[Federal Register: August 27, 2008 (Volume 73, Number 167)]
[Rules and Regulations]
[Page 50563-50570]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr27au08-6]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[EPA-HQ-OPP-2007-0604; FRL-8377-7]
Dichlobenil; Pesticide Tolerances
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: This regulation establishes tolerances for combined residues
of dichlobenil and its metabolite, 2,6-dichlorbenzamide, in or on
bushberry subgroup 13-07B, caneberry subgroup 13-07A and rhubarb. It
also removes existing tolerances on individual members of bushberry
subgroup 13-07B (blueberry) and caneberry subgroup 13-07A (blackberry
and raspberry) that are superseded by the new crop subgroup tolerances
at the same tolerance levels. Interregional Research Project Number 4
(IR-4) requested these tolerances under the Federal Food, Drug, and
Cosmetic Act (FFDCA).
DATES: This regulation is effective August 27, 2008. Objections and
requests for hearings must be received on or before October 27, 2008,
and must be filed in accordance with the instructions provided in 40
CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION ).
ADDRESSES: EPA has established a docket for this action under docket
identification (ID) number EPA-HQ-OPP-2007-0604. To access the
electronic docket, go to http://www.regulations.gov, select ``Advanced
Search,'' then ``Docket Search.'' Insert the docket ID number where
indicated and select the ``Submit'' button. Follow the instructions on
the regulations.gov website to view the docket index or access
available documents. All documents in the docket are listed in the
docket index available in regulations.gov. Although listed in the
index, some information is not publicly available, e.g., Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute. Certain other material, such as copyrighted
material, is not placed on the Internet and will be publicly available
only in hard copy form. Publicly available docket materials are
available in the electronic docket at http://www.regulations.gov, or,
if only available in hard copy, at the OPP Regulatory Public Docket in
Rm. S-4400, One Potomac Yard (South Bldg.), 2777 S. Crystal Dr.,
Arlington, VA. The Docket Facility is open from 8:30 a.m. to 4 p.m.,
Monday through Friday, excluding legal holidays. The Docket Facility
telephone number is (703) 305-5805.
FOR FURTHER INFORMATION CONTACT: Susan Stanton, Registration Division
(7505P), Office of Pesticide Programs, Environmental Protection Agency,
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone
number: (703) 305-5218; e-mail address: stanton.susan@epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this Action Apply to Me?
You may be potentially affected by this action if you are an
agricultural producer, food manufacturer, or pesticide manufacturer.
Potentially affected entities may include, but are not limited to those
engaged in the following activities:
Crop production (NAICS code 111).
Animal production (NAICS code 112).
Food manufacturing (NAICS code 311).
Pesticide manufacturing (NAICS code 32532).
This listing is not intended to be exhaustive, but rather to
provide a guide for readers regarding entities likely to be affected by
this action. Other types of entities not listed in this unit could also
be affected. The North American Industrial Classification System
(NAICS) codes have been provided to assist you and others in
determining whether this action might apply to certain entities. If you
have any questions regarding the applicability of this action to a
particular entity, consult the person listed under FOR FURTHER
INFORMATION CONTACT.
B. How Can I Access Electronic Copies of this Document?
In addition to accessing an electronic copy of this Federal
Register document through the electronic docket at http://
www.regulations.gov, you may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr. You may also access a
frequently updated electronic version of EPA's tolerance regulations at
40 CFR part 180 through the Government Printing Office's pilot e-CFR
site at http://www.gpoaccess.gov/ecfr.
C. Can I File an Objection or Hearing Request?
Under section 408(g) of FFDCA, any person may file an objection to
any aspect of this regulation and may also request a hearing on those
objections. You must file your objection or request a hearing on this
regulation in accordance with the instructions provided in 40 CFR part
178. To ensure proper receipt by EPA, you must identify docket ID
number EPA-HQ-OPP-2007-0604 in the subject line on the first page of
your submission. All requests must be in writing, and must be mailed or
delivered to the Hearing Clerk as required by 40 CFR part 178 on or
before October 27, 2008.
In addition to filing an objection or hearing request with the
Hearing Clerk as described in 40 CFR part 178, please submit a copy of
the filing that does not contain any CBI for inclusion in the public
docket that is described in ADDRESSES. Information not marked
confidential pursuant to 40 CFR part 2 may be disclosed publicly by EPA
without prior notice. Submit this copy, identified by docket ID number
EPA-HQ-OPP-2007-0604, by one of the following methods:
Federal eRulemaking Portal: http://www.regulations.gov.
Follow the on-line instructions for submitting comments.
Mail: Office of Pesticide Programs (OPP) Regulatory Public
Docket (7502P), Environmental Protection Agency, 1200 Pennsylvania
Ave., NW., Washington, DC 20460-0001.
Delivery: OPP Regulatory Public Docket (7502P),
Environmental Protection Agency, Rm. S-4400, One Potomac Yard (South
Bldg.), 2777 S. Crystal Dr., Arlington, VA. Deliveries are only
accepted during the Docket's normal hours of operation (8:30 a.m. to 4
p.m., Monday through Friday, excluding legal holidays). Special
arrangements should be made for deliveries of boxed information. The
Docket Facility telephone number is (703) 305-5805.
II. Petition for Tolerance
In the Federal Register of August 22, 2007 (72 FR 47010) (FRL-8142-
5), EPA issued a notice pursuant to section 408(d)(3) of FFDCA, 21
U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP
7E7230) by Interregional Research Project Number 4 (IR-4), 500 College
Road East, Suite 201W, Princeton, NJ 08540-6635. The petition requested
that 40 CFR 180.231 be amended by establishing tolerances for combined
residues of the herbicide dichlobenil, 2,6-dichlorobenzonitrile, and
its metabolite, 2,6-
[[Page 50564]]
dichlorobenzamide, in or on rhubarb at 0.15 parts per million (ppm);
caneberry, subgroup 13a and wild raspberry at 0.1 ppm; and bushberry,
subgroup 13b; aronia berry; bluberry, lowbush; buffalo currant; chilian
guava; european barberry; highbush cranberry; honeysuckle; jostaberry;
juneberry; lingonberry; native currant; salal; and sea buckthorn at
0.15 ppm. That notice referenced a summary of the petition prepared by
Chemtura USA Corporation, the registrant, which is available to the
public in the docket, http://www.regulations.gov. There were no
comments received in response to the notice of filing.
Based upon review of the data supporting the petition and recent
changes in EPA's crop grouping regulations, EPA has revised the
tolerance level for rhubarb and the commodity terms for the berry
tolerances. The reasons for these changes are explained in Unit IV.C.
III. Aggregate Risk Assessment and Determination of Safety
Section 408(b)(2)(A)(i) of FFDCA allows EPA to establish a
tolerance (the legal limit for a pesticide chemical residue in or on a
food) only if EPA determines that the tolerance is ``safe.'' Section
408(b)(2)(A)(ii) of FFDCA defines ``safe'' to mean that ``there is a
reasonable certainty that no harm will result from aggregate exposure
to the pesticide chemical residue, including all anticipated dietary
exposures and all other exposures for which there is reliable
information.'' This includes exposure through drinking water and in
residential settings, but does not include occupational exposure.
Section 408(b)(2)(C) of FFDCA requires EPA to give special
consideration to exposure of infants and children to the pesticide
chemical residue in establishing a tolerance and to ``ensure that there
is a reasonable certainty that no harm will result to infants and
children from aggregate exposure to the pesticide chemical
residue....''
2,6-Dichlorobenzamide (BAM) is a common metabolite and soil
degradate of dichlobenil and the fungicide fluopicolide. BAM is the
major residue detected in plants following dichlobenil use and is,
therefore, a residue of concern. For this reason, aggregate exposure
and risk associated with BAM were assessed separately from dichlobenil.
In assessing aggregate exposure and risk for BAM, EPA considered
exposures associated with both dichlobenil and fluopicolide uses.
Consistent with section 408(b)(2)(D) of FFDCA, and the factors
specified in section 408(b)(2)(D) of FFDCA, EPA has reviewed the
available scientific data and other relevant information in support of
this action. EPA has sufficient data to assess the hazards of and to
make a determination on aggregate exposure for the petitioned-for
tolerances for combined residues of dichlobenil and its metabolite,
2,6-dichlorobenzamide (BAM) on bushberry subgroup 13-07B, caneberry
subgroup 13-07A and rhubarb at 0.15 ppm, 0.10 ppm and 0.06 ppm,
respectively. EPA's assessment of exposures and risks associated with
establishing tolerances follows.
A. Toxicological Profile
EPA has evaluated the available toxicity data and considered its
validity, completeness, and reliability as well as the relationship of
the results of the studies to human risk. EPA has also considered
available information concerning the variability of the sensitivities
of major identifiable subgroups of consumers, including infants and
children.
In acute toxicity tests, dichlobenil demonstrated moderate acute
toxicity via the oral, dermal and inhalation routes. It is neither a
dermal irritant, eye irritant, nor a dermal sensitizer. In the
subchronic and chronic oral toxicity studies in hamsters, rats and
dogs, the liver was the primary target organ. For example, in a 90-day
oral toxicity study in rats, inflammation and necrosis were observed in
the liver of males, and increased liver weight and liver histopathology
(swelling and vacuolation of hepatocytes) were observed in females. In
a 90-day oral toxicity study in hamsters, increased liver weight,
enlarged liver (with rough surface) and swollen hepatocytes were
observed in females. In addition, decreased weight of the prostate and
mineralization of the prostate were reported in males. Increased liver
weights and hepatic enzymes, as well as liver histopathology, were
observed at lower doses in two chronic dog toxicity studies, as well as
in the combined chronic toxicity/carcinogenicity study in the rat.
In addition to the liver, the nose is considered a target organ for
dichlobenil. Olfactory toxicity was observed following dermal and
inhalation exposures in toxicity studies that were either published in
the open literature (dermal) or submitted to the Agency (inhalation).
In each study, degeneration of the olfactory epithelium, which is
composed of olfactory sensory neurons, was observed. Olfactory toxicity
was not observed in the chronic oral (capsule) toxicity study in the
dog. No other evidence of neurotoxicity was seen in the toxicity
studies for dichlobenil.
EPA classified dichlobenil as a Group C (possible human) carcinogen
based on the results of carcinogenicity studies in hamsters and rats
and its structural similarity to bromoxynil and thiobenzamide, which
are associated with hepatocellular tumors in rodents. In a high-dose
hamster study, there was a treatment-related increase in liver adenomas
and combined adenomas/carcinomas in males at the highest dose tested;
however, this dose was considered excessive, based on decreased body
weight gains and severe hepatotoxicity. In a second hamster study,
performed at lower, but adequate doses, there was no treatment-related
increase in the incidence of any tumor type. In the rat study, there
was a treatment-related increase in the incidence of hepatocellular
tumors in females only. Based on the weight of the evidence, EPA
classified dichlobenil as a possible human carcinogen but determined
that the chronic dietary risk assessment based on the cPAD would be
protective of any potential cancer effects for the following reasons:
The liver tumors seen in male hamsters occurred only at an excessively
high dose. The increases in liver tumors in the rat were statistically
significant in only one sex (females), while tumors were predominantly
benign adenomas and supporting evidence was weak at best. Although the
tumor type (hepatocellular) is considered unusual for the strain of rat
tested, tumors did not occur to an unusal degree or with an early
onset. Further, dichlobenil was determined to be non-mutagenic in
bacteria and mammalian cells, as well as non-clastogenic in several
mammalian assays (in vitro and in vivo).
In the rat prenatal developmental toxicity study, maternal effects
(decreased body weight gain, food consumption and food efficiency) were
seen at the mid- and high doses, whereas no prenatal developmental
effects occurred at any dose. In the rabbit developmental toxicity
study, prenatal effects (an increase in total resorptions/dam, post-
implantation loss, as well as external, visceral, and skeletal
anomalies) occurred in the presence of maternal toxicity (severe
decreases in body weight gain (120%) and food consumption (30%)). In
the rat reproduction study, effects in the pups (decreased body weight
during weaning in both F1 (16-23%) and F2 (19-22%) generation pups)
occurred at a lower dose than that which resulted in parental toxicity
(decreases in premating and gestation body weight gain and premating
food consumption
[[Page 50565]]
in both parental and F1 generation adults), indicating increased
quantitative susceptibility of the pups.
Delayed maturity of the uterus was observed in all high-dose
females tested in the chronic oral (capsule) toxicity study in the dog.
A marked decrease in mean uterine weight at the high dose confirmed
this finding. Ovarian weights were also decreased in high-dose females,
but no alterations were observed microscopically. These results are
suggestive of modulation of the female endocrine system in this study;
however, the dose utilized in the dichlobenil risk assessment for the
chronic RfD is almost forty times lower than that at which the effects
were observed and is considered protective of any potential endocrine
modulation.
BAM demonstrated moderate acute toxicity via the oral route of
exposure. In subchronic and chronic toxicity studies, the primary oral
effects seen in the rat and dog were body weight changes. Adverse liver
effects were also observed but at doses of BAM that were higher than
those of dichlobenil. There is no evidence that BAM is either mutagenic
or clastogenic; nor is there evidence of endocrine mediated toxicity.
BAM is considered to be neurotoxic, based on clinical signs of
neurotoxicity following oral exposure in several short-term assays, in
addition to toxicity to the olfactory sensory neurons observed
following single intraperitoneal exposures of mice to BAM. In the
absence of carcinogenicity study data for a second species (a rat study
is available), the EPA has assumed that BAM's carcinogenic potential is
similar to that of dichlobenil, the parent compound having the greatest
carcinogenicity potential. Dichlobenil is classified as a ``group C,
possible human carcinogen.'' Quantification of cancer risk is based on
the cPAD approach which requires comparison of the chronic exposure to
the cPAD. Using this methodology will adequately account for all
chronic toxic effects, including carcinogenicity, likely to result from
exposure to dichlobenil and, therefore, to BAM.
Specific information on the studies received and the nature of the
adverse effects caused by dichlobenil and BAM, as well as the no-
observed-adverse-effect-level (NOAEL) and the lowest-observed-adverse-
effect-level (LOAEL) from the toxicity studies, can be found at http://
www.regulations.gov in the documents Dichlobenil; Human Health Risk
Assessment for Proposed Uses on Rhubarb; Caneberry, Subgroup 13-07A;
and Bushberry, Subgroup 13-07B, page 37 and 2,6-Dichlorobenzamide (BAM
); 2,6-Dichlorobenzamide (BAM ) as a Metabolite/Degradate of
Fluopicolide and Dichlobenil. Human Health Risk Assessment for Proposed
Uses of Rhubarb, Dichlobenil on Caneberries (Subgroup 13-07A), and
Bushberries (Subgroup 13-07B, page 17 in docket ID number EPA-HQ-OPP-
2007-0604.
B. Toxicological Endpoints
For hazards that have a threshold below which there is no
appreciable risk, a toxicological point of departure (POD) is
identified as the basis for derivation of reference values for risk
assessment. The POD may be defined as the highest dose at which no
adverse effects are observed (the NOAEL) in the toxicology study
identified as appropriate for use in risk assessment. However, if a
NOAEL cannot be determined, the lowest dose at which adverse effects of
concern are identified (the LOAEL) or a Benchmark Dose (BMD) approach
is sometimes used for risk assessment. Uncertainty/safety factors (UFs)
are used in conjunction with the POD to take into account uncertainties
inherent in the extrapolation from laboratory animal data to humans and
in the variations in sensitivity among members of the human population
as well as other unknowns. Safety is assessed for acute and chronic
dietary risks by comparing aggregate food and water exposure to the
pesticide to the acute population adjusted dose (aPAD) and chronic
population adjusted dose (cPAD). The aPAD and cPAD are calculated by
dividing the POD by all applicable UFs. Aggregate short-, intermediate-
, and chronic-term risks are evaluated by comparing food, water, and
residential exposure to the POD to ensure that the margin of exposure
(MOE) called for by the product of all applicable UFs is not exceeded.
This latter value is referred to as the Level of Concern (LOC).
For non-threshold risks, the Agency assumes that any amount of
exposure will lead to some degree of risk. Thus, the Agency estimates
risk in terms of the probability of an occurrence of the adverse effect
greater than that expected in a lifetime. For more information on the
general principles EPA uses in risk characterization and a complete
description of the risk assessment process, see http://www.epa.gov/
pesticides/factsheets/riskassess.htm.
A summary of the toxicological endpoints for dichlobenil and BAM
used for human risk assessment can be found at http://
www.regulations.gov in the documents Dichlobenil; Human Health Risk
Assessment for Proposed Uses on Rhubarb; Caneberry, Subgroup 13-07A;
and Bushberry, Subgroup 13-07B, page 19 and 2,6-Dichlorobenzamide (BAM
); 2,6-Dichlorobenzamide (BAM ) as a Metabolite/Degradate of
Fluopicolide and Dichlobenil. Human Health Risk Assessment for Proposed
Uses of Rhubarb, Dichlobenil on Caneberries (Subgroup 13-07A), and
Bushberries (Subgroup 13-07B, page 5 in docket ID number EPA-HQ-OPP-
2007-0604.
C. Exposure Assessment
1. Dietary exposure from food and feed uses. In evaluating dietary
exposure to dichlobenil, EPA considered exposure under the petitioned-
for tolerances as well as all existing dichlobenil tolerances in 40 CFR
180.231. In evaluating dietary exposure to BAM, EPA considered exposure
resulting from all proposed and registered uses of dichlobenil and
fluopicolide. EPA assessed dietary exposures from dichlobenil and BAM
in food as follows:
i. Acute exposure. Quantitative acute dietary exposure and risk
assessments are performed for a food-use pesticide, if a toxicological
study has indicated the possibility of an effect of concern occurring
as a result of a 1-day or single exposure.
a. Dichlobenil. An effect of concern attributable to a single
exposure was not identified for the general population, including
infants and children; however, such effects (an increase in total
resorptions/dam, post-implantation loss, as well as external, visceral,
and skeletal anomalies) were identified for the population subgroup
females, 13 to 49 years old. In estimating acute dietary exposure of
females, 13 to 49 years old, EPA used food consumption information from
the United States Department of Agriculture (USDA) 1994-1996 Nationwide
Continuing Surveys of Food Intake by Individuals (CSFII). As to residue
levels in food, EPA assumed that 100 percent of all crops with
established or pending tolerances are treated with dichlobenil and
contain tolerance-level residues.
b. BAM. EPA identified an effect of concern attributable to a
single exposure for the general population (lethargy after a single
dose in a dose range finding assay for an in vivo mouse erythrocyte
micronucleus assay) and for females 13 to 49 years old (increased
incidences of late abortion and skeletal and visceral anomalies in a
rabbit developmental toxicity study). In estimating acute dietary
exposure, EPA used food consumption information from the United States
Department of Agriculture (USDA) 1994-1996 and 1998 Nationwide
Continuing Surveys of Food Intake by Individuals (CSFII). As to residue
levels in food, EPA used
[[Page 50566]]
maximum residues of BAM from fluopicolide and dichlobenil field trials
on food commodities with established/pending tolerances. The
assessments assumed 100 percent crop treated (PCT) for all commodities
except apples, blueberries, cherries, peaches, pears and raspberries.
ii. Chronic exposure. a. Dichlobenil. In conducting the chronic
dietary exposure assessment, EPA used food consumption information from
the United States Department of Agriculture (USDA) 1994-1996 and 1998
Nationwide Continuing Surveys of Food Intake by Individuals (CSFII). As
to residue levels in food, EPA assumed that 100 percent of all crops
with established or pending tolerances are treated with dichlobenil and
contain tolerance-level residues.
b. BAM. In conducting the chronic dietary exposure assessment, EPA
used food consumption information from the United States Department of
Agriculture (USDA) 1994-1996 and 1998 Nationwide Continuing Surveys of
Food Intake by Individuals (CSFII). As to residue levels in food, EPA
used maximum residues of BAM from fluopicolide and dichlobenil field
trials on food commodities with established/pending tolerances. The
assessments assumed 100 PCT for all commodities except apples,
blueberries, cherries, cranberries, peaches, pears and raspberries.
iii. Cancer. EPA classified dichlobenil as a Group C, possible
human, carcinogen but determined that the chronic dietary risk
assessment based on the cPAD would be protective of any potential
cancer effects. The weight of the evidence supporting this
determination is discussed in unit III.A. (Toxicological Profile). EPA
has assumed that BAM's carcinogenic potential is similar to that of
dichlobenil, the parent compound having the greatest carcinogenicity
potential. As with dichlobenil, the chronic dietary risk assessment
based on the cPAD is expected to protect for any potential cancer
effects. Separate cancer exposure assessments are not needed for
dichlobenil or BAM.
iv. Anticipated residue and PCT information. EPA did not use
anticipated residues in the dietary risk assessments for dichlobenil
but did use anticipated residues (maximum field trial residues) for
BAM. Section 408(b)(2)(E) of FFDCA authorizes EPA to use available data
and information on the anticipated residue levels of pesticide residues
in food and the actual levels of pesticide residues that have been
measured in food. If EPA relies on such information, EPA must require
pursuant to FFDCA section 408(f)(1) that data be provided 5 years after
the tolerance is established, modified, or left in effect,
demonstrating that the levels in food are not above the levels
anticipated. For the present action, EPA will issue such data call-ins
as are required by FFDCA section 408(b)(2)(E) and authorized under
FFDCA section 408(f)(1). Data will be required to be submitted no later
than 5 years from the date of issuance of these tolerances.
Section 408(b)(2)(F) of FFDCA states that the Agency may use data
on the actual percent of food treated for assessing chronic dietary
risk only if:
Condition a: The data used are reliable and provide a
valid basis to show what percentage of the food derived from such crop
is likely to contain the pesticide residue.
Condition b: The exposure estimate does not underestimate
exposure for any significant subpopulation group.
Condition c: Data are available on pesticide use and food
consumption in a particular area, the exposure estimate does not
understate exposure for the population in such area.
In addition, the Agency must provide for periodic evaluation of any
estimates used. To provide for the periodic evaluation of the estimate
of PCT as required by FFDCA section 408(b)(2)(F), EPA may require
registrants to submit data on PCT.
The Agency used PCT information as follows:
The Agency did not use PCT information in the dichlobenil dietary
risk assessments. For the BAM acute assessment, maximum PCT estimates
were used for the following commodities: Apples, blueberries, cherries,
peaches and pears, each at 2.5%; and raspberries at 5%. For the BAM
chronic assessment, average PCT estimates were used for the following
commodities: Apples, blueberries, cherries, peaches and pears, each at
1%; raspberries at 5%; and cranberries at 45%.
In most cases, EPA uses available data from United States
Department of Agriculture/National Agricultural Statistics Service
(USDA/NASS), proprietary market surveys, and the National Pesticide Use
Database for the chemical/crop combination for the most recent 6 years.
EPA uses an average PCT for chronic dietary risk analysis. The average
PCT figure for each existing use is derived by combining available
public and private market survey data for that use, averaging across
all observations, and rounding to the nearest 5%, except for those
situations in which the average PCT is less than one. In those cases,
1% is used as the average PCT and 2.5% is used as the maximum PCT. EPA
uses a maximum PCT for acute dietary risk analysis. The maximum PCT
figure is the highest observed maximum value reported within the recent
6 years of available public and private market survey data for the
existing use and rounded up to the nearest multiple of 5%.
The Agency believes that the three conditions discussed in Unit
III.C.1.iv. have been met. With respect to Condition a, PCT estimates
are derived from Federal and private market survey data, which are
reliable and have a valid basis. The Agency is reasonably certain that
the percentage of the food treated is not likely to be an
underestimation. As to Conditions b and c, regional consumption
information and consumption information for significant subpopulations
is taken into account through EPA's computer-based model for evaluating
the exposure of significant subpopulations including several regional
groups. Use of this consumption information in EPA's risk assessment
process ensures that EPA's exposure estimate does not understate
exposure for any significant subpopulation group and allows the Agency
to be reasonably certain that no regional population is exposed to
residue levels higher than those estimated by the Agency. Other than
the data available through national food consumption surveys, EPA does
not have available reliable information on the regional consumption of
food to which dichlobenil may be applied in a particular area.
2. Dietary exposure from drinking water. The Agency used screening
level water exposure models in the dietary exposure analysis and risk
assessments for dichlobenil and BAM in drinking water. These simulation
models take into account data on the physical, chemical, and fate/
transport characteristics of dichlobenil and BAM. Further information
regarding EPA drinking water models used in pesticide exposure
assessment can be found at http://www.epa.gov/oppefed1/models/water/
index.htm.
Based on the Pesticide Root Zone Model /Exposure Analysis Modeling
System (PRZM/EXAMS) and Screening Concentration in Ground Water (SCI-
GROW) models, the estimated drinking water concentrations (EDWCs) of
dichlobenil for acute exposures are estimated to be 298 parts per
billion (ppb) for surface water and 0.93 ppb for ground water. The
estimated drinking water concentrations (EDWCs) of dichlobenil for
chronic exposures for non-cancer assessments are estimated to
[[Page 50567]]
be 4.6 ppb for surface water and 0.93 ppb for ground water.
Based on the Pesticide Root Zone Model /Exposure Analysis Modeling
System (PRZM/EXAMS) and Screening Concentration in Ground Water (SCI-
GROW) models, the estimated drinking water concentrations (EDWCs) of
BAM for acute exposures are estimated to be 21 parts ppb for surface
water and 56.2 ppb for ground water. The estimated drinking water
concentrations (EDWCs) of BAM for chronic exposures for non-cancer
assessments are estimated to be 8.6 ppb for surface water and 56.2 ppb
for ground water.
Modeled estimates of drinking water concentrations were directly
entered into the dietary exposure model. For acute dietary risk
assessment for dichlobenil, the water concentration value of 298 ppb
was used to assess the contribution to drinking water. For chronic
dietary risk assessment for dichlobenil, the water concentration value
of 4.6 ppb was used to assess the contribution to drinking water. For
acute and chronic dietary risk assessment for BAM, the water
concentration value of 56.2 ppb was used to assess the contribution to
drinking water.
3. From non-dietary exposure. The term ``residential exposure'' is
used in this document to refer to non-occupational, non-dietary
exposure (e.g., for lawn and garden pest control, indoor pest control,
termiticides, and flea and tick control on pets).
There are several dichlobenil products that may be used around
roses and other woody ornamentals in established residential plantings.
Since they are approved for professional applicator use only,
residential handler exposures are not expected. Post-application
exposure of adults and children to dichlobenil and BAM from the use of
dichlobenil products on ornamental plantings is expected to be
negligible and, therefore, was not assessed.
Fluopicolide is currently registered for the following uses that
could result in residential exposure to the metabolite/degradate BAM:
Residential turfgrass and recreational sites. EPA assessed residential
exposure to BAM using the following assumptions: Residential handler
exposure was not evaluated for turf uses, because the metabolite BAM is
believed to form slowly in plants and soil after the product containing
parent fluopicolide has been applied. Residential post-application
exposure via the dermal route is likely for adults and children
entering treated lawns; however, post-application exposure via the
inhalation route is expected to be negligible. Toddlers may also be
exposed via incidental ingestion (i.e., hand-to-mouth, object-to-mouth
(turfgrass), and soil ingestion) during post-application activities on
treated turf. Post-application exposures are expected to be of short
and intermediate duration.
4. Cumulative effects from substances with a common mechanism of
toxicity. Section 408(b)(2)(D)(v) of FFDCA requires that, when
considering whether to establish, modify, or revoke a tolerance, the
Agency consider ``available information'' concerning the cumulative
effects of a particular pesticide's residues and ``other substances
that have a common mechanism of toxicity.''
Unlike other pesticides for which EPA has followed a cumulative
risk approach based on a common mechanism of toxicity, EPA has not made
a common mechanism of toxicity finding as to dichlobenil (parent) or
its metabolite BAM and any other substances. For the purposes of this
tolerance action, therefore, EPA has not assumed that dichlobenil
(parent) or its metabolite BAM has a common mechanism of toxicity with
other substances. EPA has aggregated BAM exposure from both use of
dichlobenil and fluopicolide. For information regarding EPA's efforts
to determine which chemicals have a common mechanism of toxicity and to
evaluate the cumulative effects of such chemicals, see EPA's website at
http://www.epa.gov/pesticides/cumulative.
D. Safety Factor for Infants and Children
1. In general. Section 408(b)(2)(c) of FFDCA provides that EPA
shall apply an additional tenfold (10X) 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 database on toxicity
and exposure unless EPA determines based on reliable data that a
different margin of safety will be safe for infants and children. This
additional margin of safety is commonly referred to as the FQPA safety
factor (SF). In applying this provision, EPA either retains the default
value of 10X, or uses a different additional safety factor when
reliable data available to EPA support the choice of a different
factor.
2. Prenatal and postnatal sensitivity. The pre- and postnatal
toxicology database for dichlobenil includes rat and rabbit
developmental toxicity studies and a 2-generation reproduction toxicity
study in rats. There was no evidence of increased qualitative or
quantitative susceptibility of in utero rats or rabbits in the
developmental toxicity studies for dichlobenil. In the rat reproduction
study, effects in the pups (decreased body weight during weaning)
occurred at a lower dose than that which resulted in parental toxicity
(decreases in premating and gestation body weight gain and premating
food consumption), indicating increased quantitative susceptibility of
the pups. However, the degree of concern for the body weight changes in
pups is low. There are clear NOAELs for effects in both the pups and
parental animals; and EPA is using the pup NOAEL, which is 6-fold lower
than the dose at which decreased pup body weight was observed, to
assess incidental oral exposure of children.
There was no evidence of increased prenatal susceptibility in the
rabbit developmental toxicity study for BAM. In this study, an increase
in the incidences of late abortion, as well as visceral and skeletal
anomalies, was observed at the high dose. However, severe maternal
toxicity (severely decreased body weight gain and food consumption and
late abortion) was also observed at the same dose.
3. Conclusion-i. Dichlobenil. EPA has determined that the 10X FQPA
SF must be retained for all prechronic (i.e., acute and subchronic)
oral exposure scenarios. EPA has also determined that reliable data
show the safety of infants and children would be adequately protected
if the FQPA SF were reduced to 1X for all other (i.e., chronic, dermal
or inhalation) exposure scenarios. These decisions are based on the
following findings:
a. The dichlobenil database is incomplete to the extent that the
existing data have not assayed the potential for dichlobenil to induce
olfactory toxicity following short-term (prechronic) oral exposure.
Olfactory toxicity has been assayed and demonstrated after dermal,
inhalation and intraperitoneal exposure of rodents to dichlobenil. No
oral studies, to date, have reported olfactory toxicity for
dichlobenil; however, olfactory toxicity was assayed in only one study
- a chronic dog study - submitted to the Agency. In the chronic dietary
dog study, no effects on the nasal epithelium from long term exposure
were observed. Due to the uncertainty regarding the potential for
dichlobenil to induce olfactory toxicity following oral exposure of
prechronic duration, EPA has retained the 10X FQPA SF. For chronic
exposures and prechronic dermal and inhalation exposure scenarios, the
10X SF is not needed to account for database uncertainty. Olfactory
toxicity was not observed in the chronic oral dog study, and the
[[Page 50568]]
doses selected for dermal and inhalation exposure risk assessments are
based on a very sensitive and conservative endpoint (olfactory
histopathology - epithelial damage). This is a conservative endpoint
because it is unknown whether this olfactory histopathology would have
an adverse effect on the function of the sense of smell.
b. Apart from the degenerative effects of dichlobenil on olfactory
sensory neurons, there are no other indications of neurotoxicity in any
of the studies available for dichlobenil. The 10X FQPA SF being
retained for prechronic oral exposure scenarios is adequate to account
for olfactory neurotoxicity. For dermal and inhalation exposure
scenarios, EPA is using a very sensitive endpoint that should be
protective of all populations, including infants and children.
c. There is no evidence that dichlobenil results in increased
susceptibility in in utero rats or rabbits in the prenatal
developmental toxicity studies. Although there is evidence of
quantitative susceptibility in the 2-generation reproduction study in
rats, the degree of concern is low, and the Agency did not identify any
residual uncertainties after establishing toxicity endpoints and
traditional UFs to be used in the risk assessment of dichlobenil.
d. There are no residual uncertainties identified in the exposure
databases. The dietary food exposure assessments were performed
assuming 100 PCT and tolerance-level residues. EPA made conservative
(protective) assumptions in the ground and surface water modeling used
to assess exposure to dichlobenil in drinking water. Residential
exposure of infants and children to dichlobenil is expected to be
negligible. These assessments will not underestimate the exposure and
risks posed by dichlobenil.
ii. BAM: EPA has retained the 10X FQPA SF for BAM for those
exposure scenarios that do not rely on dichlobenil toxicity data. These
scenarios are acute dietary for the general population (including
infants and children) and females 13-49 years of age; chronic dietary;
and incidental oral non-dietary. Although EPA has developmental,
reproduction, and subchronic and chronic toxicity studies for the
metabolite BAM, and a structure activity analysis indicates EPA has
identified its principal toxicological effects and level of toxicity,
EPA is retaining the FQPA 10X SF due to remaining questions regarding
the systemic neurotoxic potential of BAM, including olfactory toxicity
via the oral route of exposure and the use of a LOAEL in assessing
acute dietary risk for the general population. For the dermal and
inhalation routes of exposures, for which the Agency is relying on
dichlobenil toxicity data, EPA has reduced the FQPA SF for BAM toxicity
to 1X, based on a comparison of toxicity via the intraperitoneal route
of exposure showing that higher doses of BAM are needed to induce
levels of olfactory toxicity that are similar to those caused by
dichlobenil. Olfactory toxicity, the most sensitive endpoint, was the
endpoint chosen for these exposure scenarios. Other factors EPA
considered in the FQPA SF decisions for BAM include the following:
a. To compensate for deficiencies in the toxicology database for
BAM, EPA performed a comparative analysis of the toxicity of BAM and
the parent compounds, dichlobenil and fluopicolide, using the available
animal data and DEREK analysis. DEREK is a toxicology application that
uses structure-activity relationships to predict a broad range of
toxicological properties based on a comprehensive analysis of a
compound's molecular structure. Based on the available animal data and
Derek analyses, BAM does not appear to cause different organ specific
toxicities compared to fluopicolide and dichlobenil. The kidney and
liver toxicities are common to all three compounds. With respect to
relative toxicity, conclusions from the evaluation of the animal
studies appear to confirm that both fluopicolide and dichlobenil appear
to be more or equally toxic compared to BAM. A full discussion of EPA's
comparative toxicity analysis of BAM, dichlobenil and fluopicolide can
be found at http://www.regulations.gov in the document Comparative
Toxicity using Derek analysis for Dichlobenil, Fluopicolide and BAM in
docket ID number EPA-HQ-OPP-2007-0604. Based on the results of the
available animal data and the DEREK analysis, EPA concludes that the
safety factors discussed in the previous paragraph are adequate.
b. There is no evidence that BAM results in increased
susceptibility of in utero rabbits in the prenatal developmental
toxicity study.
c. There are no residual uncertainties identified in the exposure
databases. The dietary food exposure assessments were refined using
reliable PCT information and anticipated residue values calculated from
residue field trial results. EPA made conservative (protective)
assumptions in the ground and surface water modeling used to assess
exposure to BAM in drinking water. EPA used similarly conservative
assumptions to assess post[dash]application exposure of children as
well as incidental oral exposure of toddlers. These assessments will
not underestimate the exposure and risks posed by BAM.
E. Aggregate Risks and Determination of Safety
EPA determines whether acute and chronic pesticide exposures are
safe by comparing aggregate exposure estimates to the aPAD and cPAD.
The aPAD and cPAD represent the highest safe exposures, taking into
account all appropriate SFs. EPA calculates the aPAD and cPAD by
dividing the POD by all applicable UFs. For linear cancer risks, EPA
calculates the probability of additional cancer cases given the
estimated aggregate exposure. Short-, intermediate-, and chronic-term
risks are evaluated by comparing the estimated aggregate food, water,
and residential exposure to the POD to ensure that the MOE called for
by the product of all applicable UFs is not exceeded.
1. Acute risk. An acute aggregate risk assessment takes into
account exposure estimates from acute dietary consumption of food and
drinking water. Using the exposure assumptions discussed in this unit
for acute exposure, the acute dietary exposure from food and water to
dichlobenil will occupy 33% of the aPAD for females, 13 to 49 years
old, the only subpopulation at risk from acute exposure to dichlobenil.
EPA performed two different acute risk assessments for BAM - one
focusing on females 13 to 49 years old and designed to protect against
prenatal effects and the other focusing on acute effects relevant to
all other population groups. The more sensitive acute endpoint was seen
as to prenatal effects rather than other acute effects. For females 13
to 49 years old, the acute dietary exposure from food and water will
occupy 28% of the aPAD addressing prenatal effects. As to acute effects
other than prenatal effects, the acute dietary exposure from food and
water to BAM will occupy 28% of the aPAD for infants less than 1 year
old, the population subgroup with the highest estimated acute dietary
exposure to BAM.
2. Chronic risk. Using the exposure assumptions described in this
unit for chronic exposure, EPA has concluded that chronic exposure to
dichlobenil from food and water will utilize 30% of the cPAD for
children, 1 to 2 years old, the population group receiving the greatest
dichlobenil exposure. Chronic exposure to BAM from food and water
[[Page 50569]]
will utilize 93% of the cPAD for infants, less than 1 year old, the
population group receiving the greatest BAM exposure. Based on the
explanation in Unit III.C.3., regarding residential use patterns,
chronic residential exposure to residues of dichlobenil or BAM is not
expected.
3. Short-/intermediate-term risk. Short- and intermediate-term
aggregate exposure takes into account short- or intermediate-term
residential exposure plus chronic exposure to food and water
(considered to be a background exposure level). Although dichlobenil is
registered for use on ornamentals in residential areas, residential
handler exposures are not expected and post-application exposures of
adults and children are expected to be negligible. Therefore, the
short-term aggregate risk is the sum of the risk from exposure to
dichlobenil through food and water and will not be greater than the
chronic aggregate risk.
Fluopicolide is currently registered for uses that could result in
short- and intermediate-term residential exposure to its metabolite,
BAM, and the Agency has determined that it is appropriate to aggregate
chronic exposure through food and water with short- and intermediate-
term oral residential exposures to BAM. It is not appropriate to
aggregate dietary (i.e., oral) exposures and dermal exposures because
the toxic effects identified for the oral and dermal exposure pathways
differ. Using the exposure assumptions described in this unit for
short- and intermediate-term exposures, EPA has concluded the combined
short-term food, water, and residential exposures aggregated result in
aggregate MOEs of 3,200 for infants and 5,400 for children, 1 to 2
years old. The aggregate MOEs for infants and children include food and
drinking water exposures to BAM from all existing and new uses of
dichlobenil and fluopicolide, as well as post-application incidental
oral exposures from activities on lawns treated with fluopicolide. MOEs
for dermal exposures on treated lawns are 10,000 for adults and 6,000
for infants/children. As noted above, it is not appropriate to
aggregate chronic exposure from food and water with oral exposures.
Post-application inhalation exposure of adults and children is expected
to be negligible.
4. Aggregate cancer risk for U.S. population. The Agency has
determined that quantification of human cancer risk is not necessary
for dichlobenil or BAM and that the chronic risk assessments based on
the established cPADs are protective of potential cancer effects. Based
on the results of the chronic risk assessments discussed in Unit
III.E.2, EPA concludes that dichlobenil and BAM are not expected to
pose a cancer risk.
5. Determination of safety. Based on these risk assessments, EPA
concludes that there is a reasonable certainty that no harm will result
to the general population, or to infants and children from aggregate
exposure to dichlobenil or BAM residues.
IV. Other Considerations
A. Analytical Enforcement Methodology
Adequate enforcement methodology (Pesticide Analytical Manual (PAM)
Vol. II, Method A, a gas-liquid chromatography/electroconductivity
detector (GLC/ECD) method) is available to enforce the tolerance
expression. In addition, dichlobenil is completely recovered using the
multiresidue methods in PAM Vol. I Sections 302 and 304. BAM is
completely recovered using Section 302.
B. International Residue Limits
No CODEX, Canadian or Mexican maximum residue limits (MRLs) have
been established for dichlobenil.
C. Revisions to Petitioned-For Tolerances
Based upon review of the data supporting the petition and recent
changes in EPA's crop grouping regulations, EPA has revised the
tolerance level for rhubarb and the commodity terms for the berry
tolerances. The tolerance for rhubarb was reduced from 0.15 ppm to 0.06
ppm, the lower limit of method validation (LLMV), based on the absence
of detectable residues in the field trials.
IR-4 petitioned for individual tolerances on caneberry, subgroup
13a and wild raspberry; bushberry, subgroup 13b; aronia berry;
bluberry, lowbush; buffalo currant; chilian guava; european barberry;
highbush cranberry; honeysuckle; jostaberry; juneberry; lingonberry;
native currant; salal; and sea buckthorn. In the Federal Register of
December 7, 2007 (72 FR 69150) (FRL-8340-6), EPA issued a final rule
that revised the crop grouping regulations. As part of this action, EPA
expanded and revised berries group 13. Changes to crop group 13
(berries) included adding new commodities, revising existing subgroups
and creating new subgroups (including Caneberry subgroup 13-07A and
Bushberry subgroup 13-07B, which include the berry commodities
requested in IR-4's petition and cultivars, varieties, and/or hybrids
of these).
EPA indicated in the December 7, 2007 final rule as well as the
earlier May 23, 2007 proposed rule (72 FR 28920 (FRL-8126-1) that, for
existing petitions for which a Notice of Filing had been published, the
Agency would attempt to conform these petitions to the rule. Therefore,
consistent with this rule, EPA is establishing tolerances on Caneberry
subgroup 13-07A and Bushberry subgroup 13-07B. All of the berry
commodities for which IR-4 requested tolerances are included in these
revised subgroups.
EPA concludes it is reasonable to revise the petitioned-for
tolerances so that they agree with the recent crop grouping revisions
because:
1. Although the new crop groups/subgroups include several new
commodities, the added commodities are closely related minor crops
which contribute little to overall dietary or aggregate exposure and
risk; and dichlobenil/BAM exposure from these added commodities was
considered when EPA conducted the dietary and aggregate risk
assessments supporting this action; and
2. The representative commodities for the revised crop group/
subgroups have not changed.
V. Conclusion
Therefore, tolerances are established for combined residues of
dichlobenil, 2,6-dichlorobenzonitrile, and its metabolite, 2,6-
dichlorobenzamide, in or on bushberry subgroup 13-07B at 0.15 ppm;
caneberry subgroup 13-07A at 0.10 ppm; and rhubarb at 0.06 ppm. The
existing tolerances on individual members of bushberry subgroup 13-07B
(blueberry) and caneberry subgroup 13-07A (blackberry and raspberry)
that are superseded by the new crop subgroup tolerances at the same
tolerance levels are being removed.
VI. Statutory and Executive Order Reviews
This final rule establishes tolerances under section 408(d) of
FFDCA in response to a petition submitted to the Agency. The Office of
Management and Budget (OMB) has exempted these types of actions from
review under Executive Order 12866, entitled Regulatory Planning and
Review (58 FR 51735, October 4, 1993). Because this final rule has been
exempted from review under Executive Order 12866, this final rule is
not subject to Executive Order 13211, Actions Concerning Regulations
That Significantly Affect Energy Supply, Distribution, or Use (66 FR
28355, May 22, 2001) or Executive Order 13045, entitled Protection of
Children from Environmental Health Risks and Safety
[[Page 50570]]
Risks (62 FR 19885, April 23, 1997). This final rule does not contain
any information collections subject to OMB approval under the Paperwork
Reduction Act (PRA), 44 U.S.C. 3501 et seq., nor does it require any
special considerations under Executive Order 12898, entitled Federal
Actions to Address Environmental Justice in Minority Populations and
Low-Income Populations (59 FR 7629, February 16, 1994).
Since tolerances and exemptions that are established on the basis
of a petition under section 408(d) of FFDCA, such as the tolerance in
this final rule, do not require the issuance of a proposed rule, the
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et
seq.) do not apply.
This final rule directly regulates growers, food processors, food
handlers, and food retailers, not States or tribes, nor does this
action alter the relationships or distribution of power and
responsibilities established by Congress in the preemption provisions
of section 408(n)(4) of FFDCA. As such, the Agency has determined that
this action will not have a substantial direct effect on States or
tribal governments, on the relationship between the national government
and the States or tribal governments, or on the distribution of power
and responsibilities among the various levels of government or between
the Federal Government and Indian tribes. Thus, the Agency has
determined that Executive Order 13132, entitled Federalism (64 FR
43255, August 10, 1999) and Executive Order 13175, entitled
Consultation and Coordination with Indian Tribal Governments (65 FR
67249, November 9, 2000) do not apply to this final rule. In addition,
this final rule does not impose any enforceable duty or contain any
unfunded mandate as described under Title II of the Unfunded Mandates
Reform Act of 1995 (UMRA) (Public Law 104-4).
This action does not involve any technical standards that would
require Agency consideration of voluntary consensus standards pursuant
to section 12(d) of the National Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272
note).
VII. Congressional Review Act
The Congressional Review Act, 5 U.S.C. 801 et seq., generally
provides that before a rule may take effect, the agency promulgating
the rule must submit a rule report to each House of the Congress and to
the Comptroller General of the United States. EPA will submit a report
containing this rule and other required information to the U.S. Senate,
the U.S. House of Representatives, and the Comptroller General of the
United States prior to publication of this final rule in the Federal
Register. This final rule is not a ``major rule'' as defined by 5
U.S.C. 804(2).
List of Subjects in 40 CFR Part 180
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated: August 15, 2008.
Lois Rossi,
Director, Registration Division, Office of Pesticide Programs.
0
Therefore, 40 CFR chapter I is amended as follows:
PART 180--[AMENDED]
0
1. The authority citation for part 180 continues to read as follows:
Authority: 21 U.S.C. 321(q), 346a and 371.
0
2. Section 180.231 is amended by removing the commodities Blackberry,
Blueberry and Raspberry and alphabetically adding the following
commodities to the table in paragraph (a) to read as follows:
Sec. 180.231 Dichlobenil; tolerances for residues.
(a) * * *
----------------------------------------------------------------------------------------------------------------
Commodity Parts per million
----------------------------------------------------------------------------------------------------------------
* * * * *
Bushberry subgroup 13-07B............................. 0.15
Caneberry subgroup 13-07A............................. 0.10
* * * * *
Rhubarb............................................... 0.06
----------------------------------------------------------------------------------------------------------------
* * * * *
[FR Doc. E8-19859 Filed 8-26-08; 8:45 am]
BILLING CODE 6560-50-S