[Federal Register Volume 73, Number 167 (Wednesday, August 27, 2008)]
[Rules and Regulations]
[Pages 50563-50570]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E8-19859]


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

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.

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

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and raspberry) that are superseded by the new crop subgroup tolerances 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: <a href="/cdn-cgi/l/email-protection#5c2f283d32283332722f292f3d321c392c3d723b332a"><span class="__cf_email__" data-cfemail="ec9f988d82988382c29f999f8d82ac899c8dc28b839a">[email protected]</span></a>.

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:
    <bullet> Crop production (NAICS code 111).
    <bullet> Animal production (NAICS code 112).
    <bullet> Food manufacturing (NAICS code 311).
    <bullet> 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:
    <bullet> Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the on-line instructions for submitting comments.
    <bullet> Mail: Office of Pesticide Programs (OPP) Regulatory Public 
Docket (7502P), Environmental Protection Agency, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460-0001.
    <bullet> 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:
    <bullet> 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.
    <bullet> Condition b: The exposure estimate does not underestimate 
exposure for any significant subpopulation group.
    <bullet> 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


</pre><script data-cfasync="false" src="/cdn-cgi/scripts/5c5dd728/cloudflare-static/email-decode.min.js"></script></body>
</html>