[Federal Register Volume 74, Number 93 (Friday, May 15, 2009)]
[Rules and Regulations]
[Pages 23046-23095]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E9-11396]
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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
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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
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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.
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28. Dose-time response modeling of rat brain AChE activity:
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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:
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32. Dumaz, N., Hayward, R., Martin, J., Ogilvie, L., Hedley, D.,
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Water Risk Assessment for Carbofuran. From Carbofuran Scientific
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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)
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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
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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
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(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,
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45. Final report on cholinesterase inhibition study of carbofuran:
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47. Fite, Edward, Randall, Donna, Young, Dirk, Odenkirchen, Edward
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99. USEPA. 2000a. Assigning Values to Nondetected/Nonquantified
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101. USEPA. 2000c. Choosing a Percentile of Acute Dietary Exposure
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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.
114. USGS. The Quality of Our Nation's Waters: Pesticides in the
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.
115. USGS. 2008. USGS Ground-Water Data for the Nation. database
last updated December , 2008. http://nwis.waterdata.usgs.gov/nwis/gw..
116. WARF. 1978. Rao, G.N., Davis, G.J., Giesler, P. et al. 1978.
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).
117. Watershed Regressions for Pesticides (WARP) Model Estimates
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
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111, No. 5, pp. 749-756).
119. Williams, C.H. and Casterline, J.L., Jr. (1969). A comparison
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