Federal Register / Vol. 73, No. 167 / Wednesday, August 27, 2008 / Rules and Regulations 50563 

* * * * * 

[FR Doc. E8–19858 Filed 8–26–08; 8:45 am] 

BILLING CODE 6560–50–S 

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superseded by the new crop subgroup 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: 

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- 


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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 


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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-adverseeffect-level (NOAEL) and the lowestobserved-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 


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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 


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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 noncancer 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 nonoccupational, 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. Postapplication 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 postapplication exposure via the dermal 

route is likely for adults and children 

entering treated lawns; however, postapplication exposure via the inhalation 

route is expected to be negligible. 

Toddlers may also be exposed via 

incidental ingestion (i.e., hand-tomouth, object-to-mouth (turfgrass), and 

soil ingestion) during post-application 

activities on treated turf. Postapplication 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 


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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-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 


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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 postapplication 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 intermediateterm 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 postapplication 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 


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50570 Federal Register / Vol. 73, No. 167 / Wednesday, August 27, 2008 / Rules and Regulations 

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. 

■ Therefore, 40 CFR chapter I is 

amended as follows: 

PART 180—[AMENDED] 

■ 1. The authority citation for part 180 

continues to read as follows: 

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

■ 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: 

§ 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 

FEDERAL COMMUNICATIONS 

COMMISSION 

47 CFR Part 27 

[WT Docket No. 02–353; FCC 03–251] 

Service Rules for Advanced Wireless 

Services 

AGENCY: Federal Communications 

Commission. 

ACTION: Final rule; correction. 

SUMMARY: In this document the Federal 

Communications Commission corrects 

an inadvertent error that occurred when 

the Commission adopted final rules for 

the Advanced Wireless Services in the 

1710–1755 MHz and 2110–2155 MHz 

bands, including provisions for 

application, licensing, operating and 

technical rules, and for competitive 

bidding. These rules were published in 

the Federal Register on Friday, 

February 6, 2004 (69 FR 5711). 

Specifically, the error occurred in a 

table to the rules concerning 

interference protection at certain 

Federal Government operations in the 

1710–1755 MHz band. As a result of this 

correction, the table will be amended as 

intended by the Commission. 

DATES: Effective August 27, 2008. 

FOR FURTHER INFORMATION CONTACT: John 

Spencer at 202–418–2487. 

SUPPLEMENTARY INFORMATION: This is a 

correction to a summary of the 

Commission’s Report and Order in WT 

Docket No. 02–353, FCC 03–251, 

adopted on October 16, 2003 and 

released on November 25, 2003. The 

Report and Order adopted licensing, 

technical, and competitive bidding rules 

to govern the use of the spectrum at 

1710–1755 MHz and 2110–2155 MHz, 

which had previously been allocated for 

advanced wireless services, in a manner 

that would enable service providers to 

put this spectrum to use for any purpose 

consistent with its allocation. 

Need for Correction 

As published, the final rules contain 

an error in § 27.1134 in Table 1. The 

Commission inadvertently omitted the 

abbreviation for the word kilometers 

(km) after the category heading ‘Radius 

of Operation’ in Table 1: Protected 

Department of Defense Facilities. This 

correction restores the information that 

was inadvertently omitted. 


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