChE 
inhibition data are not reliable due to lack of data at the low end of 
the dose response curve. As an alternative approach, EPA has used the 
ratio of brain to RBC AChE inhibition at the BMD50, since 
there are quality data at or near the 50% response level such that a 
reliable estimate can be calculated. There is, however, an assumption 
associated with using the 50% response level--namely that the magnitude 
of difference between RBC and brain AChE inhibition is constant across 
dose. In other words, EPA is assuming the RBC and brain AChE dose 
response curves are parallel. There are currently no data to test this 
assumption for carbofuran.
    The Agency has determined that a children's safety factor of 4X is 
appropriate based on a weight-of-evidence approach. This safety factor 
is calculated using the ratio of RBC and brain AChE inhibition, using 
the data on administered dose for the PND11 animals from the EPA-ORD 
studies and the FMC studies combined. In other words, EPA estimated the 
BMD50 for PND11 animals for RBC and brain from each quality 
study and used the ratio from the combined analysis, resulting in a 
BMD50 ratio of 4.1X. EPA estimated the RBC to brain potency 
ratio using EPA's data for RBC (the only reliable RBC data in PND11 
animals for carbofuran) and all available data in PND11 animals for 
brain.
    EPA also compared the BMD50 ratios for PND17 pups (who 
are slightly less sensitive than 11-day olds; see Figure 2) in the EPA-
ORD study, to confirm that the differences in sensitivity between RBC 
and brain were not unique to the PND11 data. The result of EPAs 
modeling shows a BMD50 ratio of 2.6\4\ X between brain and 
RBC in the PND17 pups.
---------------------------------------------------------------------------

    \4\ One commenter noted that EPA had inadvertently failed in its 
BMD analysis of the PND17 data, to convert the units from hours to 
minutes. EPA has corrected its error, and has recalculated the 
BMD50s for the PND17 animals, using the corrected times. 
The BMD50 ratio for brain and RBC is now 2.6, rather than 
the 3.3 originally estimated based on its original oversight.
---------------------------------------------------------------------------

    On the basis of the available data, EPA believes that application 
of a 4X factor will be ``safe'' for infants and children. This 
selection was made based on: (1) The remaining uncertainty regarding 
lack of an appropriate measure of peripheral toxicity (i.e., lack of 
RBC AChE inhibition data at the low end of the dose response curve), 
and (2) the RBC to brain AChE ratio at the BMD50 for PND11 
animals of 4.1X.

[[Page 23076]]

[GRAPHIC] [TIFF OMITTED] TR15MY09.001

    EPA presented its dietary risk assessment of carbofuran to the 
FIFRA SAP, and requested comment on the Agency's approach to selecting 
the PoD and the children's safety factor. As described in the proposal, 
the Agency believes that the Panel's responses unambiguously support 
the Agency's approach with regard to carbofuran's hazard identification 
and hazard characterization (73 FR 44864). In addition, EPA believes 
that, on balance, the application of a 4X children's safety factor is 
consistent with the SAP's advice. Additional detail on the SAP's advice 
and EPA's responses can be found at Reference 34.
    EPA received the greatest number of comments for the proposed 
tolerance revocation on the children's safety factor. However, none of 
the commenters provided any new data nor information that changes the 
Agency's major conclusions with regard to the uncertainty factor, and 
the methodology used to assess risks as a result of dietary exposures 
to carbofuran.
    In sum, EPA has concluded that there is reliable data to support 
the application of a 4X safety factor and has therefore applied this 
safety factor in its dietary risk estimates.

D. Hazard Characterization and Point of Departure Conclusions.

    The doses and toxicological endpoints selected and Margins of 
Exposures for various exposure scenarios are summarized below.

                                  Table 1.--Toxicology Endpoint Selection Table
----------------------------------------------------------------------------------------------------------------
                                                                    FQPA factor and
          Exposure Scenario               Dose Used in Risk        Endpoint for Risk     Study and Toxicological
                                            Assessment, UF             Assessment                Effects
----------------------------------------------------------------------------------------------------------------
Acute Dietary Infants and Children     BMDL10 = 0.03 mg/kg/day  Children's SF = 4X       Comparative AChE
                                       UF = 100...............  aPAD = 0.000075 mg/kg/    Studies in PND11 rats
                                       Acute RfD = 0.0003 mg/    day.                     (FMC and EPA-ORD)
                                        kg/day.                                          BMD10 = 0.04 mg/kg/day
                                                                                         BMDL10 = 0.03 mg/kg/
                                                                                          day, based on brain
                                                                                          AChE inhibition of
                                                                                          postnatal day 11
                                                                                          (PND11) pups
----------------------------------------------------------------------------------------------------------------
Acute Dietary Youth (13 and older)     BMDL10 = 0.02 mg/kg/day  aRfD = 0.0002 mg/kg/day  Comparative AChE Study
 and Adults                            UF = 100...............                            (EPA-ORD), Padilla et
                                       Acute RfD = 0.00024 mg/                            al (2007), McDaniel et
                                        kg/day.                                           al (2007)
                                                                                         BMD10 = 0.06 mg/kg/day
                                                                                         BMDL10 = 0.02 mg/kg/
                                                                                          day, based on RBC AChE
                                                                                          inhibition in adult
                                                                                          rat
----------------------------------------------------------------------------------------------------------------


[[Page 23077]]

E. Dietary Exposure and Risk Assessment

    1. Dietary exposure to carbofuran--Food--a. EPA methodology and 
background. As noted earlier, in their September 29, 2008 comments on 
the Agency's risk assessment, FMC requested cancellation of a large 
number of domestic food uses, including, among other uses, artichokes, 
peppers, and all cucurbits except pumpkins. EPA granted the request, 
and accordingly, conducted a refined (Tier 3) acute probabilistic 
dietary risk assessment for the remaining carbofuran residues in food. 
The remaining sources of ``food'' exposures are from the domestic uses 
of field corn, potato, sunflower, pumpkins, as well as milk (indirect 
residues through use on corn, potatoes and sunflower), and from four 
import tolerances (bananas, coffee, sugarcane, and rice). To conduct 
the assessment, EPA relied on DEEM-FCID\(TM)\, Version 2.03, which uses 
food consumption data from the USDA's CSFII from 1994-1996 and 1998.
    Using data on the percent of the crop actually treated with 
carbofuran and data on the level of residues that may be present on the 
treated crop, EPA developed estimates of combined anticipated residues 
of carbofuran and 3-hydroxycarbofuran on food. 3-hydroxycarbofuran is a 
degradate of carbofuran and is assumed to have toxic potency equivalent 
to carbofuran (Refs. 16 and 20). Anticipated residues of carbofuran for 
most foods were derived using USDA PDP monitoring data from recent 
years (through 2006 for all available commodities). In some cases, 
where PDP data were not available for a particular crop, EPA translated 
PDP monitoring data from surrogate crops based on the characteristics 
of the crops and the use patterns. For example, PDP data for winter 
squash were used to derive anticipated residues for pumpkins.
    The PDP analyzed for parent carbofuran and its metabolite of 
concern, 3-hydroxycarbofuran. Most of the samples analyzed by the PDP 
were measured using a high Level of Detection (LOD) and contained no 
detectable residues of carbofuran or 3-hydroxycarbofuran. Consequently, 
the acute assessment for food assumed a concentration equal to one-half 
of the LOD for PDP monitoring samples with no detectable residues, and 
zero ppm carbofuran to account for the percent of the crop not treated 
with carbofuran.
    An additional source of data on carbofuran residues was provided by 
a market basket survey of NMC pesticides in single-serving samples of 
fresh fruits and vegetables collected in 1999-2000 (Ref. 18), which was 
sponsored by the Carbamate Market Basket Survey Task Force. EPA relied 
on these data to construct the residue distribution files for bananas 
because the use of these data resulted in more refined exposure 
estimates. The combined Limits of Quantitation (LOQs) for carbofuran 
and its metabolite in the Market Basket Survey (MBS) were between 
tenfold and twentyfold lower than the combined LODs in the PDP 
monitoring data.
    For certain crops where PDP data were not available (sugarcane, and 
sunflower seed), anticipated residues were based on field trial data. 
EPA also relied on field trial data for particular food commodities 
that are blended during marketing (field corn and rice), as use of PDP 
data can result in significant overestimates of exposure when 
evaluating blended foods. Field trial data are typically considered to 
overestimate the residues that are likely to occur in food as actually 
consumed because they reflect the maximum application rate and shortest 
preharvest interval allowed by the label. However, for crops that are 
blended during marketing, such as corn or wheat, use of field trial 
data can provide a more refined estimate than PDP data, by allowing EPA 
to better account for the percent of the crop actually treated with 
carbofuran.
    EPA used average and maximum PCT estimates for most crops, 
following the guidance provided in HED SOP 99.6 (Classification of Food 
Forms with Respect to level of Blending; 8/20/99), and available 
processing and/or cooking factors. The maximum PCT estimates were used 
to refine the acute dietary exposure estimates. Maximum PCT ranged from 
<1 to 10%. The estimated percent of the crop imported was applied to 
crops with tolerances currently maintained solely for import purposes 
(banana, coffee, sugarcane, and rice).
    b. Acute dietary exposure (food alone) conclusions. The estimated 
acute dietary exposure from carbofuran residues in food alone (i.e., 
assuming no additional carbofuran exposure from drinking water), are 
below EPA's level of concern for the U.S. Population and all population 
subgroups. Children 1 to 2 years of age (78% aPAD) were the most highly 
exposed population subgroup when food only was included. The major 
driver of the acute dietary exposure risk (food only) for Children 1 to 
2 years is milk at greater than 90% of the exposure. (See results from 
Table 2 below).

                       Table 2.--Results of Acute Dietary Exposure Analysis for Food Alone
----------------------------------------------------------------------------------------------------------------
                                                                   99th Percentile          99.9th Percentile
                                                 aPAD (mg/kg/---------------------------------------------------
              Population Subgroup                    day)       Exposure                  Exposure
                                                              (mg/kg/day)     % aPAD    (mg/kg/day)     % aPAD
----------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                          0.000075     0.000013           18     0.000039           52
----------------------------------------------------------------------------------------------------------------
Children 1-2 years old                              0.000075     0.000024           32     0.000058           78
----------------------------------------------------------------------------------------------------------------
Children 3-5 years old                              0.000075     0.000015           20     0.000034           45
----------------------------------------------------------------------------------------------------------------
Children 6-12 years old                             0.000075     0.000010           13     0.000022           29
----------------------------------------------------------------------------------------------------------------

    Exposure estimates for all of the major food contributors were 
based on PDP monitoring data adjusted to account for the percent of the 
crop treated with carbofuran and, therefore, may be considered highly 
refined.
    As noted previously, in response to comments, the Agency revised 
its PCT estimates for the bananas from 78% to 25%. The Agency also 
developed a regional PCT estimate for potatoes of 5% based on projected 
limited use in the Northwest, and has applied that estimate in its 
revised dietary risk assessment (Ref. 71). Based on the estimated 5% 
crop treated for potato, which is the highest PCT of any feed stuff 
that can be treated with carbofuran, EPA estimated a 5% CT for milk.

[[Page 23078]]

    The Agency notes that these PCT changes on bananas, potatoes and 
milk had relatively modest effects on the dietary exposure estimates. 
The PCT estimates are used by the Agency to account for the fact that 
not all samples are treated, and that some fraction of samples 
(specifically, the complement to the PCT fraction) actually have 
residues of zero. This allows the Agency to incorporate a residue 
concentration of zero (a true zero) for that fraction of the crop which 
is not treated and a residue concentration of [frac12] the analytical 
limit of detection for that portion of the crop which is treated, but 
show no detectable residues because of insufficient sensitivity of the 
analytical method. Specifically in this case, if one were to assume for 
banana, potatoes, and milk that all samples without detectable residues 
were not treated and are thus ``true zeroes,'' then exposure at the per 
capita 99.9th percentile falls only slightly: from 77.8% to 75.2% of 
the aPAD for children 1 to 2 years old, and from 45.4% to 44.1% of the 
aPAD for children 3-5 years old.
    The relative insensitivity of exposure estimates to PCT found under 
EPA's most recent risk assessment based on the September 2008 revised 
label, is counter to earlier sensitivity analyses that the Agency 
performed that indicate exposures at the per capita 99.9th percentile 
fall by about 50% when all non-detects were set at 0 ppm (Ref. 70). 
Those effects were due to the watermelons and other commodities 
(cucumbers, cantaloupes) that were the primary source of unacceptable 
single exposures. The Half LODs for the four domestic uses that the 
commenters currently are interested in retaining, and milk, are 
relatively low, such that exposures from residues at Half LOD 
concentrations produce nominal contributions to high-end exposures.
    As a further consequence of the cancellation of the use on melons 
and cucmbers, the risk assessment now shows that single exposures from 
food alone are not expected to be the source of unacceptable single 
eating events. However, as discussed in Unit VIII.E.2. below, concerns 
still remain that children will receive unacceptable exposures from a 
single consumption of contaminated drinking water. Further, even after 
accounting for carbofuran's reversibility throughout the day and the 
fact that drinking water can be consumed over multiple occasions during 
the day, EPA has concluded that carbofuran exposures through the 
drinking water pathway exceed the Agency's level of concern for infants 
and children.
    2. Drinking water exposures. EPA's drinking water assessment uses 
both monitoring data for carbofuran and modeling methods, and takes 
into account contributions from both surface water and ground water 
sources (Refs. 17, 54, 58, 61, and 84). Concentrations of carbofuran in 
drinking water, as with any pesticide, are in large part determined by 
the amount, method, timing and location of pesticide application, the 
chemical properties of the pesticide, the physical characteristics of 
the watersheds and/or aquifers in which the community water supplies or 
private wells are located, and other environmental factors, such as 
rainfall, which can cause the pesticide to move from the location where 
it was applied. While there is a considerable body of monitoring data 
that has measured carbofuran residues in surface and ground water 
sources, the locations of sampling and the sampling frequencies 
generally are not sufficient to capture peak concentrations of the 
pesticide in a watershed or aquifer where carbofuran is used. Capturing 
these peak concentrations is particularly important for assessing risks 
from carbofuran because the toxicity end-point of concern results from 
single-day exposure (acute effects). Because pesticide loads in surface 
water tend to move in relatively quick pulses in flowing water, 
frequent targeted sampling is necessary to reliably capture peak 
concentrations for surface water sources of drinking water. Pesticide 
concentrations in ground water, however, are generally the result of 
longer-term processes and less frequent sampling can better 
characterize peak ground water concentrations. However, such data must 
be targeted at vulnerable aquifers in locations where carbofuran 
applications are documented in order to capture peak concentrations. As 
a consequence, monitoring data for both surface and ground water tends 
to underestimate exposure for acute endpoints. Simulation modeling 
complements monitoring by making estimations at vulnerable sites and 
can be used to represent daily concentration profiles, based on a 
distribution of weather conditions. Thus, modeling can account for the 
cases when a pesticide is used in drinking water watersheds at any rate 
and is applied to a substantial proportion of the crop. It can also 
account for stochastic processes, such as rainfall represented by 30 
years of existing weather data maintained by NOAA.
    a. Exposure to carbofuran from drinking water derived from ground 
water sources. Drinking water taken from shallow wells is highly 
vulnerable to contamination in areas where carbofuran is used around 
sandy, highly acidic soil, although sites that are less vulnerable 
(e.g., deeper aquifer, higher organic matter) could still be prone to 
have concentrations exceeding acceptable exposures. The results of the 
ground water modeling simulations from the South-Central Wisconsin 
scenario show that the persistence of carbofuran in ground water is 
dependent on soil and water pH, and what might appear as relatively 
small variations in soil pH can have a significant impact on estimates 
of carbofuran in ground water. Estimated 1-in-10-year peak ground water 
concentrations at pH 7 are 1.6 x 10-3 [mu]g/L; however, the 
estimated 1-in-10-year peak ground water concentration at pH 6.5 is 16 
[mu]g/L, nearly 4 orders of magnitude greater. Because of carbofuran's 
sensitivity to pH, EPA has concerns that any given set of mitigation 
measures will not successfully protect ground water source drinking 
water. Data indicate that pH varies across an agricultural field, and 
also with depth (Ref. 64). In particular, the pH can be different in 
ground water than in the overlying soil. The upper bound of the 
carbofuran concentrations estimated by EPA at pH 6.5 is much greater 
than the concentrations FMC report in their comments.
    In EPA's revised assessment, ground water concentrations were 
estimated for all remaining crops on carbofuran labels, and used two 
new Tier 2 scenarios. Based on a new corn scenario, representative of 
potentially vulnerable areas in the upper Midwest, EPA estimated 1-in-
10-year concentrations for ground water source drinking water of 16 to 
1.6 x 10-3 [mu]g/L, for pH 6.5 and 7, respectively. A potato scenario 
representing use in the Northwest estimated no measurable 
concentrations of carbofuran in ground water. Other remaining uses were 
modeled using a Tier 1 ground water model (Screening Concentration in-
Groundwater) with estimated peak 90-day concentrations of 48 - 178 
[mu]g/L, depending on application rate. Well setback prohibitions of 50 
feet were proposed on the new label for the flowable and granular 
formulations in select counties in Kentucky (seven counties), Louisiana 
(one county), Minnesota (one county), and Tennessee (one county). 
Analysis of the impact of these setbacks for the use on corn indicated 
that the setbacks would not reduce concentrations significantly at 
locations where exposure to carbofuran in ground water is of concern 
because

[[Page 23079]]

at acid pHs, carbofuran does not degrade sufficiently during the travel 
time from the application site to the well to substantially reduce the 
concentration.
    Exposure estimates for this assessment are drawn primarily from 
EPA's modeling. To conduct its modeling, EPA examined readily available 
data with respect to ground water and soil pH to evaluate the spatial 
variability of pH. Ground water pH values can span a wide range; this 
is especially true for shallow ground water systems, where local 
conditions can greatly affect the quality and characteristics of the 
water (higher or lower pHs compared to average values). Thus, average 
ground water pH values for a given area do not truly characterize the 
(temporal and especially spatial) heterogeneity common in most areas. 
This can be seen by comparing differences in pH values between counties 
within a state, and noting that even within each county specific area, 
wells will consistently yield ground water with either above- or below-
average pH values for that county. The ground water simulations reflect 
variability in pH by modeling carbofuran leaching in four different pH 
conditions (pH 5.25, 6.5, 7.0, and 8.7), representing the range in the 
Wisconsin aquifer system. The upper and lower bound of pH values that 
EPA chose for this assessment were measured values from the aquifer, 
and the remaining two values were chosen to reflect common pH values 
between the measured values.
    The Idaho potato scenario is representative of areas where ground 
water is relatively deep and the soils have a relatively alkaline pH. 
The results from the Idaho potato ground water simulation estimated no 
measurable concentrations of carbofuran in ground water. This is 
consistent with EPA's findings above, as soils where potatoes are 
typically grown are more alkaline.
    The results of EPA's revised corn modeling, based on a new scenario 
in Wisconsin, are consistent with the results of the PGW study 
developed by the registrant in Maryland in the early 1980s. Using 
higher use rates than currently permitted, the peak concentration 
measured in the PGW study was 65 ppb; when scaled to current use rates, 
the estimated peak concentration was 11 ppb. EPA's modeling is also 
consistent with a number of other targeted ground water studies 
conducted in the 1980s showing that high concentrations of carbofuran 
can occur in vulnerable areas; the results of these studies as well as 
the PGW study are summarized in References 17 and 84. For example, a 
study in Manitoba, Canada assessed the movement of carbofuran into tile 
drains and ground water from the application of liquid carbofuran to 
potato and corn fields. The application rates ranged between 0.44-0.58 
pounds a.i./acre, and the soils at the site included fine sand, loamy 
fine sand, and silt loam, with pH ranging between 6.5-8.3. 
Concentrations of carbofuran in ground water samples ranged between 0 
(non-detect) and 158 ppb, with a mean of 40 ppb (Refs. 17 and 84).
    While there have been additional ground water monitoring studies 
that included carbofuran as an analyte since that time, there has been 
no additional monitoring targeted to carbofuran use in areas where 
aquifers are vulnerable. However, as discussed in the next section, 
data compiled in 2002 by EPA's Office of Water show that carbofuran was 
detected in treated drinking water at a few locations. Based on samples 
collected from 12,531 ground water supplies in 16 states, carbofuran 
was found at one public ground water system at a concentration of 
greater than 7 ppb and in two ground water systems at concentrations 
greater than 4 ppb (measurements below this limit were not reported). 
An infant receiving these concentrations receive 220% of the aPAD or 
130% aPAD, respectively, based on a single 8 ounce serving of water. As 
this monitoring was not targeted to carbofuran, the likelihood is low 
that these samples capture peak concentrations. Given the lack of 
targeted monitoring, EPA has primarily relied on modeling to develop 
estimates of carbofuran residues in ground water sources of drinking 
water.
    Based on EPA's assessment, the maximum 1-in-10-year peak carbofuran 
concentrations in vulnerable ground water for a single application on 
corn in Wisconsin, at a rate of 1 pound per acre were estimated to 
range from a low of less than 1 ppb based on a pH of 7 or higher, to a 
high of 16 ppb, based on a pH of 6.5\5\. Because the degradate, 3-
hydroxycarbofuran, which is assumed to be of equal potency with the 
parent compound, was not measured in the PGW study, and key 
environmental fate data are not available to use in modeling, exposure 
was not estimated. Although the failure to include the degradate is 
expected to underestimate exposure to some degree, the extent to which 
it would contribute to exposure is unclear.
---------------------------------------------------------------------------

    \5\ Although higher estimates were generated at a pH of 5.25, 
use should be precluded in such sites based on the September 2008 
labels.
---------------------------------------------------------------------------

    EPA compiled a distribution of estimated carbofuran concentrations 
in water based on these estimates that were used to generate 
probabilistic assessments of the potential exposures from drinking 
water derived from vulnerable ground water sources. The results of 
EPA's probabilistic assessments are represented below in Table 3. As 
discussed in the previous section, it is important to remember that the 
aPAD for carbofuran is quite low, hence, relatively low concentrations 
of carbofuran monitored or estimated in vulnerable ground water can 
have a significant impact on the aPAD utilized.

Table 3.--Results of Acute Dietary (Ground Water Only) Exposure Analysis Using DEEM-FCID\(TM)\ and Incorporating the Wisconsin Ground Water Scenario, pH
                                                           of 6.5 (Representing Private Wells)
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                      95th Percentile         99th Percentile        99.9th Percentile
                                                                     aPAD (mg/kg/-----------------------------------------------------------------------
                        Population Subgroup                              day)       Exposure                Exposure                Exposure
                                                                                  (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD
--------------------------------------------------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                                              0.000075     0.001602      2,100     0.003536      4,700     0.007078      9,400
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 1-2 years old                                                  0.000075     0.000677        900     0.001481      2,000     0.003163      4,200
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 3-5 years old                                                  0.000075     0.000623        830     0.001345      1,800     0.002845      3,800
--------------------------------------------------------------------------------------------------------------------------------------------------------

[[Page 23080]]

 
Children 6-12 years old                                                 0.000075     0.000431        570     0.000934      1,200     0.002015      2,700
--------------------------------------------------------------------------------------------------------------------------------------------------------
Youth 13-19 years old                                                     0.0002     0.000334        170     0.000756        380     0.001743        870
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 20-49 years old                                                    0.0002     0.000414        210     0.000893        450     0.001890        950
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 50+ years old                                                      0.0002     0.000413        210     0.000852        430     0.001546        770
--------------------------------------------------------------------------------------------------------------------------------------------------------

    While the registrant has attempted to address drinking water 
exposure from ground water sources by including additional restrictions 
on their September 2008 proposed labels, EPA's analyses show that these 
do not sufficiently reduce exposures to acceptable levels. The proposed 
labels include well setback prohibitions at 50-foot-distances for the 
flowable and granular formulations in a select set of counties in 
Kentucky, Louisiana, Minnesota, and Tennessee. The impact of the well 
setbacks was modeled for the corn use using the approach developed for 
the NMC cumulative assessment (Ref. 107), resulting in reductions in 
concentrations that vary with pH (to account for degradation of the 
compound in subsurface flow from the application site to a private well 
down gradient). At acid pHs the slow degradation rate reduced the 
effectiveness of a 50-foot well setback at the well head (1-in-10-year 
peak concentration of 16 to 14 [mu]g/L, a reduction factor of 0.73 at 
pH 6.5). Additional setback distances (100, and 300 ft) were evaluated 
using an aquifer pH of 6.5, resulting in reduction factors of 0.54 and 
0.16, respectively. At alkaline pH, the 50-foot setback is effective, 
but concentrations at these sites are already low due to hydrolytic 
degradation occurring during recharge. These results suggest that a 50-
foot well setback is less effective in low pH environments due to the 
persistence of carbofuran under these conditions.
    In addition, the revised labels prohibit use throughout the 
Atlantic Coastal plain, and prohibit application to areas with soils 
greater than 90% sand and less than 1% organic matter, acidic soil and 
water conditions, and where shallow water tables predominate (e.g., 
where ground water is less than 30 feet). While EPA agrees in principle 
that precluding use in sites vulnerable to leaching can mitigate the 
risks, and even presuming that the methodology used by FMC adequately 
identifies those sites, these criteria are not sufficient to prohibit 
use in all areas that could reasonably be expected to be vulnerable to 
ground water contamination from carbofuran use. Based on carbofuran's 
characteristics, a diversity of soil conditions in the remaining 
proposed use area, and available monitoring data, there are valid 
scientific reasons to believe that additional soil and site 
characteristics could result in ground water contamination. For 
example, water table depth can vary with the time of the year, 
depending on such factors as the amount of rainfall that has occurred 
in the recent past, and how much irrigation has been applied to a field 
or removed from the aquifer. It is difficult to determine how the depth 
to the water table varies throughout fields, and the definition of a 
``shallow'' water table on the September 2008 label is indeterminate 
(e.g., less than 30 ft.). Furthermore, the vulnerability associated 
with depth varies with location, for example, deeper aquifers may be 
vulnerable in areas with greater precipitation and rapid recharge. The 
September 2008 label restrictions in no way addressed these less 
sensitive, but still vulnerable, sites (Refs. 94 and 111). Accordingly, 
EPA continues to believe that its assessment of drinking water from 
ground water sources based on current labels is a reasonable assessment 
of potential exposures to those portions of the population consuming 
drinking water from shallow wells in highly vulnerable areas.
    b. Exposure from drinking water derived from surface water sources. 
EPA's evaluation of environmental drinking water concentrations of 
carbofuran from surface water, as with its evaluation of ground water, 
takes into account the results of both surface water monitoring and 
modeling.
    Data compiled in 2002 by EPA's Office of Water show that carbofuran 
was detected in treated drinking water at a few locations. Based on 
samples collected from 12,531 ground water and 1,394 surface water 
source drinking water supplies in 16 states, carbofuran was found at no 
public drinking water supply systems at concentrations exceeding 40 ppb 
(the MCL). Carbofuran was found at one public ground water system at a 
concentration of greater than 7 ppb and in two ground water systems and 
one surface water public water system at concentrations greater than 4 
ppb (measurements below this limit were not reported). Sampling is 
costly and is conducted typically four times a year or less at any 
single drinking water facility. The overall likelihood of collecting 
samples that capture peak exposure events is, therefore, low. For 
chemicals with acute risks of concern, such as carbofuran, higher 
concentrations and resulting risk is primarily associated with these 
peak events, which are not likely to be captured in monitoring unless 
the sampling rate is very high.
    Unlike drinking water derived from private ground water wells, 
drinking water from public water supplies (surface water or ground 
water source) will generally be treated before it is distributed to 
consumers. An evaluation of laboratory and field monitoring data 
indicate that carbofuran may be effectively removed (60 - 100%) from 
drinking water by lime softening and activated carbon; other treatment 
processes are less effective in removing carbofuran (Ref. 107). The 
detections between 4 and 7 ppb, reported above, represent 
concentrations in samples collected post-treatment. As such, these 
levels are of particular concern to the Agency. An infant who consumes 
a single 8-ounce serving of water with a concentration of 4 ppb, as 
detected in the monitoring, would receive approximately 130% of the 
aPAD from water consumption alone. An infant who consumes a single 8-
ounce serving of water with the higher detected concentration of 7 ppb, 
as detected in the monitoring, would receive approximately 220% of the 
aPAD from water consumption alone.
    To further characterize carbofuran concentrations in surface water 
(e.g.,

[[Page 23081]]

streams or rivers) that may drain into drinking water reservoirs, EPA 
analyzed the extensive source of national water monitoring data for 
pesticides, the USGS NAWQA program. The NAWQA program focuses on 
ambient water rather than on drinking water sources, is not 
specifically targeted to the high use area of any specific pesticide, 
and is sampled at a frequency (generally weekly or bi-weekly during the 
use season) insufficient to provide reliable estimates of peak 
pesticide concentrations in surface water. For example, significant 
fractions of the data may not be relevant to assessing exposure from 
carbofuran use, as there may be no use in the basin above the 
monitoring site. Unless ancillary usage data are available to determine 
the amount and timing of the pesticide applied, it is difficult to 
determine whether non-detections of carbofuran were due to a low 
tendency to move to water or from a lack of use in the basin. The 
program, rather, provides a good understanding on a national level of 
the occurrence of pesticides in flowing water bodies that can be useful 
for screening assessments of potential drinking water sources. A 
detailed description of the pesticide monitoring component of the NAWQA 
program is available on the NAWQA Pesticide National Synthesis Project 
(PNSP) web site (http://ca.water.usgs.gov/pnsp/).
    A summary of the first cycle of NAWQA monitoring from 1991 to 2001 
indicates that carbofuran was the most frequently detected carbamate 
pesticide in streams and ground water in agricultural areas. Overall, 
where carbofuran was detected, these non-targeted monitoring results 
generally found carbofuran at levels below 0.5 ppb. In the NMC 
assessment, EPA summarized NAWQA monitoring for carbofuran between 1991 
and 2004. Maximum surface-water concentrations exceeded 1 ppb in 
approximately nine agricultural watershed-based study units, with 
detections in the sub-parts per billion range reported in additional 
watersheds (Ref. 107). The highest concentrations of carbofuran are 
reported from a sampling station on Zollner Creek, in Oregon. Zollner 
Creek, located in the Molalla-Pudding sub-basin of the Willamette 
River, is not directly used as a drinking water source. This creek is a 
low-order stream and its watershed is small (approximately 40 
km2) and intensively farmed, with a diversity of crops 
grown, including plant nurseries. USGS monitoring at that location from 
1993 to 2006 detected carbofuran annually in 40-100 % of samples. 
Although the majority of concentrations detected there are also in the 
sub-part per billion range, concentrations have exceeded 1 ppb in 8 of 
the 14 years of sampling. The maximum measured concentration was 32.2 
ppb, observed in the spring of 2002. The frequency of detections 
generally over a 14-year period suggests that standard use practices 
rather than aberrational misuse incidents in the region are responsible 
for high concentration levels at this location.
    While available monitoring from other portions of the country 
suggests that the circumstances giving rise to high concentrations of 
carbofuran may be rare, overall, the national monitoring data indicate 
that EPA cannot dismiss the possibility of detectable carbofuran 
concentrations in some surface waters under specific use and 
environmental conditions. Even given the limited utility of the 
available monitoring data, there have been relatively recent measured 
concentrations of carbofuran in surface water systems at levels above 4 
ppb and levels of approximately 1 to 10 ppb measured in streams 
representative of those in watersheds that support drinking water 
systems (Ref. 107). Based on this analysis, and since monitoring 
programs have not been sampling at a frequency sufficient to detect 
daily-peak concentrations that are needed to assess carbofuran's acute 
risk, the available monitoring data, in and of themselves, are not 
sufficient to establish that the risks posed by carbofuran in surface 
drinking water are below thresholds of concern. Nor can the non-
detections in the monitoring data be reasonably used to establish a 
lower bound of potential carbofuran risk through this route of 
exposure.
    To further characterize carbofuran risk through drinking water 
derived from surface water sources, EPA modeled estimated daily 
drinking water concentrations of carbofuran using PRZM to simulate 
field runoff processes and EXAMS to simulate receiving water body 
processes. These models were summarized in Unit V.B.2.
    There are sources of uncertainty associated with estimating 
exposure of carbofuran in surface water source drinking water. Several 
of the most significant of these are the effect of treatment in 
removing carbofuran from finished drinking water before it is delivered 
to the consumer supply system, the impact of percent crop treated 
assumptions, and the variation in pH across the landscape. The effect 
of the percent crop treated assumption in the case of carbofuran is 
discussed in detail in EPA's assessment of additional data submitted by 
the registrant (Refs. 22 and 94) and summarized below. Available data 
on the degree to which carbofuran may be removed from treatment systems 
was summarized previously and is discussed in more detail in Appendix 
E-3 of the Revised NMC CRA (Ref. 107). Although EPA is aware of the 
mitigating effects of specific treatment processes, the processes 
employed at public water supply utilities across the country vary 
significantly both from location to location and throughout the year, 
and therefore are difficult to incorporate quantitatively in drinking 
water exposure estimates. For example, lime softening would likely 
reduce carbofuran concentrations. That process is used in 3 to 21% of 
drinking water treatment systems in the United States (Ref. 19). 
Activated carbon has been shown to also reduce carbofuran 
concentrations, but is used in 1 to 15% of drinking water treatment 
facilities (Ref. ibid.). Therefore, EPA assumes that there is no 
reduction in carbofuran concentrations in surface water source drinking 
water due to treatment, which is a source of conservatism in surface 
water exposure estimates used for human health risk assessment. While 
it is well established that carbofuran will degrade at higher rates 
when the pH is above 7, and lower rates when below pH 7, due to the 
high variation of pH across the country for many of the scenarios, a 
neutral pH (pH 7) default value was used to estimate water 
concentrations. Finally, available environmental fate studies do not 
show formation of 3-hydroxycarbofuran through most environmental 
processes except soil photolysis, where in one study it was detected in 
very low amounts. Although 3-hydroxycarbofuran was not explicitly 
considered as a separate entity in the drinking water exposure 
assessment, it is unclear whether it would significantly add to 
exposure estimates.
    EPA compiled a distribution of estimated carbofuran concentrations 
in surface water in order to conduct probabilistic assessments of the 
potential exposures from drinking water. For the IRED, EPA modeled 
crops representing 80 percent of total carbofuran use at locations that 
would be considered among the more vulnerable where the crops are 
grown. Subsequently, for a refined dietary risk assessment, EPA 
generated distributions for 13 different scenarios representing all 
labeled uses of carbofuran treated at maximum label rates and adjusted 
with PCA factors (Refs. 17, 53, and 84).
    EPA subsequently conducted several rounds of modeling to refine 
estimates for specific uses and agricultural practices. One set of 
refinements addressed use of carbofuran on corn at

[[Page 23082]]

typical rather than maximum label rates, another set included 
simulation of different types of applications to corn (e.g., 
applications to control European corn borer, a rescue treatment for 
corn rootworm, and an in-furrow application at plant).
    For this final rule, EPA conducted additional refined modeling, 
based on the September 2008 label submitted by FMC. The modeling 
addressed all of the domestic uses that remain registered, and included 
certain refinements to better understand the impacts of varying pH. EPA 
also conducted modeling to assess the impact of the proposed spray 
drift buffer requirements and other spray drift measures included on 
the September label.
    EPA estimated carbofuran concentrations resulting from the use on 
pumpkins by adjusting the EDWCs from a previous run simulating melons 
in Missouri; adjustments accounted for differences in application rate 
and row spacing. Two EDWCs were calculated for pumpkins: One based on a 
36-inch row spacing, representing pumpkins for consumption (77.6 [mu]g/
L); and a second based on a 60-inch row spacing, representing 
decorative pumpkins (46.6 [mu]g/L).
    EPA had previously evaluated the corn rootworm rescue treatment at 
seven representative sites, representing use in states with extensive 
carbofuran usage at locations more vulnerable than most in each state 
in areas corn is grown. Using measured rainfall values, and assuming 
typical rather than maximum use rates, peak concentrations for the corn 
rescue treatments simulated for Illinois, Iowa, Indiana, Kansas, 
Minnesota, Nebraska, and Texas ranged from 16.6 - 36.7 ppb (Ref. 61). 
Under the revised assessment to account for the new use restrictions, 
concentrations for corn, calculated including the proposed spray drift 
buffers in Kansas and Texas, decreased 5.1% and 4.7%, respectively, 
from simulations with no buffer from the previous assessment (Ref. 61). 
In Kansas, the 1-in-10-year peak EDWCs decreased from 33.5 to 31.8 ppb 
when a 300-foot buffer was added, and in Texas, from 29.9 to 28.5 ppb 
with the addition of a 66-foot buffer.
    For the sunflower use, 12 simulations were performed for 
sunflowers, 9 in Kansas, and 3 in North Dakota. The North Dakota 
scenario was used to represent locations where sunflowers are grown 
that are vulnerable to pesticide movement to surface water while the 
Kansas scenario represents places that are not particularly vulnerable, 
based on the limited rainfall and generally well-drained soils 
(hydrologic group B soils) that are found in that area. Estimated 1-in-
10-year concentrations ranged from 11.6 to 32.7 [mu]g/L. When 
simulating three applications, one at plant and two foliar with a 14-
day interval between the two foliar applications and a 66-foot buffer, 
the 1-in-10-year peak EDWC for North Dakota was 22.4 [mu]g/L. In 
contrast, the same three applications in Kansas with a 14-day interval 
between the foliar applications and a 300-foot buffer produced a 1-in-
10-year peak EDWC of 20.5 [mu]g/L. The 1-in-10-year peak EDWCs assuming 
that carbofuran is applied only at plant were 14.0 and 16.0 [mu]g/L in 
Kansas and North Dakota respectively. EPA also evaluated the impact of 
pH on carbofuran concentrations for sunflowers, resulting in a 10% 
decrease in 1-in-10-year peak concentrations assuming high pH in the 
reservoir. Spray drift buffers of 66 and 300 feet decreased 
concentrations 4.7 and 5.1% for corn and 10.0% and 16.0% for 
sunflowers, respectively, in comparison to previous labels that had no 
spray drift buffer requirements. Additional details on these 
assessments can be found at Reference 111. Consistent with the analysis 
summarized above these predicted carbofuran water concentrations are 
similar or lower than the peak concentrations reported in the USGS-
NAWQA monitoring data and similar to or not more than tenfold higher 
than the 4 ppb reported in finished water from a surface water drinking 
plant.
    There are few surface water field-scale studies targeted to 
carbofuran use that could be compared with modeling results. Most of 
these studies were conducted in fields that contain tile drains, which 
is a common practice throughout midwestern states to increase drainage 
in agricultural fields (Ref. 17). Drains are common in the upper 
Mississippi river basin (Illinois, Iowa, and the southern part of 
Minnesota), and the northern part of the Ohio River Basin (Indiana, 
Ohio, and Michigan) (Ref. 74). Although it is not possible to directly 
correlate the concentrations found in most of the studies with drinking 
water concentrations, these studies confirm that carbofuran use under 
such circumstances can contaminate surface water, as tile drains have 
been identified as a conduit to transport water and contaminants from 
the field to surface waters. For example, one study conducted in the 
United Kingdom in 1991 and 1992 looked at concentrations in tile drains 
and surface water treated at a rate of 2.7 lbs a.i. per acre (granular 
formulation). Resulting concentrations in surface water downstream of 
the field ranged from 49.4 ppb almost 2 months after treatment to 0.02 
ppb 6 months later, and were slightly lower than concentrations 
measured in the tile drains, which were a transport pathway. Even with 
the factors that limit the study's relevance to the majority of current 
carbofuran use--the high use rate and granular formulation--the study 
clearly confirms that tile drains can serve as a source of significant 
surface water contamination. Although EPA's models do not account for 
tile drain pathways, and acknowledging the uncertainties in comparing 
carbofuran monitoring data to the concentrations predicted from the 
exposure models, as noted previously, estimated (model-derived) peak 
concentrations of carbofuran are similar to peak concentrations 
reported in stream monitoring studies. These are no more than tenfold 
higher than a value reported from a drinking water plant where it is 
unlikely the sample design would have ensured that water was sampled on 
the day of the peak concentration.
    EPA conducted dietary exposure analyses based on the modeling 
scenarios for the proposed September 2008 label. Exposures from all 
modeled scenarios substantially exceeded EPA's level of concern (Ref. 
16). For example, a Kansas sunflower scenario, assuming two foliar 
applications at a typical 1-lb a.i. per acre use rate, applied at 14-
day intervals, estimated a 1-in-10-year peak carbofuran water 
concentration of 11.6 ppb. Exposures at the 99.9th percentile based on 
this modeled distribution ranged from 160% of the aPAD for youths 13 to 
19 years, to greater than 2,000% of the aPAD for infants. As previously 
noted, this scenario is intended to be representative of sites that are 
less vulnerable than most on which sunflowers could be grown. By 
contrast, exposure estimates from a comparable North Dakota sunflower 
scenario, intended to represent more vulnerable sites, estimated a 1-
in-10-year peak concentration of 22.4 ppb. These concentrations would 
result in estimated exposures ranging between 450% aPAD for youths 13 
to 19 years, to 5,500% aPAD for infants. Similarly, exposures based on 
a Washington surface water potato scenario, and using a 3 lb a.i. acre 
rate, ranged from 230% of the aPAD for children 6 to 12 years to 890% 
of the aPAD for infants, with a 1-in-10-year peak carbofuran 
concentration of 7.2 ppb. Although other crop scenarios resulted in 
higher exposures, estimates for these two crops are presented here, as 
they are major

[[Page 23083]]

crops on which a large percentage of carbofuran use occurs. More 
details on these assessments, as well as the assessments EPA conducted 
for other crop scenarios, can be found in References 16, 61, and 84.
    Restricting the sunflower application to a single at-plant 
application from three applications reduces the 1-in-10-year peak EDWCs 
from 32.7 to 16.0 [mu]g/L for the North Dakota scenario and from 20.5 
to 14.0 [mu]g/L in western Kansas. These concentrations would result in 
estimated exposures, based on the North Dakota scenario ranging between 
350% aPAD for youths 13 to 19 years, to 4,300% aPAD for infants. Based 
on the Kansas scenario, the estimated exposures would range between 
250% aPAD for youths 13 to 19 years, to 3,100% aPAD for infants.
    Table 4 below presents the results of one of EPA's refined exposure 
analyses that is based on a Nebraska corn rootworm ``rescue treatment'' 
scenario, and assumes a single aerial application at a typical rate of 
1-pound a.i. per acre. To simulate an application made post-plant, at 
or near rootworm hatch, EPA modeled an application of carbofuran 30 
days after crop emergence. EPA used a crop specific PCA of 0.46 which 
is the maximum proportion of corn acreage in a HUC-8-sized basin in the 
United States. (The USGS has classified all watersheds in the United 
States into basins of various sizes, according to hydrologic unit 
codes, in which the number of digits indicates the size of the basin). 
The full distribution of daily concentrations over a 30-year period was 
used in the probabilistic dietary risk assessment. The 1-in-10-year 
peak concentration of the distribution of values for the Nebraska corn 
rescue treatment was 22.3 ppb. More details on these assessments, as 
well as the assessments EPA conducted for other crop scenarios, can be 
found in References 16, 61, and 84.

           Table 4.--Results of Acute Dietary (Surface Water Only) Exposure Analysis Incorporating the Nebraska Corn Rootworm Rescue Scenario
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                      95th Percentile         99th Percentile        99.9th Percentile
                                                                     aPAD (mg/kg/-----------------------------------------------------------------------
                        Population Subgroup                              day)       Exposure                Exposure                Exposure
                                                                                  (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD
--------------------------------------------------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                                              0.000075     0.000424        560     0.001201      1,600     0.002895      3,900
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 1-2 years old                                                  0.000075     0.000182        240    0.0005047        670     0.001261      1,700
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 3-5 years old                                                  0.000075     0.000169        230     0.000461        620     0.001137      1,500
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 6-12 years old                                                 0.000075     0.000117        160     0.000320        430     0.000794      1,100
--------------------------------------------------------------------------------------------------------------------------------------------------------
Youth 13-19 years old                                                     0.0002     0.000087         43     0.000248        120     0.000760        380
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 20-49 years old                                                    0.0002     0.000113         57     0.000305        150     0.000760        380
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 50+ years old                                                      0.0002     0.000120         60     0.000300        150     0.000672        340
--------------------------------------------------------------------------------------------------------------------------------------------------------

    The populations described in the ``Nebraska corn'' assessments are 
those people who consume water from a reservoir located in a small 
watershed predominated by corn production (with the assumption that 
treatment does not reduce carbofuran concentrations). The only crop 
treated by carbofuran in the watershed is corn, and all of that crop is 
assumed treated with carbofuran at the rate of 1 lb per acre. To the 
extent a drinking water plant drawing water from the reservoir normally 
treats the raw intake water with lime softening or activated carbon 
processes the finished water concentrations could be reduced from 60 to 
100% with the resultant aPADs ranging from approximately 198% to 2,340% 
of the aPAD to 0% of the aPAD, respectively, at the 99.9th percentile 
of exposure.
    As discussed in the previous sections, it is important to remember 
that carbofuran's aPAD is quite low, hence relatively low 
concentrations of carbofuran monitored or estimated in surface water 
can have a significant impact on the percent of the aPAD utilized. 
Thus, while the refined carbofuran water concentrations for the corn 
``rescue'' treatment in the range of approximately 16.6 to 36.7 ppb are 
comparable to maximum peak concentrations reported in the monitoring 
studies, these concentrations can result in very significant 
exceedences of the aPAD for various age groups, primarily because 
carbofuran is inherently very toxic.
    As noted, EPA's modeling indicates that while there is some 
mitigation value in the use of spray drift buffers, the loading to 
surface water is dominated by runoff even in semi-arid locations such 
as western Kansas, and the proposed mitigation measures do not 
substantially reduce exposure to carbofuran in surface water source 
drinking water systems.
    It is important to note that spray drift calculations have been 
conducted assuming that certain BMPs were used during the aerial spray 
application. Those practices are [frac12] swath displacement windward, 
a 10 foot release, wind speed no greater than 10 mph, and a spray boom 
less than 75% of the aircraft's wing (Ref. 106). There is advisory 
language on the revised labels regarding wind speed (``Drift potential 
increases at wind speeds less the 3 mph (due to inversion potential) or 
more than 10 mph,'' and boom height (``setting the boom to the lowest 
height (if specified) which provides uniform coverage reduces the 
exposure of droplets to evaporation and wind.''). The boom width is 
specifically restricted (``the boom length should not exceed [frac34] 
the wing or rotor length.''). There is no language on the label 
regarding swath displacement. While these ``best management practices'' 
are frequently used by aerial applicators, they are not used 
universally. To the extent these management practices are not used, 
EPA's assessment would underestimate the additional loading expected to 
result from spray drift.
    Equally important is that EPA only assumed that the buffers would 
be effective in reducing spray drift from neighboring fields, rather 
than assuming that the buffers would be effective in preventing or 
mitigating field runoff. As explained in the proposed rule, EPA 
disagrees that these measures will be effective in reducing 
carbofuran's movement to surface water. The proposed buffers were for 
fields where

[[Page 23084]]

soils were considered to be highly erodible. Buffer widths varied, and 
were to be vegetated with ``crop, seeded with grass, or other suitable 
crop.'' In 2000, EPA participated in the development of a guidance 
document on how to reduce pesticide runoff using conservation buffers 
(Ref. 98). Results of this effort found that properly designed buffers 
can reduce runoff of weakly absorbed pesticides like carbofuran by 
increasing filtration so that the pesticide can be trapped and degraded 
in the buffer. However, it is of critical importance that sheet flow be 
maintained across the buffer in order for this to occur. To ensure 
sheet flow, buffers need to be specifically designed for that purpose 
and they must be well-maintained, as over time sediment trapped in the 
buffer causes flow to become more channelized and the buffer then 
becomes ineffective. The guidance concludes that un-maintained, un-
vegetated buffers around water bodies, often referred to a `setback,' 
are ineffective in reducing pesticide movement to surface water.
    As discussed in Unit VII.C.2., FMC has criticized EPA's assessment 
for failing to account more fully for the percent of the crop likely to 
be treated in its modeling. In response to FMC's concerns, EPA 
performed a sensitivity analysis of an exposure assessment using a PCT 
in the watershed to determine the extent to which some consideration of 
this factor could meaningfully affect the outcome of the risk 
assessment. The registrant has at different times, suggested the 
application of a 5 or 10% crop treated factor based on county sales 
data. While substantial questions remain as to the support for these 
percentages for a given basin where carbofuran may be used, EPA used 
the upper figure for the purpose of conducting a sensitivity analysis. 
To be clear, this means that EPA assumed that 10% of the 46% of the 
watershed on which corn could be grown, would be treated with 
carbofuran, resulting in less than 5% of the watershed treated with 
carbofuran--an assumption that clearly underestimates exposures in many 
highly agricultural areas, such as Nebraska, and as discussed 
previously, requires several unrealistic assumptions. The results 
suggest that, even at levels below 10% crop treated, exposures from 
drinking water derived from surface waters can contribute significantly 
to the aggregate dietary risks, particularly for infants and children. 
For example, applying a 10% crop treated figure to the Nebraska corn 
scenario described above, in addition to the corn-PCA of 0.46 
incorporated into that scenario, results in estimated exposures from 
water alone, ranging from 110% of the aPAD for children 6 to 12 years 
to 390% of the aPAD for infants, assuming water treatment processes do 
not affect concentrations in drinking water consumed. Details on the 
assessments EPA conducted for other crop scenarios, which showed higher 
contributions from drinking water, can be found in References 16, 17, 
and 84. Accordingly, these assessments suggest that EPA's use of PCA 
alone, rather than in conjunction with PCT, will not meaningfully 
affect the carbofuran risk assessment, as even if EPA were to apply an 
extremely low PCT, aggregate exposures would still exceed 100% of the 
aPAD.
    In response to this sensitivity analysis, which had been presented 
in the proposed rule, FMC complained that EPA had failed to account in 
these analyses for the rapid nature of carbofuran's recovery. Or in 
other words, the commenter wanted EPA to both apply a PCT figure and 
conduct an Eating Occasion Analysis, claiming that this analysis would 
show that carbofuran ``passed.''
    EPA disagrees that conducting the analysis the commenter suggests 
would be appropriate, or would provide any information on which EPA 
could properly rely to support a determination of safety. As previously 
explained, the available information and methodology does not allow EPA 
to generate PCT estimates with any degree of confidence, and certainly 
not with the ``reasonable certainty'' demanded by the statute. EPA 
conducted its analysis purely in an attempt to understand the extent to 
which its assumption of PCT affected the risk assessment conclusions. 
It is not necessary to gain an understanding of the PCT impact, to 
compound the uncertainty by adding assumptions about the reversibility 
of carbofuran's effects.
    The commenter provided the results of their dietary assessment, in 
which they appear to have conducted the analysis suggested above, and 
reported that the aPAD for infants from aggregate exposures (i.e., food 
+ water) was 107.06%. As previously discussed, the commenter did not 
provide any of the underlying support documentation for these reported 
results, and EPA was unable to replicate them. However, in its efforts 
to replicate the commenter's analysis, the lowest aggregate exposure 
EPA was able to estimate for infants using the commenter's PCT and 
half-life inputs was 126% of the aPAD, a figure that, for reasons 
discussed subsequently, is certainly an underestimate of exposure. 
Further discussion of the Eating Occasion Analyses EPA conducted for 
carbofuran is presented in Unit VIII.E.1.d. and in Reference 112.
    In conclusion, the large difference between concentrations seen in 
the monitoring data on the low side, and the simulation modeling on the 
high side, is an indication of the uncertainty in the assessment for 
surface-water source drinking water exposure. The majority of drinking 
water concentrations resulting from use of carbofuran are likely to be 
occurring at higher concentrations than those measured in most 
monitoring studies, but below those estimated with simulation modeling; 
however the exact values within the range obtained from the monitoring 
and the model simulations are uncertain. However, the monitoring data 
show a consistent pattern of low concentrations, with the occasional, 
infrequent spike of high concentrations. Those infrequent high 
concentrations are consistent with EPA's modeling, which is intended to 
capture the exposure peaks. For a chemical with an acute risk, like 
carbofuran, the spikes or peaks in exposures, even though infrequent, 
are the most relevant for assessing the risks. And, as previously 
noted, the available monitoring has its own limitations for estimating 
exposure for risk assessment.
    Further, the results of the modeling analyses provide critical 
insights regarding locations in the country where the potential for 
carbofuran contamination to surface water and associated drinking water 
sources is more likely. These locations include areas with soils prone 
to runoff (such as those high in clay or containing restrictive 
layers), in regions with intensive agriculture with crops on which 
carbofuran is used (e.g., corn), which have high rainfall amounts and/
or are subject to intense storm events in the spring around the times 
applications are being made. Drinking water facilities with small 
basins tend to be more vulnerable, as it is more likely that a large 
proportion of the crop acreage will be treated in small basins.
    3. Aggregate dietary exposures (food and drinking water). EPA 
conducted a number of probabilistic analyses to combine the national 
food exposures with the exposures from the individual region and crop-
specific drinking water scenarios. As discussed in Unit V.B.3., 
although food is distributed nationally, and residue values are 
therefore not expected to vary substantially throughout the country, 
drinking water is locally derived and concentrations of pesticides in 
source water fluctuate over

[[Page 23085]]

time and location for a variety of reasons. Consequently, EPA conducted 
several estimates of aggregate dietary risks by combining exposures 
from food and drinking water. These estimates showed that, because 
drinking water exposures from any of the crops on the label exceed safe 
levels, aggregate exposures from food and water are unsafe. Although 
EPA's assessments showed that, based on the Idaho potato scenarios, 
exposures from ground water from use on potatoes would be safe, surface 
water exposures from carbofuran use on potatoes far exceed the safety 
standard. More details on the individual aggregate assessments 
presented below, as well as the assessments EPA conducted for other 
regional and crop scenarios, can be found in References 16 and 17.
    Table 5 reflects the results of aggregate exposures from food and 
from drinking water derived from ground water in extremely vulnerable 
areas (i.e., from shallow wells associated with sandy soils and acidic 
aquifers, such as are found in Wisconsin). The estimates range between 
780% of the aPAD for adults, to 9,400% of the aPAD for infants.

             Table 5.--Results of Acute Dietary (Food and Water) Exposure Analysis incorporating the Wisconsin Ground Water Scenario pH 6.5
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                      95th Percentile         99th Percentile        99.9th Percentile
                                                                     aPAD (mg/kg/-----------------------------------------------------------------------
                        Population Subgroup                              day)       Exposure                Exposure                Exposure
                                                                                  (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD
--------------------------------------------------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                                              0.000075     0.001602      2,100     0.003537      4,700     0.007053      9,400
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 1-2 years old                                                  0.000075     0.000680        910     0.001490      2,000     0.003180      4,200
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 3-5 years old                                                  0.000075     0.000626        840     0.001350      1,800     0.002845      3,800
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 6-12 years old                                                 0.000075     0.000432        580     0.000935      1,200     0.002019      2,700
--------------------------------------------------------------------------------------------------------------------------------------------------------
Youth 13-19 years old                                                     0.0002     0.000334        170     0.000751        380     0.001721        860
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 20-49 years old                                                    0.0002     0.000415        210     0.000896        450     0.001906        950
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 50+ years old                                                      0.0002     0.000415        210     0.000853        430     0.001552        780
--------------------------------------------------------------------------------------------------------------------------------------------------------

    The peak concentration estimates in the Wisconsin ground water 
scenario time series are consistent with monitoring data from wells in 
vulnerable areas where carbofuran was used. For example, the maximum 
water concentration from the time series is 34 ppb while maximum values 
from a targeted ground water monitoring study in Maryland, with a 
higher application rate, was 65 ppb, with studies at other sites having 
similar or higher peak concentrations (Refs. 17 and 84). For studies 
with multiple measurements at each well, central tendency estimates 
were also in the same range as the time series. For example, the mean 
carbofuran concentration from wells under no-till agriculture in 
Queenstown, MD was 7 ppb, while the median for the modeling was 15.5 
ppb. The 90-day average concentration, based on the registrant's PGW 
study conducted on corn in the Delmarva (adjusted for current maximum 
application rates) is 11 ppb.
    Table 6 presents the results of aggregate exposure from food and 
water derived from one of the least conservative surface water 
scenarios: Kansas sunflower, with two foliar applications. This table 
reflects the risks only for those people in watersheds with 
characteristics similar to that used in the scenario, and assuming that 
water treatment does not remove carbofuran. As discussed previously, 
the estimated water concentrations are comparable to the maximum peak 
concentrations reported in monitoring studies that were not designed to 
detect peak, daily concentrations of carbofuran in vulnerable 
locations.

  Table 6.--Results of Acute Dietary (Food and Water) Exposure Analysis Using The DEEM-FCID\(TM)\ and Incorporating the Kansas Surface Water Sunflower
                                                           Foliar Application pH 7.8 Scenario
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                      95th Percentile         99th Percentile        99.9th Percentile
                                                                     aPAD (mg/kg/-----------------------------------------------------------------------
                        Population Subgroup                              day)       Exposure                Exposure                Exposure
                                                                                  (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD   (mg/kg/day)    % aPAD
--------------------------------------------------------------------------------------------------------------------------------------------------------
All Infants (< 1 year old)                                              0.000075     0.000087        120     0.000425        570     0.001555       2100
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 1-2 years old                                                  0.000075     0.000044         59     0.000185        250     0.000660        880
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 3-5 years old                                                  0.000075     0.000039         53     0.000172        230     0.000610        800
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children 6-12 years old                                                 0.000075     0.000027         36     0.000117        160     0.000416        560
--------------------------------------------------------------------------------------------------------------------------------------------------------
Youth 13-19 years old                                                     0.0002     0.000019         10     0.000089         45     0.000330        160
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 20-49 years old                                                    0.0002     0.000026         13     0.000114         57     0.000395        200
--------------------------------------------------------------------------------------------------------------------------------------------------------
Adults 50+ years old                                                      0.0002     0.000028         14     0.000119         60     0.000373        190
--------------------------------------------------------------------------------------------------------------------------------------------------------


[[Page 23086]]

    More details on this assessment, as well as the assessments EPA 
conducted for other crop scenarios, can be found in References 16, 61, 
and 84. For example, in the proposed rule, EPA presented the results 
from aggregate exposures resulting from a Nebraska surface water 
scenario based on a Nebraska corn rootworm ``rescue treatment.'' 
Estimated exposures from that scenario ranged from 330% of the aPAD for 
youths 13 to 19 years to 3,900% of the aPAD for infants.
    As noted previously, EPA's food and water exposure assessments 
typically sum exposures over a 24-hour period, and EPA used this 24-
hour total in developing its acute dietary risk assessment for 
carbofuran. Because of the rapid nature of carbofuran toxicity and 
recovery, EPA considered durations of exposure less than 24 hours. 
Accordingly, EPA has conducted an analysis using information about 
dietary exposure, timing of exposure within a day, and half-life of 
AChE inhibition from rats to estimate risk to carbofuran at durations 
less than 24 hours. Specifically, EPA has evaluated individual eating 
and drinking occasions and used the AChE half-life to recovery 
information (herein called half-life information) to estimate the 
residual effects from carbofuran from previous exposures within the 
day. The carbofuran analyses are described in the 2009 aggregate 
(dietary) memo (Ref. 71).
    EPA used the same approach for considering the impact of 
carbofuran's rapid reversibility on exposure estimates in the food and 
drinking water risk assessments that had been previously used in the 
cumulative risk assessment of the NMC pesticides and/or risk 
assessments for other NMC pesticides (e.g., methomyl and aldicarb) 
(Ref. 107).
    Using the two FMC time course studies in rat pups, EPA calculated 
half-lives for recovery of 186 and 426 minutes. The two values were 
derived from two different studies using rat pups of the same age 
(Refs. 30 and 31); the two values provide an indication that half-lives 
to recovery can vary among juvenile rats. By extension, children are 
expected to vary in their ability to recover from AChE inhibition where 
longer recoveries would be associated with a potentially higher 
``persisting dose'' (as described below). Incorporating Eating Occasion 
Analysis and the 186-minute or 426-minute recovery half-lives for 
carbofuran into the food only analysis does not significantly change 
the risk estimates when compared to baseline levels (for which a total 
daily consumption basis - and not eating occasion - was used). From 
this, it is apparent that modifying the analysis such that information 
on eating (i.e., food) occasions and carbofuran half-life is 
incorporated results in only minor reductions in estimated risk from 
food alone.
    Regarding drinking water exposure, accounting for drinking water 
consumption throughout the day and using the half-life to recovery 
information, risk is reduced by approximately 2-3X. Consequently, risk 
estimates for which food and drinking water are jointly considered and 
incorporated (i.e., Food + Drinking Water) are also reduced 
considerably--by a factor of two or more in some cases--compared to 
baseline. This is not unexpected, as infants receive much of their 
exposures from indirect drinking water in the form of water used to 
prepare infant formula, as shown in the above example. But even though 
the risk estimates from aggregate exposure are reduced, they 
nonetheless still substantially exceed EPA's level of concern for 
infants and children. Using drinking water derived from the surface 
water from the Idaho potato surface water scenario, which estimated one 
of the lowest exposure distributions, aggregate exposures at the 99.9th 
percentile ranged from 328% of the aPAD under the scenario for which 
infants rapidly metabolize carbofuran (e.g., 186 minute half-life), to 
a high of 473% of the aPAD under the scenario for which infants 
metabolize carbofuran more slowly, (e.g., scenarios in which a 426 
minute half life is assumed).
    Moreover, even accounting for the estimated decreased risk from 
accounting for carbofuran's rapid reversibility, the Agency remains 
concerned about the risks from single eating or drinking events, as 
illustrated in the following example, based on an actual food 
consumption diary from the CSFII survey. A 4-month old male non-nursing 
infant weighing 10 kg is reported to have consumed a total of 1,070 
milliters (ml) of indirect water over eight different occasions during 
the day. The first eating occasion occurred at 6:30 a.m., when this 4 
month old consumed 8 fluid ounces of formula prepared from powder. The 
FCID food recipes indicate that this particular food item consists of 
approximately 87.7% water, and therefore, 8 ounces of formula contains 
approximately 214 ml (or grams) of indirect water; with the powder 
(various nutrients, dairy, soy, oils, etc.) accounting for the 
remaining 12.3%. This infant also reportedly consumed a full 8-ounce 
bottle of formula at 12 p.m., 4 p.m., and 8 p.m. that day. The food 
diary also indicates that the infant consumed about 1 tablespoon of 
water (14.8 ml) added to prepare rice cereal at 10:00 a.m., about 2 
ounces of water (59.3 ml) added to pear juice at 11 a.m., another 
[frac12] tsp of water (2.5 ml) to prepare more rice cereal at 8:30 
p.m.; and finally, he consumed another 4 ounces of formula (107 ml) at 
9:30 p.m.
    The infant's total daily water intake (1,070 ml, or approximately 
107 ml/kg/day) is not overly conservative, and represents substantially 
less than the 90th percentile value from CSFII on a ml water/kg 
bodyweight (ml/kg/bw) basis. As noted, carbofuran has been detected in 
finished water at concentrations of 4 ppb. For this 10 kg body weight 
infant, an 8-ounce bottle of formula prepared from water containing 
carbofuran at 4 ppb leads to drinking water exposures of 0.0856 
micrograms of active ingredient/kilogram of bodyweight ([mu]g ai/kg 
bw), or 114% of the aPAD. Based on the total daily water intake of 
1,070 ml/day (no reversibility), total daily exposures from water at 4 
ppb concentration would amount to 0.4158 [mu]g ai/kg bw, or 555% of the 
aPAD; this is the amount that would be used for this person-day in the 
Total Daily Approach.
    Peak inhibition occurs following each occasion on which the infant 
consumed 8 fluid ounces of formula (6 a.m., 12 p.m., 4 p.m. and 8 
p.m.); however, the maximum persisting dose occurs following the 9:30 
p.m. eating occasion, based on a 186-minute half-life parameter. This 
produces a maximum persisting dose of 0.1457 [mu]g ai/kg bw, or about 
30% of the total daily exposure of 0.4158 [mu]g ai/kg bw derived above, 
or expressed as a fraction of the level of concern, the maximum 
persisting dose amounts to about 194% of the aPAD (or 30% of 554%). 
Note that with drinking water concentration at 4 ppb, an infant 
consuming one 8 oz bottle of formula - prepared from powder and tap 
water containing carbofuran at 4 ppb will obtain exposures of 
approximately 114% of aPAD. Since many infants consume the equivalent 
of this amount on a single eating occasion, accounting for 
reversibility over multiple occasions is not essential to ascertain 
that infants quite likely have obtained drinking water exposures to 
carbofuran exceeding the level of concern based on drinking water 
concentrations found in public drinking water supplies.
    The approach discussed above is used to evaluate the extent to 
which the Agency's 24-hour approach to dietary risk assessment 
overestimates risk from carbofuran exposure. The results of both 
approaches indicate that the risk from carbofuran is indeed not 
substantively overestimated using the current

[[Page 23087]]

exposure models and the 24-hour approach.
    In this regard, it is important to note EPA's Eating Occasion 
Analyses underestimate exposures to the extent that they do not take 
into account carry-over effects from previous days, and because 
drinking water concentrations are randomly picked from the entire 30-
year distribution. As discussed previously, DEEM-FCID\(TM)\ is a single 
day dietary exposure model, and the DEEM-based Eating Occasion Analysis 
accounts for reversibility within each simulated person-day. All of the 
empirical data regarding time and amounts consumed (and corresponding 
exposures based on the corresponding residues) from the CSFII survey 
are used, along with the half-life to assess an equivalent persisting 
dose that produced the peak inhibition expected over the course of that 
day. This is a reasonable assumption for food alone; since the time 
between exposure events across 2 days is relatively high (compared to 
the half-life)--most children (>9 months) tend to sleep through the 
night--and the time between dinner and breakfast the following morning 
is long enough it is reasonable to ``ignore'' persisting effects from 
the previous day. A single day exposure model will underestimate the 
persisting effects from drinking water exposures (formula) among 
infants, and newborns in particular (<3 months), since newborns tend to 
wake up every 2 to 4 hours to feed. Any carry over effects may be 
important, especially if exposures from the previous day are relatively 
high, since the time between the last feeding (formula) of the day and 
the first feeding of the subsequent day is short. A single day model 
also does not account for the effect of seasonal variations in drinking 
water concentrations, which will make this effect more pronounced 
during the high use season (i.e., the time of year when drinking water 
concentrations are high). Based on these analyses, the Agency concludes 
that the current exposure assessment methods used in the carbofuran 
dietary assessment provide realistic and high confidence estimates of 
risk to carbofuran exposure through food and water.
    The result of all of these analyses clearly demonstrates that 
aggregate exposure from all uses of carbofuran fail to meet the FFDCA 
section 408 safety standard, and revocation of the associated 
tolerances is warranted. EPA's analyses show that those individuals-
both adults as well as children--who receive their drinking water from 
vulnerable sources are also exposed to levels that exceed EPA's level 
of concern--in some cases by orders of magnitude. This primarily 
includes those populations consuming drinking water from ground water 
from shallow wells in acidic aquifers overlaid with sandy soils that 
have had crops treated with carbofuran. It could also include those 
populations that obtain their drinking water from reservoirs located in 
small agricultural watersheds, prone to runoff, and predominated by 
crops that are treated with carbofuran, although there is more 
uncertainty associated with these exposure estimates.
    Although the recent cancellation of several registered uses has 
reduced the dietary risks to children, EPA's analyses still show that 
estimated exposures significantly exceed EPA's level of concern for 
children.
    While the registrant claims to have conducted an alternate analysis 
showing that aggregate carbofuran exposures to children will be safe, 
FMC failed to provide the data and details of that assessment to the 
Agency. They have also failed to provide several critical components 
that served to support key inputs into that assessment. And for several 
of these, EPA was unable to replicate the claimed results based on the 
information contained in the comments. In the absence of such critical 
components, the Agency cannot accept the validity or utility of the 
analyses, let alone rely on the results.
    But based on the summary descriptions provided in their comments, 
it is clear that the commenters' analyses contain a critical flaw. The 
commenters' determination of safety rests on the presumption that under 
real world conditions, events will always occur exactly as hypothesized 
by the multiple assumptions in their assessment. For example, they 
assume, despite all available evidence to the contrary, that children 
will not be appreciably more sensitive to carbofuran's effects than 
adults. They assume that carbofuran's effects will be highly 
reversible, and that children will be uniformly sensitive, such that 
the effects will be adequately accounted for by the assumption of a 
150-minute half-life. They further assume that there will be no carry 
over effect from the preceding day's exposures for infants. They assume 
that the cancellation of use on alfalfa will reduce carbofuran residues 
in milk by over 70%. They assume that residues will decrease between 19 
and 23% as a result of the buffer requirements on the September 2008 
label, even though the label does not require the use of all of the 
recommended ``best management practices'' (e.g., no language regarding 
swath displacement), and applicators do not universally use such 
practices in the absence of any requirement. They assume that average 
ground water pH adequately characterizes the temporal and spatial 
heterogeneity common in most areas, despite the available evidence to 
the contrary. Finally, they assume that PCT in watersheds will never 
exceed 5% CT, despite varying pest pressures, consultant 
recommendations, and individual grower decisions. Leaving aside that 
EPA believes most, if not all of these assumptions are not supported by 
the available evidence, as described throughout this final rule, the 
probability of all these assumptions always simultaneously holding true 
under real world conditions is unreasonably low, and certainly does not 
approach the degree of certainty necessary for EPA to conclude that 
children's exposures will be safe.
    Determining whether residues will be safe for U.S. children is not 
a theoretical paper exercise; it cannot suffice to hypothesize a unique 
set of circumstances that make residues ``fit in the box.'' There must 
be a reasonable certainty that under the variability that exists under 
real world conditions, exposures will be ``safe.'' EPA's assessments 
incorporate a certain degree of conservatism precisely to account for 
the fact that assumptions must be made that may not prove accurate. 
This consideration is highly relevant for carbofuran, because as 
refined as EPA's assessments are, areas of uncertainty remain with 
regard to carbofuran's risk potential. For example, a recent 
epidemiological study reported that 45% of maternal and cord blood 
samples in a cohort of New York City residents of Northern Manhattan 
and the South Bronx between 2000 and 2004, contained low, but 
measurable residues of carbofuran (Ref. 118). The Agency is currently 
unable to account for the source of such sustained exposures at this 
frequency.
    A further consideration is that the risks of concern are acute 
risks to children. For acute risks, the higher values in a 
probabilistic risk assessment are often driven by relatively high 
values in a few exposures rather than relatively lower values in a 
greater number of exposures. This is due to the fact that an acute 
assessment looks at a narrow window of exposure where there are 
unlikely to be a great variety of consumption sources. Thus, to the 
extent that there is a high exposure it will be more likely due to a 
high residue value in a single consumption event. Additionally 
worrisome in this regard is that carbofuran is a highly potent (i.e.,

[[Page 23088]]

has a very steep dose-response curve), acute toxicant, and therefore 
any aPAD exceedances are more likely to have greater significance in 
terms of the potential likelihood of actual harm.
    In sum, these results strongly support EPA's conclusion that 
aggregate exposures to carbofuran are not safe.

IX. Procedural Matters

A. When Do These Actions Become Effective?

    The revocations of the tolerances for all commodities will become 
effective December 31, 2009. EPA had proposed to establish an extended 
effective date for artichokes and sunflower seed; however, EPA 
ultimately agrees with those commenters who raised concern that 
continuance of use for an additional year on these crops would be 
inconsistent with the acute risks that carbofuran poses to children. 
Accordingly, the revocation for tolerances on these two crops will now 
be effective December 31, 2009. The Agency has set the effective date 
in December because this is the quickest time frame in which the 
decision could be practically implemented, given that some additional 
time will be necessary to allow the process applicable to stay requests 
to be completed. In addition, this time frame ensures that growers will 
have a reasonable amount of time to make reasoned decisions about their 
pest management strategies, and to exhaust any stocks of carbofuran 
currently in their possession.
    Any commodities listed in this rule treated with the pesticide 
subject to this rule, and in the channels of trade following the 
tolerance revocations, shall be subject to FFDCA section 408(l)(5). 
Under this section, any residues of these pesticides in or on such food 
shall not render the food adulterated so long as it is shown to the 
satisfaction of the Food and Drug Administration that:
    1. The residue is present as the result of an application or use of 
the pesticide at a time and in a manner that was lawful under FIFRA, 
and
    2. The residue does not exceed the level that was authorized at the 
time of the application or use to be present on the food under a 
tolerance or exemption from tolerance. Evidence to show that food was 
lawfully treated may include records that verify the dates when the 
pesticide was applied to such food.

B. Request for Stay of Effective Date

    A person filing objections to this final rule may submit with the 
objections a petition to stay the effective date of this final rule. 
Such stay petitions must be received by the Hearing Clerk on or before 
July 14, 2009. A copy of the stay request filed with the Hearing Clerk 
shall be submitted to the Office of Pesticide Programs Docket Room. A 
stay may be requested for a specific time period or for an indefinite 
time period. The stay petition must include a citation to this final 
rule, the length of time for which the stay is requested, and a full 
statement of the factual and legal grounds upon which the petitioner 
relies for the stay.
    EPA received comments asserting that a hearing would definitely be 
requested, and requesting a stay pending resolution of that hearing.
    Until EPA has published its final rule, any request for a stay is 
purely speculative. EPA is only authorized to issue a stay of the 
regulation, ``if after issuance of such regulation or order, objections 
are filed with respect to such regulation...'' 21 U.S.C. 346a(g)(1). No 
objections have been filed, nor could they be until EPA publishes its 
final rule. Further, no demonstration has yet been made that any 
hearing is warranted, nor indeed, could the commenters have done so at 
this stage of the tolerance revocation process. See, 40 CFR 178 Subpart 
B. EPA's regulations require all parties who request a stay to justify 
the request with a statement of the factual and legal grounds upon 
which the petitioner relies. To the extent the commenters still wish to 
seek a stay of EPA's final rule, they will have the opportunity to do 
so, as discussed above.
    In determining whether to grant a stay, EPA will consider the 
criteria set out in the Food and Drug Administration's regulations 
regarding stays of administrative proceedings at 21 CFR 10.35. Under 
those rules, a stay will be granted if it is determined that:
    (1) The petitioner will otherwise suffer irreparable injury;
    (2) The petitioner's case is not frivolous and is being pursued in 
good faith;
    (3) The petitioner has demonstrated sound public policy grounds 
supporting the stay;
    (4) The delay resulting from the stay is not outweighed by public 
health or other public interests.
    Under FDA's criteria, EPA may also grant a stay if EPA finds such 
action is in the public interest and in the interest of justice.
    Any person wishing to comment on any stay request may submit such 
comments and objections to a stay request to the Hearing Clerk, on or 
before July 29, 2009. Any subsequent decisions to stay the effect of 
this order, based on a stay request filed, will be published in the 
Federal Register, along with EPA's response to comments on the stay 
request.

X. Are The Agency's Actions Consistent With International Obligations?

    The tolerance revocations in this final rule are not discriminatory 
and are designed to ensure that both domestically-produced and imported 
foods meet the food safety standard established by the FFDCA. The same 
food safety standards apply to domestically produced and imported 
foods.
    EPA considers Codex Maximum Residue Limits (MRLs) in setting U.S. 
tolerances and in reassessing them. MRLs are established by the Codex 
Committee on Pesticide Residues, a committee within the Codex 
Alimentarius Commission, an international organization formed to 
promote the coordination of international food standards. It is EPA's 
policy to harmonize U.S. tolerances with Codex MRLs to the extent 
possible, provided that the MRLs achieve the level of protection 
required under FFDCA. EPA's effort to harmonize with Codex MRLs is 
summarized in the tolerance reassessment section of individual 
Reregistration Eligibility Decision documents. EPA has developed 
guidance concerning submissions for import tolerance support (65 FR 
35069, June 1, 2000) (FRL-6559-3). This guidance will be made available 
to interested persons. Electronic copies are available on the internet 
at http://www.epa.gov/. On the Home Page select ``Laws, Regulations, 
and Dockets,'' then select Regulations and Proposed Rules and then look 
up the entry for this document under ``Federal Register--Environmental 
Documents.'' You can also go directly to the ``Federal Register'' 
listings at http://www.epa.gov/fedrgstr/.

XI. Statutory and Executive Order Reviews

    In this final rule, EPA is revoking specific tolerances established 
under FFDCA section 408. The Office of Management and Budget (OMB) has 
exempted tolerance regulations from review under Executive Order 12866, 
entitled Regulatory Planning and Review (58 FR 51735, October 4, 1993). 
Because this final rule has been exempted from review under Executive 
Order 12866, this final rule is not subject to Executive Order 13211, 
Actions Concerning Regulations That Significantly Affect Energy Supply, 
Distribution, or Use (66 FR 28355, May 22, 2001) or Executive Order 
13045, entitled Protection of Children from

[[Page 23089]]

Environmental Health Risks and Safety Risks (62 FR 19885, April 23, 
1997), which both apply to regulation actions reviewed under Executive 
Order 12866. This final rule does not contain any information 
collections subject to OMB approval under the Paperwork Reduction Act 
(PRA), 44 U.S.C. 3501 et seq., or impose any enforceable duty or 
contain any unfunded mandate as described under Title II of the 
Unfunded Mandates Reform Act of 1995 (UMRA) (Public Law 104-4). Nor 
does it require any special considerations as required by Executive 
Order 12898, entitled Federal Actions to Address Environmental Justice 
in Minority Populations and Low-Income Populations (59 FR 7629, 
February 16, 1994). This action does not involve any technical 
standards that would require Agency consideration of voluntary 
consensus standards pursuant to section 12(d) of the National 
Technology Transfer and Advancement Act of 1995 (NTTAA), Public Law 
104-113, section 12(d) (15 U.S.C. 272 note).
    In addition, the Agency has determined that this action will not 
have a substantial direct effect on States, on the relationship between 
the national government and the States, or on the distribution of power 
and responsibilities among the various levels of government, as 
specified in Executive Order 13132, entitled Federalism (64 FR 43255, 
August 10, 1999). This final rule directly regulates growers, food 
processors, food handlers and food retailers, not States. This action 
does not alter the relationships or distribution of power and 
responsibilities established by Congress in the preemption provisions 
of section 408(n)(4) of the FFDCA. For these same reasons, the Agency 
has determined that this final rule does not have any ``tribal 
implications'' as described in Executive Order 13175, entitled 
Consultation and Coordination with Indian Tribal Governments (65 FR 
67249, November 6, 2000). This final rule will not have substantial 
direct effects on tribal governments, on the relationship between the 
Federal Government and Indian tribes, or on the distribution of power 
and responsibilities between the Federal Government and Indian tribes, 
as specified in Executive Order 13175. Thus, Executive Order 13175 does 
not apply to this final rule.
    The Regulatory Flexibility Act (RFA) 5 USC 601 et.seq, generally 
requires an agency to prepare a regulatory flexibility analysis of any 
rule subject to notice and comment rulemaking requirements under the 
Administrative Procedures Act or any other statute. This is required 
unless the agency certifies that the rule will not have a significant 
economic impact on a substantial number of small entities. Small 
entities include small businesses, small organizations, and small 
governmental jurisdictions. The Agency has determined that no small 
organizations or small governmental jurisdictions are impacted by 
today's rulemaking. For purposes of assessing the impacts of today's 
determination on businesses, a small business is defined either by the 
number of employees or by the annual dollar amount of sales/revenues. 
The level at which an entity is considered small is determined for each 
North American Industry Classification System (NAICS) code by the Small 
Business Administration (SBA). Farms are classified under NAICS code 
111, Crop Production, and the SBA defines small entities as farms with 
total annual sales of $750,000 or less.
    The Agency has examined the potential effects today's final rule 
may have on potentially impacted small businesses. EPA prepared an 
analysis for the proposal and certified that its proposed rule would 
not have a significant economic impact on a substantial number of small 
entities. EPA received no comments on its analysis or certification. 
Based on its analysis, EPA concludes that the Agency can certify that 
revoking the food tolerances for carbofuran will not have a significant 
economic impact on a substantial number of small entities for alfalfa, 
artichoke, banana, chili pepper, coffee, cotton, cucurbits (cucumber, 
melons, pumpkin, and squash), grape, grains (barley, flax, oats, and 
wheat), field corn, potato, soybean, sorghum, sugarbeet, sugarcane, 
sunflower, and sweet corn. Even in a worst-case scenario, in which a 
grower obtains income only from a single crop and his/her entire 
acreage is affected, the impact generally amounts to less than 2% of 
gross income and would be felt by fewer than 3% of affected small 
producers. Estimates of impacts to corn growers were refined to account 
for the sporadic nature of need for carbofuran while still maintaining 
some assumptions that would bias the estimates upward. Refined 
estimates were also made for artichoke and sunflower, which consider 
the diversity in growers' revenue. The largest impact may be felt by 
artichoke growers, with impacts as high as 5% of gross revenue, but 
fewer than five growers are likely to be affected. Moreover, as the 
registrant has voluntarily cancelled the use of carbofuran on 
artichokes, any impact is more properly traced to the registrant's 
decision to cancel the registration, than to the revocation of the 
tolerance. EPA could not quantify the impacts to banana, sugarcane, and 
sweet corn producers, but the number of impacted farms is less than 2% 
of the farms subject to the action. Additional detail on the analyses 
EPA conducted in support of this certification can be found in 
Reference 85.

XII. Congressional Review Act

    The Congressional Review Act, 5 U.S.C. 801 et seq., generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report to each House of the Congress and 
the Comptroller General of the United States. EPA will submit a report 
containing this rule and other required information to the U.S. Senate, 
the U.S. House of Representatives, and the Comptroller General of the 
United States prior to publication of the rule in the Federal Register. 
This rule is not a ``major rule'' as defined by 5 U.S.C. 804(2).

XIII. References

    The following is a list of the documents that are specifically 
referenced in this final rule and placed in the docket that was 
established under Docket ID number EPA-HQ-OPP-2005-0162. The public 
docket includes information considered by EPA in developing this final 
rule, such as the documents specifically referenced in this action that 
are listed in this unit, documents that are referenced in the documents 
that are in the docket, any public comments received, and other 
information related to this action. For information on accessing the 
docket, refer to the ADDRESSES unit at the beginning of this document.
    1. Abou-Donia, M.B., Khan, W.A., Dechkovskaia, A.M., Goldstein, 
L.B., Bullman, S.L., Abdel-Rahman, A., In utero exposure to nicotine 
and chlorpyrifos alone, and in combination produces persistent 
sensorimotor deficits and Purkinje neuron loss in the cerebellum of 
adult offspring rats. Arch Toxicol. 2006 Sep;80(9):620-31. Epub 2006 
Feb 16.
    2. Abramovitch, R., Tavor, E., Jacob-Hirsch, J., Zeira, E., 
Amariglio, N., Pappo, O., Rechavi, G., Galun, E., Honigman, A., A 
pivotal role of cyclic AMP-responsive element binding protein in tumor 
progression. Cancer Research. 2004 Feb 15;64(4):1338-46.
    3. Acute oral (gavage) dose range-finding study of cholinesterase 
depression from carbofuran technical in juvenile (day 11) rats. 
Hoberman, 2007. MRID 47143703 (unpublished FMC study) EPA-HQ-OPP-2007-
1088-0062.

[[Page 23090]]

    4. Acute oral (gavage) time course study of cholinesterase 
depression from carbofuran technical in adult and juvenile (day 11 
postpartum) rats. Hoberman, 2007. MRID 47143704 (unpublished FMC study) 
EPA-HQ-OPP-2007-1088-0063.
    5. Acute Dose-Response Study of Carbofuran Technical Administered 
by Gavage to Adult and Postnatal Day 11 Male and Female CD (Sprague-
Dawley) Rats: Tyl and Myers. 2005. MRID. 46688914.
    6. Aller, L., Bennet, T., Lehr, J.H., Petty, R.J., and Hackett, G. 
1987. DRASTIC: A standardized system for evaluating groundwater 
pollution potential using hydrogeologic setting. EPA/600/2-87/035. 
Robert S. Kerr Environmental Research Laboratory, U.S. Environmental 
Protection Agency, 622 pp.
    7. An In-Depth Investigation to Estimate Surface Water 
Concentrations of Carbofuran within Indiana Community Water Supplies. 
Performed by Waterborne Environmental, Inc., Leesburg, VA, Engel 
Consulting, and Fawcett Consulting. Submitted by FMC. Corporation, 
Philadelphia, PA. WEI No 528.01, FMC Report No. PC-0378. MRID 47221603. 
EPA-HQ-OPP-2007-1088-0023.
    8. An Investigation into the Potential for Carbofuran Leaching to 
Ground Water Based on Historical and Current Use Practices. Submitted 
by FMC. Corporation, Philadelphia, PA. Report No. PC-0363. MRID 
47221602. EPA-HQ-OPP-2007-1088-0022.
    9. An Investigation into the Potential for Carbofuran Leaching to 
Ground Water Based on Historical and Current Use Practices: 
Supplemental Report on Twenty-one Additional States. Submitted by FMC 
Corporation, Philadelphia, PA. Report No. PC-0383. MRID 47244901. EPA-
HQ-OPP-2007-1088-0025.
    10. Angier, Jonathan. 2005. Tier 2 Drinking Water Assessment for 
Aldicarb and its Major Degradates Aldicarb Sulfoxide and Aldicarb 
Sulfone. (DP 316754) Internal EPA Memorandum to Robert McNally dated 
May 10, 2005.
    11. Benchmark dose analysis of cholinesterase inhibition data in 
neonatal and adult rats (MRID no. 46688914) following exposure to 
carbofuran (A.Lowit, 1/19/06, D325342, TXR no. 0054034). EPA-HQ-OPP-
2007-1088-0045.
    12. Benjamins, J.A., and McKhann, G.M. 1981. Development, 
regeneration, and aging of the brain. In: Basic Neurochemistry. 3rd 
edition. Edited by Siegel, G.J., Albers, R.W., Agranoff, B.W., and 
Katzman, R. Little, Brown and Co., Boston. pp 445-469;.
    13. Best Management Practices to Reduce Carbofuran Losses to Ground 
And Surface Water. Submitted by FMC. Corporation, Philadelphia, PA. 
Report No. PC-0362. MRID 47279201. EPA-HQ-OPP-2005-0162-0464.
    14. Bretaud, S., Toutant, J.P., Saglio, P. 2000. Effects of 
carbofuran, diuron, and nicosulfuron on acetylcholinesterase activity 
in goldfish (Carassius auratus). Ecotoxicol Environ Saf. 2000 Oct; 
47(2):117-24.
    15. California Department of Pesticide Regulation. Risk 
Characterization Document for Carbofuran. January 23, 2006. 219 pgs. 
Available at: http://www.cpdr.ca.gov/docs/risk/red/carbofuran.pdf.
    16. Carbofuran Acute Aggregate Dietary (Food and Drinking Water) 
Exposure and Risk Assessments for the Reregistration Eligibility 
Decision (T. Morton, 7/22/08, D351371). EPA-HQ-OPP-2005-0162-0508.
    17. Carbofuran Environmental Risk Assessment and Human Drinking 
Water Exposure Assessment for IRED. March 2006. EPA-HQ-OPP-2005-0162-
0080.
    18. Carringer, 2000. Carbamate Market Basket Survey. Reviewed by S. 
Piper, D267539, 8/8/02. (MRID 45164701 S. Carringer, 5/12/00).
    19. Carbofuran. HED Revised Risk Assessment for the Reregistration 
Eligibility Decision (RED) Document (Phase 6). (PC 090601) D 330541, 
July 26, 2006. EPA-HQ-OPP-2005-0162-0307.
    20. Carbofuran. HED Revised Risk Assessment for the Notice of 
Intent to Cancel . (PC 090601) D 347038, January 2007. EPA-HQ-OPP-2007-
1088-0034.
    21. Cholinesterase depression in juvenile (day 11) and adult rats 
following acute oral (gavage) dose of carbofuran technical. Hoberman, 
2007. MRID 47143705 (unpublished FMC study). EPA-HQ-OPP-2007-1088-0066.
    22. Context Document for Carbofuran Risk Assessment Issues not 
Specifically Addressed in the FIFRA SAP Charge Questions (M. Panger, C. 
Salice, R. David Jones, E. Odenkirchen, I. Sunzenauer, 1/08 D348292). 
EPA-HQ-OPP-2007-1088-0071.
    23. Crumpton T.L., Seidler, F.J., Slotkin, T.A. Developmental 
neurotoxicity of chlorpyrifos in vivo and in vitro: Effects on nuclear 
transcription factors involved in cell replication and differentiation. 
Brain Research. 2000 Feb 28;857(1-2):87-98.
    24. Data Evaluation Record for Acute dose-response study of 
carbofuran technical administered by gavage to adult and postnatal day 
11 male and female CD[reg](Sprague-Dawley) rats. MRID 46688914. EPA-HQ-
OPP-2007-1088-0045.
    25. Data Evaluation Record for Cholinesterase depression in 
juvenile (day 11) and adult rats following acute oral (gavage) dose of 
carbofuran technical. MRIDs 47143703, 47143704 and 47143705. EPA-HQ-
OPP-2005-0162-0468.
    26. Davison, A.N. and Dobbing, J. 1966. Myelination as a vulnerable 
period in brain development. British Medical Bulletin. 22:40-44.
    27. Dobbing, J. and Smart, J.L. (1974) Vulnerability of developing 
brain and behaviour. British Medical Bulletin. 30:164-168.
    28. Dose-time response modeling of rat brain AChE activity: 
carbofuran gavage dosing 10/5/07 (Carbofuran-RatBrainDR.pdf) EPA-HQ-
OPP-2007-1088-0053.
    29. Dose-time response modeling of rat RBC-AChE activity: 
carbofuran gavage dosing 10/23/07 (RatRBC--DR.pdf). EPA-HQ-OPP-2007-
1088-0029.
    30. Dose-Time Response Modeling of Rat Brain AChE Activity: 
Carbofuran Gavage Dosing: BMD50s for PND11 animals, January 
14, 2009.
    31. Dose-Time Response Modeling of Rat RBC AChE Activity: 
Carbofuran Gavage Dosing: BMD50s for PND11 Animals, January 
14, 2009.
    32. Dumaz, N., Hayward, R., Martin, J., Ogilvie, L., Hedley, D., 
Curtin, J.A., Bastian, B.C., Springer, C., Marais, R. In Melanoma, RAS 
Mutations Are Accompanied by Switching Signaling from BRAF to CRAF and 
Disrupted Cyclic AMP Signaling. Cancer Resarch. 2006 Oct 1;66(19):9483-
91.
    33. Bernard, Engel, Fawcett, Richard S. and Williams, W. Martin. 
2008. Comments to the FIFRA Scientific Advisory Panel - Volume V: The 
Water Risk Assessment for Carbofuran. From Carbofuran Scientific 
Advisory Panel Meeting, Feb. 5-8, 2008, Docket ID Number: EPA-HQ-OPP-
2007-1088 FMC Corporation, Agricultural Products Group Written 
Comments.
    34. EPA Response to the Transmittal of Meeting Minutes of the FIFRA 
Scientific Advisory Panel Meeting Held February 5-8 2008 on the 
Agency's Proposed Action under FIFRA 6(b) Notice of Intent to Cancel 
Carbofuran (E.Reaves, A. Lowit, J. Liccione 7/2008 D352315).
    35. Estimated Drinking Water Concentrations (email communication D. 
Young to D. Drew, March 8, 2006).
    36. Fawcett, R., Engel, B., Williams, W. 2007. An Investigation 
into the Potential for Carbofuran Leaching to Ground Water Based on 
Historical and Current Product Uses. (MRID 47221602)

[[Page 23091]]

Project Number PC/0363. 32 p. EPA-HQ-OPP-2005-0162-0454.1.
    37. FIFRA SAP. 1998. ``A set of Scientific Issues Being Considered 
by the Agency in Connection with Proposed Methods for Basin-scale 
Estimation of Pesticide Concentrations in Flowing Water and Reservoirs 
for Tolerance Reassessment.'' Final Report from the FIFRA Scientific 
Advisory Panel Meeting of July 29-30, 1998 (Report dated September 2, 
1998). Available at: http://www.epa.gov/scipoly/sap/meetings/1998/july/final1.pdf.
    38. FIFRA SAP. 1999. ``Sets of Scientific Issues Being Considered 
by the Environmental Protection Agency Regarding Use of Watershed-
derived Percent Crop Areas as a Refinement Tool in FQPA Drinking Water 
Exposure Assessments for Tolerance Reassessment.'' Final Report from 
the FIFRA Scientific Advisory Panel Meeting of February 5-7, 2002 
(Report dated May 25, 1999). SAP Report 99-03C. Available at: http://www.epa.gov/scipoly/sap/meetings/1999/may/final.pdf.
    39. SAP. 2001a. REPORT: FIFRA Scientific Advisory PanelMeeting, 
September 29, 2000, held at the Sheraton Crystal City Hotel, Arlington, 
Virginia. Session VI - A Set of Scientific Issues Being Considered by 
the Environmental Protection Agency Regarding: Progress Report on 
Estimating Pesticide Concentrations in Drinking Water and Assessing 
Water Treatment Effects on Pesticide Removal and Transformation: A 
Consultation. SAP Report No 2002-2.
    40. FIFRA SAP. 2002a. ``Methods Used to Conduct a Preliminary 
Cumulative Risk Assessment for Organophosphate Pesticides.'' Final 
Report from the FIFRA Scientific Advisory Panel Meeting of February 5-
7, 2002 (Report dated March 19, 2002). FIFRA Scientific Advisory Panel, 
Office of Science Coordination and Policy, Office of Prevention, 
Pesticides and Toxic Substances, U.S. Environmental Protection Agency. 
Washington, DC. SAP Report 2002-01.
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Safety Factor(s) in the Organophosphorous Pesticide Cumulative Risk 
Assessment: Susceptibility and Sensitivity to the Common Mechanism, 
Acetylcholinesterase Inhibition Meeting Minutes from the FIFRA 
Scientific Advisory Panel Meeting of June 26-27, 2002 (Minutes dated 
July 19, 2002). FIFRA Scientific Advisory Panel, Office of Science 
Coordination and Policy, Office of Prevention, Pesticides and Toxic 
Substances, U.S. Environmental Protection Agency. Washington, DC.
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Methyl Carbamate Cumulative Risk Assessment: Pilot Cumulative 
Analysis.'' Final Report from the FIFRA Scientific Advisory Panel 
Meeting of February15-18, 2005. (report dated April 15, 2005) Available 
at: http://www.epa.gov/scipoly/sap/2005/february/minutes.pdf.
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Preliminary N-Methyl Carbamate Cumulative Risk Assessment.'' Final 
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26, 2005. Available at: http://www.epa.gov/scipoly/sap/2005/august/minutes.pdf.
    44. FIFRA Science Advisory Panel (SAP). 2008. ``Final report on the 
Agency's Proposed Action under FIFRA 6(b) Notice of Intent to Cancel 
Carbofuran.'' Report from the FIFRA Scientific Advisory Panel Meeting 
of February 5-8, 2008. Available at: http://www.epa.gov/scipoly/sap/meetings/2008/february/carbofuransapfinal.pdf.
    45. Final report on cholinesterase inhibition study of carbofuran: 
PND17 rats. MRID 47167801 (ORD study). EPA-HQ-OPP-2007-1088-0064.
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and adult rats following acute oral (gavage) dose of carbofuran 
technical. Study by Charles River Laboratories for FMC. May 31, 2007. 
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and Salice, Christopher. 2006. Reregistration Eligibility Science 
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(SAP) Friday, September 29, 2000. http://www.epa.gov/scipoly/sap/meetings/2000/september/sept00_sap_dw_0907.pdf.
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cholinergic neurochemistry. Journal of Toxicology and Environmental 
Health. 84, 352-59.
    83. Report on cholinesterase sensitivity study of carbofuran: Adult 
and PND11 MRID 47289001 (ORD study). EPA-HQ-OPP-2007-1088-0065.
    84. Revised Drinking Water Assessment in Support of the 
Reregistration of Carbofuran (PC Code 090601) (R. David Jones, 9/5/07 
D3424057). EPA-HQ-OPP-2005-0162-0485.
    85. Screening Level analysis of the small business impacts of 
revoking carbofuran tolerances. (Wyatt, T.J. July 2008) 28 pgs. EPA-HQ-
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    86. Setzer W. 2008. Carbofuran: Updated Statistical Analysis of the 
FQPA Factor Based on the BMD50 ratio of Adult/Pup RBC Data. 
7 pgs. EPA-HQ-OPP-2005-0162-0511.
    87. Setzer W. October 23, 2007. Dose-time response modeling of rat 
RBC AChE activity: Carbofuran gavage dosing. 47 pgs. EPA-HQ-OPP-2007-
1088-0029.
    88. Setzer W. October 25, 2007. PND17 BMDs and BMDLs and recovery 
half-lives for the effect of Carbofuran on brain and blood AChE. 12 
pgs. EPA-HQ-OPP-2007-1088-0047.
    89. Setzer W. October 5, 2007. Dose-time response modeling of rat 
brain AChE activity: Carbofuran gavage dosing. 64 pgs. EPA-HQ-OPP-2007-
1088-0053.
    90. Slotkin T.A., Cousins, M.M., Tate, C.A., Seidler, F.J. 
Persistent cholinergic presynaptic deficits after neonatal chlorpyrifos 
exposure. Brain Research. 2001 Jun 1;902(2):229-43.
    91. Slotkin, T.A., Seidler, F.J. 2007. Comparative developmental 
neurotoxicity of organophosphates in vivo: Transcriptional responses of

[[Page 23093]]

pathways for brain cell development, cell signaling, cytotoxicity and 
neurotransmitter systems. Brain Research Bulletin. May 30;72(4-6):232-
74. Epub 2007 Jan 25.
    92. Slotkin, T.A., Tate, C.A., Ryde, I.T., Levin, E.D., Seidler, 
F.J. Organophosphate insecticides target the serotonergic system in 
developing rat brain regions: disparate effects of diazinon and 
parathion at doses spanning the threshold for cholinesterase 
inhibition. Environmental Health Perspectives. 2006 Oct;114(10):1542-6.
    93. Soil Survey Staff, Natural Resources Conservation Service, 
United States Department of Agriculture. 2009. NRCS Soil Data Mart Home 
Page. [Online WWW]. Accessed March, 2009. http://soildatamart.nrcs.usda.gov/.
    94. Summary Evaluation of Recently Submitted FMC Water Exposure 
Studies. (PC Code 090601) (R. David Jones, 12/26/07 D347901), 12 pgs. 
EPA-HQ-OPP-2007-1088-0016.
    95. Thelin, Gail P., and Leonard P. Gianessi. 2000. U.S. Method for 
Estimating Pesticide Use for County Areas of the Conterminous United 
States Geological Survey Open-File Report 00-250. Sacramento, 
California, 2000.
    96. Trask, Jennifer R., and Amos, Joshua. 2005.. Prepared by 
Waterborne Environmental Inc., Leesburg, VA. WEI 362.07. (MRID 
46688915) Submitted by FMC Corporation, Philadephia, PA FMC Study 
 P3786. EPA-HQ-OPP-2005-0162-0061.
    97. Transmittal of Meeting Minutes of the FIFRA Scientific Advisory 
Panel Meeting Held June 26-27, 2002. Released on July 19, 2002, 26. 
EPA-HQ-OPP-2007-1088-0146.
    98. USDA NRCS. Conservation Buffer to Reduce Pesticide Losses. 
Natural Resources Conservation Service, Fort Worth, TX, 21 pp.
    99. USEPA. 2000a. Assigning Values to Nondetected/Nonquantified 
Pesticide Residues in Human Health Dietary Exposure Assessments. March 
23, 2000. Available at: http://www.epa.gov/pesticides/trac/science/trac3b012.pdf.
    100. USEPA. 2000b. Benchmark Dose Technical Guidance Document. 
Draft report. Risk Assessment Forum, Office of Research and 
Development, U.S. Environmental Protection Agency. Washington, DC. EPA/
630/R-00/001.
    101. USEPA. 2000c. Choosing a Percentile of Acute Dietary Exposure 
as a Threshold of Regulatory Concern. March 16, 2000. Available at: 
http://www.epa.gov/pesticides/trac/science/trac2b054.pdf.
    102. USEPA. 2000d. The Use of Data on Cholinesterase Inhibition for 
Risk Assessments of Organophosphorous and Carbamate Pesticides. August 
18, 2000. Available at: http://www.epa.gov/pesticides/trac/science/cholin.pdf.
    103. USEPA. 2001a. Memorandum from Marcia Mulkey to Lois Rossi. 
``Implementation of the Determinations of a Common Mechanism of 
Toxicity for N-Methyl Carbamate Pesticides and for Certain 
Chloroacetanilide Pesticides.'' July 12, 2001. Available at: http://www.epa.gov/oppfead1/cb/csb_page/updates/carbamate.pdf.
    104. USEPA. 2001b. Pesticide Registration (PR) Notice 2001-X Draft: 
Spray and Dust Drift Label Statements for Pesticide Products. http://www.epa.gov/PR_Notices/prdraft-spraydrift801.htm.
    105. USEPA. 2002. Office of Pesticide Programs' Policy on the 
Determination of the Appropriate FQPA Safety Factor(s) For Use in 
Tolerance Assessment. Available at: http://www.epa.gov/oppfead1/trac/science/determ.pdf.
    106. USEPA. 2005. Preliminary N-Methyl Carbamate Cumulative Risk 
Assessment. Available at: http://www.epa.gov/oscpmont/sap/2005/index.htm#august.
    107. USEPA. 2007. Revised N-Methyl Carbamate Cumulative Risk 
Assessment U.S. Environmental Protection Agency, Office of Pesticide 
Programs, September 24, 2007. Available at: http://www.epa.gov/oppsrrd1/REDs/nmc_revised_cra.pdf.
    108. USEPA 2007c. Carbaryl. HED Chapter of the Reregistration 
Eligibility Decision Document (RED). PC Code: 056801, DP Barcode: 
D334770. 28 June 2007.
    109. U.S. Environmental Protection Agency. 2008a. EPA response to 
the transmittal of meeting minutes of the FIFRA Scientific Advisory 
Panel Meeting held February 5-8 on the Agency's proposed action under 
FIFRA 6(b) Notice of Intent to Cancel Carbofuran (3-26-08). E. Reaves 
et al., July 22, 2008, DP 352315).
    110. U.S. Environmental Protection Agency. 2008b. Memorandum 
(November 18, 2008) from Linda L. Taylor. ``Aldicarb: Determination of 
Whether Cited Study Fulfills Data Requirements for Comparative 
Cholinesterase Assay.'' D299880.
    111. USEPA. 2009a. Jones, R. David, Reuben Baris, and Marietta 
Echeverria. 2009. Response to comments on EPA's proposed tolerance 
revocations for carbofuran specifically related to drinking water 
exposure assessment. Internal EPA memorandum to Jude Andreasen dated 
April 29, 2009. D362182.
    112. USEPA. 2009b. Response to Comments in Opposition To Proposed 
Tolerance Revocations For Carbofuran Docket EPA-HQ-OPP-2005-0162'' 
submitted by the National Potato Council, National Corn Growers 
Association, National Cotton Council, National Sunflower Association, 
And FMC Corporation (September 29, 2008). April 29, 2009. D364288.
    113. USEPA. 2009c. Response to Comments from the Children's 
Environmental Health Network and the American Academy of Pediatrics 
(AAP) (Dated September 28. 2008) & the Natural Resources Defense 
Council and American Bird Conservancy (Dated September 28. 2008). April 
29, 2009. D364289.
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Nation's Streams and Ground Water, 1992-2001. Appendix 7A. Statistical 
summaries of pesticide compounds in stream water. http://water.usgs.gov/nawqa/pnsp/pubs/circ1291/appendix7/7a.html.
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last updated December , 2008. http://nwis.waterdata.usgs.gov/nwis/gw..
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Teratogenicity of Carbofuran in Rats: ACT 184.33. (Unpublished study 
received Dec 5, 1978 under 275-2712; prepared by WARF Institute, Inc., 
submitted by FMC Corp., Philadelphia, Pa.; CDL:236593-A).
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for Carbofuran in Illinois Watershed. Performed by Waterborne 
Environmental, Inc., Leesburg, VA. WEI 362.07. Submitted by FMC 
Corporation, Philadelphia, PA. Report No. P-3786. MRID 46688915. EPA-
HQ-OPP-2007-1088-0021.
    118. Whyatt, R., Barr, D., Camann, D., Kinney, P., Barr, J., 
Andrews, H., et al. 2003. Contemporary-use pesticides in personal air 
samples during pregnancy and blood samples at delivery among urban 
minority mothers and newborns. Environmental Health Perspectives, Vol. 
111, No. 5, pp. 749-756).
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of two methods for measurement of erythrocyte cholinesterase inhibition 
after carbamate administration to rats. Food and Cosmetic Toxicology. 
7:149-151.
    120. Williams, W.M., Engel, B., Dasgupta, S., and Hoogeweg, C.G. 
2007a. An In-Depth Investigation to Estimate Surface Water 
Concentrations of Carbofuran within Indiana Community Water Supplies. 
(MRID 47221603) Performed by Waterborne

[[Page 23094]]

Environmental, Inc., , Leesburg, VA, Engel Consulting, and Fawcett 
Consulting. Submitted by FMC. Corporation, Philadelphia, PA. WEI No 
528.01, FMC Report No. PC-0378. EPA-HQ-OPP-2005-0162-0453.
    121. Williams, W.M., Engel, B., Dasgupta, S. and Hoogeweg, C.G. 
2007b. An In-Depth Investigation to Estimate Surface Water 
Concentrations of Carbofuran within Indiana Community Water Supplies. 
Performed by Waterborne Environmental, Inc., (MRID 47272301) Leesburg, 
VA, Engel Consulting, and Fawcett Consulting. Submitted by FMC. 
Corporation, Philadelphia, PA. WEI No 528.01, FMC Report No. PC-0378. 
EPA-HQ-OPP-2005-0162-0453.
    122. Wyatt, T.J. (10/30/08). Percent crop treated estimates for 
dietary risk analysis, carbofuran on domestic potatoes and imported 
bananas (DP 357726).
    123. Winteringham, F.P.W. and Fowler, K.S. 1966. Substrate and 
dilution effects on the inhibition of acetylcholinesterase by 
carbamates. Biochemistry Journal. 101:127-134.
    124 USEPA. 2007d. Memorandum (June 29, 2007) from E Reaves. 
Carbaryl: Updated Endpoint Selection for Single Chemical Risk 
Assessment. D337054
    125. USEPA. Memorandum (December 12, 2008) Setzer. W., PND17 BMDs 
and BMDLs and Recovery Half-Lives for the Effect of Carbofuran on Brain 
and Blood AChE.
     126. Vecchia, A.V. and C. G. Crawford, 2006. Simulation Of Daily 
Pesticide Concentrations From Watershed Characteristics And Monthly 
Climatic Data USGS Scientific Investigations. USGS Report 2006-5181. 60 
pgs.

List of Subjects in 40 CFR Part 180

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


    Dated: May 11, 2009.
Debra Edwards,
Director, Office of Pesticide Programs.


0
Therefore, 40 CFR chapter I be amended as follows:

PART 180--[AMENDED]

0
1. The authority citation for part 180 continues to read as follows:

    Authority: 21 U.S.C. 321(q), 346a and 371.


0
2. Section 180.254 is amended by revising the tables in paragraphs (a) 
and (c) to read as follows:


Sec.  180.254  Carbofuran; tolerances for residues.

    (a) * * *

------------------------------------------------------------------------
                                                  Parts per  Expiration/
                    Commodity                      million    Revocation
                                                    (ppm)        date
------------------------------------------------------------------------
Alfalfa, forage (of which no more than 5 ppm are         10     12/31/09
 carbamates)....................................
Alfalfa, hay (of which no more than 20 ppm are           40     12/31/09
 carbamates)....................................
Banana..........................................        0.1     12/31/09
Barley, grain (of which not more than 0.1 ppm is        0.2     12/31/09
 carbamates)....................................
Barley, straw (of which no more than 1.0 ppm is         5.0     12/31/09
 carbamates)....................................
Beet, sugar, roots..............................        0.1     12/31/09
Beet, sugar, tops (of which no more than 1 ppm            2     12/31/09
 is carbamates).................................
Coffee, bean, green.............................        0.1     12/31/09
Corn, forage (of which no more than 5 ppm are            25     12/31/09
 carbamates)....................................
Corn, grain (including popcorn) (of which no            0.2     12/31/09
 more than 0.1 ppm is carbamates)...............
Corn, stover (of which no more than 5 ppm are            25     12/31/09
 carbamates)....................................
Corn, sweet, kernel plus cob with husks removed         1.0     12/31/09
 (of which no more than 0.2 ppm is carbamates)..
Cotton, undelinted seed (of which no more than          1.0     12/31/09
 0.2 ppm is carbamates).........................
Cranberry (of which no more than 0.3 ppm is             0.5     12/31/09
 carbamates)....................................
Cucumber (of which not more than 0.2 ppm is             0.4     12/31/09
 carbamates)....................................
Grape (of which no more than 0.2 ppm is                 0.4     12/31/09
 carbamates)....................................
Grape, raisin (of which no more than 1.0 ppm is         2.0     12/31/09
 carbamate......................................
Grape, raisin, waste (of which no more than 3.0         6.0     12/31/09
 ppm is carbamates..............................
Melon (of which not more than 0.2 ppm is                0.4     12/31/09
 carbamates)....................................
Milk (of which no more than 0.02 ppm is                 0.1     12/31/09
 carbamates)....................................
Oat, grain (of which not more than 0.1 ppm is           0.2     12/31/09
 carbamates)....................................
Oat, straw (of which not more than 1.0 ppm is           5.0     12/31/09
 carbamates)....................................
Pepper (of which no more than 0.2 ppm is                  1     12/31/09
 carbamates)....................................
Potato (of which no more than 1 ppm is                    2     12/31/09
 carbamates)....................................
Pumpkin (of which not more than 0.6 ppm is              0.8     12/31/09
 carbamates)....................................
Rice, grain.....................................        0.2     12/31/09
Rice, straw (of which no more than 0.2 ppm is             1     12/31/09
 carbamates)....................................
Sorghum, forage (of which no more than 0.5 ppm            3     12/31/09
 is carbamates).................................
Sorghum, grain, grain...........................        0.1     12/31/09
Sorghum, grain, stover (of which no more than             3     12/31/09
 0.5 ppm is carbamates).........................
Strawberry (of which no more than 0.2 ppm is            0.5     12/31/09
 carbamates)....................................
Soybean (of which not more than 0.2 ppm is              1.0     12/31/09
 carbamates)....................................
Soybean, forage (of which not more than 20.0 ppm       35.0     12/31/09
 are carbamates)................................
Soybean, hay (of which not more than 20.0 ppm          35.0     12/31/09
 are carbamates)................................
Squash (of which not more than 0.6 ppm is               0.8     12/31/09
 carbamates)....................................
Sugarcane, cane.................................        0.1     12/31/09
Sunflower, seed (of which not more than 0.5 ppm         1.0     12/31/09
 is carbamates).................................
Wheat, grain (of which not more than 0.1 ppm is         0.2     12/31/09
 carbamates)....................................
Wheat, straw (of which not more than 1.0 ppm is         5.0     12/31/09
 carbamates)....................................
------------------------------------------------------------------------

* * * * *
    (c) * * *

[[Page 23095]]



------------------------------------------------------------------------
                                                  Parts per  Expiration/
                    Commodity                      million    Revocation
                                                    (ppm)        date
------------------------------------------------------------------------
Artichoke, globe (of which not more than 0.2 ppm        0.4     12/31/09
 is carbamates).................................
------------------------------------------------------------------------

* * * * *

[FR Doc. E9-11396 Filed 5-12-09; 4:15 pm]
 BILLING CODE 6560-50-S