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-

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

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-

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.

    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

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

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

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

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).

    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

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

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.

[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

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.

[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
----------------------------------------------------------------------------------------------------------------

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.

    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

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
--------------------------------------------------------------------------------------------------------------------------------------------------------

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.,

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