Federal Register / Vol. 78, No. 236 / Monday, December 9, 2013 / Proposed Rules 73787 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 372 

[EPA–HQ–TRI–2013–0393; FRL 9903–44– 

OEI] 

Chlorsulfuron; Community Right-toKnow Toxic Chemical Release 

Reporting 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Denial of Petition. 

SUMMARY: EPA is denying a petition to 

remove chlorsulfuron from the list of 

chemicals subject to reporting under 

section 313 of the Emergency Planning 

and Community Right-to-Know Act 

(EPCRA) of 1986 and section 6607 of the 

Pollution Prevention Act (PPA) of 1990. 

EPA has reviewed the available data on 

this chemical and has determined that 

chlorsulfuron does not meet the 

deletion criterion of EPCRA section 

313(d)(3). Specifically, EPA is denying 

this petition because EPA’s review of 

the petition and available information 

resulted in the conclusion that 

chlorsulfuron meets the listing criterion 

of EPCRA section 313(d)(2)(C) due to its 

toxicity to aquatic plants. 

DATES: EPA denied this petition on 

November 18, 2013. 

FOR FURTHER INFORMATION CONTACT: 

Daniel R. Bushman, Environmental 

Analysis Division, Office of Information 

Analysis and Access (2842T), 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460; telephone number: 202–566– 

0743; fax number: 202–566–0677; email: 

bushman.daniel@epa.gov, for specific 

information on this notice. For general 

information on EPCRA section 313, 

contact the Emergency Planning and 

Community Right-to-Know Hotline, toll 

free at (800) 424–9346 (select menu 

option 3) or (703) 412–9810 in Virginia 

and Alaska or toll free, TDD (800) 553– 

7672, http://www.epa.gov/superfund/

contacts/infocenter/. 

SUPPLEMENTARY INFORMATION: 

I. General Information 

A. Does this notice apply to me? 

You may be potentially affected by 

this action if you manufacture, process, 

or otherwise use chlorsulfuron. 

Potentially affected categories and 

entities may include, but are not limited 

to: 

Category Examples of potentially affected entities 

Industry ...................... Facilities included in the following NAICS manufacturing codes (corresponding to SIC codes 20 through 39): 311*, 312*, 

313*, 314*, 315*, 316, 321, 322, 323*, 324, 325*, 326*, 327, 331, 332, 333, 334*, 335*, 336, 337*, 339*, 111998*, 

211112*, 212324*, 212325*, 212393*, 212399*, 488390*, 511110, 511120, 511130, 511140*, 511191, 511199, 

512220, 512230*, 519130*, 541712*, or 811490*. 

*Exceptions and/or limitations exist for these NAICS codes. 

Facilities included in the following NAICS codes (corresponding to SIC codes other than SIC codes 20 through 39): 

212111, 212112, 212113 (correspond to SIC 12, Coal Mining (except 1241)); or 212221, 212222, 212231, 212234, 

212299 (correspond to SIC 10, Metal Mining (except 1011, 1081, and 1094)); or 221111, 221112, 221113, 221119, 

221121, 221122, 221330 (Limited to facilities that combust coal and/or oil for the purpose of generating power for distribution in commerce) (correspond to SIC 4911, 4931, and 4939, Electric Utilities); or 424690, 425110, 425120 (Limited to facilities previously classified in SIC 5169, Chemicals and Allied Products, Not Elsewhere Classified); or 

424710 (corresponds to SIC 5171, Petroleum Bulk Terminals and Plants); or 562112 (Limited to facilities primarily engaged in solvent recovery services on a contract or fee basis (previously classified under SIC 7389, Business Services, NEC)); or 562211, 562212, 562213, 562219, 562920 (Limited to facilities regulated under the Resource Conservation and Recovery Act, subtitle C, 42 U.S.C. 6921 et seq.) (correspond to SIC 4953, Refuse Systems). 

Federal Government Federal facilities. 

This table is not intended to be 

exhaustive, but rather provides a guide 

for readers regarding entities likely to be 

affected by this action. Some of the 

entities listed in the table have 

exemptions and/or limitations regarding 

coverage, and other types of entities not 

listed in the table could also be affected. 

To determine whether your facility 

would be affected by this action, you 

should carefully examine the 

applicability criteria in part 372 subpart 

B of Title 40 of the Code of Federal 

Regulations. If you have questions 

regarding the applicability of this action 

to a particular entity, consult the person 

listed in the preceding FOR FURTHER

INFORMATION CONTACT section. 

B. How can I get copies of this document 

and other related information? 

EPA has established a docket for this 

action under Docket ID No. EPA–HQ– 

TRI–2013–0393. All documents in the 

docket are listed in the 

www.regulations.gov index. Although 

listed in the index, some information is 

not publicly available, e.g., CBI or other 

information whose disclosure is 

restricted by statute. Certain other 

material, such as copyrighted material, 

will be publicly available only in hard 

copy. Publicly available docket 

materials are available either 

electronically in www.regulations.gov or 

in hard copy at the OEI Docket, EPA/

DC, EPA West, Room 3334, 1301 

Constitution Ave. NW., Washington, 

DC. This Docket Facility is open from 

8:30 a.m. to 4:30 p.m., Monday through 

Friday, excluding legal holidays. The 

telephone number for the Public 

Reading Room is (202) 566–1744, and 

the telephone number for the OEI 

Docket is (202) 566–1752. 

II. Introduction 

Section 313 of EPCRA, 42 U.S.C. 

11023, requires certain facilities that 

manufacture, process, or otherwise use 

listed toxic chemicals in amounts above 

reporting threshold levels to report their 

environmental releases and other waste 

management quantities of such 

chemicals annually. These facilities 

must also report pollution prevention 

and recycling data for such chemicals, 

pursuant to section 6607 of the PPA, 42 

U.S.C. 13106. Congress established an 

initial list of toxic chemicals that 

comprised more than 300 chemicals and 

20 chemical categories. 

EPCRA section 313(d) authorizes EPA 

to add or delete chemicals from the list 

and sets criteria for these actions. 

EPCRA section 313(d)(2) states that EPA 

may add a chemical to the list if any of 

the listing criteria in Section 313(d)(2) 

are met. Therefore, to add a chemical, 

EPA must demonstrate that at least one 

criterion is met, but need not determine 

whether any other criterion is met. 

EPCRA section 313(d)(3) states that a 

chemical may be deleted if the 

Administrator determines there is not 

sufficient evidence to establish any of 

the criteria described in EPCRA section 

313(d)(2)(A)–(C). The EPCRA section 

313(d)(2)(A)–(C) criteria are: 

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73788 Federal Register / Vol. 78, No. 236 / Monday, December 9, 2013 / Proposed Rules 

• The chemical is known to cause or 

can reasonably be anticipated to cause 

significant adverse acute human health 

effects at concentration levels that are 

reasonably likely to exist beyond facility 

site boundaries as a result of 

continuous, or frequently recurring, 

releases. 

• The chemical is known to cause or 

can reasonably be anticipated to cause 

in humans: 

Æ cancer or teratogenic effects, or 

Æ serious or irreversible— 

D reproductive dysfunctions, 

D neurological disorders, 

D heritable genetic mutations, or 

D other chronic health effects. 

• The chemical is known to cause or 

can be reasonably anticipated to cause, 

because of: 

Æ its toxicity, 

Æ its toxicity and persistence in the 

environment, or 

Æ its toxicity and tendency to 

bioaccumulate in the environment, a 

significant adverse effect on the 

environment of sufficient seriousness, 

in the judgment of the Administrator, to 

warrant reporting under this section. 

EPA often refers to the section 

313(d)(2)(A) criterion as the ‘‘acute 

human health effects criterion;’’ the 

section 313(d)(2)(B) criterion as the 

‘‘chronic human health effects 

criterion;’’ and the section 313(d)(2)(C) 

criterion as the ‘‘environmental effects 

criterion.’’ 

Under section 313(e)(1), any person 

may petition EPA to add chemicals to or 

delete chemicals from the list. EPA 

issued a statement of petition policy and 

guidance in the Federal Register of 

February 4, 1987 (52 FR 3479) to 

provide guidance regarding the 

recommended content and format for 

submitting petitions. On May 23, 1991 

(56 FR 23703), EPA issued guidance 

regarding the recommended content of 

petitions to delete individual members 

of the section 313 metal compounds 

categories. EPA published in the 

Federal Register of November 30, 1994 

(59 FR 61432) a statement clarifying its 

interpretation of the section 313(d)(2) 

and (d)(3) criteria for modifying the 

section 313 list of toxic chemicals. 

III. What is the description of the 

petition? 

On May 18, 2012, EPA received a 

petition from DuPont Crop Protection 

(DuPont), Technology Sciences Group 

Inc. (TSG) requesting EPA to delete 

chlorsulfuron (Chemical Abstracts 

Service Registry Number (CASRN) 

64902–72–3) from the list of chemicals 

subject to reporting under EPCRA 

section 313 and PPA section 6607 

(Reference (Ref. 1)). Chlorsulfuron was 

added to the EPCRA section 313 

chemical list on November 30, 1994, 

based on concerns for developmental 

and reproductive toxicity (59 FR 61432). 

DuPont contends that newer studies 

show that chlorsulfuron does not cause 

developmental or reproductive toxicity 

and therefore no longer meets the 

EPCRA section 313(d)(2) criteria for 

listing. While the petition addressed the 

acute human health effects criterion of 

section 313(d)(2)(A) and chronic human 

health effects criterion of section 

313(d)(2)(B), it did not address the 

environmental effects criterion of 

section 313(d)(2)(C). 

IV. What is EPA’s evaluation of the 

human health toxicity of chlorsulfuron? 

EPA’s evaluation of the toxicity of 

chlorsulfuron included a review of the 

original 1994 listing decision (59 FR 

1788, January 12, 1994 and 59 FR 

61432, November 30, 1994), the 2002 

Chlorsulfuron Toxicology Chapter (Ref. 

2), the Federal Register Notice for 

Chlorsulfuron Pesticide Tolerance (67 

FR 52866, August 14, 2002), and the 

Reregistration Eligibility Decision (RED) 

for Chlorsulfuron (Ref. 3). EPA also 

reviewed the findings of relevant 

studies published since the RED for 

chlorsulfuron was published (Ref. 4). 

Unit IV.A. below outlines evidence of 

human health toxicity from these 

existing EPA hazard characterizations 

and Unit IV.B. provides a brief summary 

of the findings from recently published 

studies. Unit IV.C. provides a summary 

of the ecological toxicity of 

chlorsulfuron from the existing EPA 

hazard characterizations. 

A. Review of the Reregistration 

Eligibility Decision for Chlorsulfuron 

1. Kinetics and Metabolism 

EPA concluded that chlorsulfuron is 

rapidly absorbed, metabolized, and 

eliminated when administered orally to 

rats (Ref. 2). There are no differences in 

absorption, distribution, and 

elimination of chlorsulfuron related to 

sex, dose, or treatment regimen. In one 

study, the major routes of elimination 

were found to be urine (58–72%) and 

feces (20–35%) with small amounts 

(0.1–0.2%) remaining in tissues 

(primarily in the liver and whole blood) 

three days after dosing (Ref. 5). This 

same study identified the major 

metabolic pathway of chlorsulfuron as 

the contraction of the sulfonylurea 

linkage followed by oxidation and 

hydroxylation to form IN–70941, IN– 

70942, Metabolite P5 (desmethyl IN– 

70942), and Metabolite P4 (OHdesmethyl IN–70942). The cleavage of 

the sulfonylurea linkage to form 

Metabolite IN–E9260 was identified as 

the minor metabolic pathway. No 

additional information on the 

absorption, distribution, metabolism, 

and excretion of chlorsulfuron was 

found in the literature. 

2. Effects of Acute Exposure 

EPA concluded that chlorsulfuron has 

no significant acute toxicity (Ref. 2). The 

conclusion was based on the results of 

a dermal study (Ref. 6), an inhalation 

study (Ref. 7) and on an oral study (Ref. 

8). 

3. Effects of Repeated Exposure 

a. Effects of subchronic exposure. As 

stated in the 2002 Chlorsulfuron 

Toxicology Chapter (Ref. 2), there are 

few subchronic studies of chlorsulfuron 

in the literature. No 21- or 90-day 

dermal toxicity studies or 90-day 

inhalation studies were identified. Two 

subchronic oral toxicity studies were 

identified and summarized in the 2002 

Chlorsulfuron Toxicology Chapter (Ref. 

2). In a 90-day oral toxicity study, Smith 

et al. (Ref. 9) administered chlorsulfuron 

(100%) to 10 ChR–CD®-1 mice/sex/dose 

at dietary concentrations of 0, 500, 

2,500, 5,000, and 7,500 ppm (equivalent 

to 0, 150, 783, 1,557, 2,130 milligrams/ 

kilogram/day (mg/kg/day) in males and 

0, 220, 1,214, 2,134, 3,176 mg/kg/day in 

females). The authors reported a lowestobserved-adverse-effect level (LOAEL) 

of 2,130 mg/kg/day based on increased 

incidence of retinal dysplasia. This 

study, however, lacked clinical 

chemistry and organ weight data. In a 6- 

month oral toxicity study, Schneider et 

al. (Ref. 10) administered chlorsulfuron 

(95%) to purebred Beagle dogs (4/sex/

dose) in the diet at dose levels of 0, 100, 

500, and 2,500 ppm (equivalent to 0, 

3.7, 18.5, and 82.3 mg/kg/day). The 

authors reported a LOAEL of 82.3 mg/ 

kg/day based on decreased body weight 

gain in females. Female body weight 

decreases were slight (91%, 93%, and 

87% of control group in the low, mid, 

and high dose groups, respectively) and 

body weight decreases were observed in 

the treatment groups prior to treatment. 

The authors also noted that high-dose 

females also exhibited a lower food 

intake. Additionally, it does not appear 

that the animals were randomized by 

body weight at the beginning of the 

study, which makes these body weight 

findings more difficult to interpret. No 

other treatment-related effects were 

observed in any hematological, clinical 

chemistry, organ weights, or gross and 

microscopic pathology in animals of 

either sex. EPA concluded that the 

subchronic oral database does not 

identify toxicity to any particular target 

organ (Ref. 2). 

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b. Carcinogenicity. EPA concluded 

there is no evidence of carcinogenicity 

in rats or mice following oral exposure 

to chlorsulfuron (Ref. 2). In a chronic 

toxicity study, Wood et al., (Ref. 11) 

administered chlorsulfuron (95%) to 80 

CD® rats/sex/dose in the diet at dose 

levels of 0, 100, 500, and 2,500 

(equivalent to 0, 5, 25, and 125 mg/kg/ 

day) for two years. The authors reported 

that the unilateral incidence of 

interstitial cell tumors was within the 

known spontaneous range for CD® rats 

and that there were no other changes 

suggestive of a treatment-related 

tumorigenic effect in the testes. In a 

similar carcinogenicity study, Wood et 

al., (Ref. 12) administered chlorsulfuron 

(91.9–95%) to 80 CD–1 mice/sex/dose 

in the diet at dose levels of 0, 100, 500, 

and 5,000 ppm (equivalent to 0, 15, 108, 

and 750 mg/kg/day) for two years. The 

authors reported no treatment-related 

increase in tumor incidence. No 

additional carcinogenicity studies were 

identified in the literature. 

4. Reproductive and Developmental 

Toxicity 

While the rabbit toxicity study cited 

in the 1994 Federal Register TRI listing 

of chlorsulfuron (59 FR 1788, January 

12, 1994) reported a treatment-related 

increase in fetal resorptions and 

decrease in the mean incidence of live 

fetuses per litter at 75 mg/kg/day (Ref. 

13), the results were not strongly 

indicative of a dose-response effect, 

were not able to be replicated in a 

follow-up study, and have recently been 

reanalyzed with improved methods. In 

this 1980 study cited in the original TRI 

listing of chlorsulfuron, Hoberman (Ref. 

13) administered chlorsulfuron to 

pregnant female New Zealand white 

rabbits by oral intubation at doses of 0, 

10, 25, and 75 mg/kg on days 6–19 of 

gestation. The author reported no 

significant changes in maternal body 

weight, uterine weight, ovarian weight, 

corpora lutea, visceral anomalies, or 

implantations. The author concluded 

that the increased mean incidence of 

resorptions in the highest dose group 

(31.3% versus 11.6% in the control 

group) and the decreased mean of live 

fetuses in the highest dose group (59.8% 

versus 88.5% in the control group) were 

significant treatment-related effects. A 

subsequent 1991 study performed in 

accordance with EPA guidelines (Ref. 

14), however, was not able to replicate 

these findings using similar methods 

and higher doses (Ref. 15). This study 

concluded that chlorsulfuron does not 

cause an increase in fetal resorptions or 

decrease in fetal viability in rabbits up 

to 1,000 mg/kg/day, the highest dose 

tested (Ref. 15). Moreover, the 2002 

Chlorsulfuron Toxicology Chapter (Ref. 

2), the Federal Register Notice on 

Chlorsulfuron Pesticide Tolerance (67 

FR 52866, August 14, 2002), and the 

Reregistration Eligibility Decision for 

Chlorsulfuron (Ref. 3) do not include 

fetal resorptions or decreased fetal 

viability as a part of the chlorsulfuron 

hazard characterization. 

The 1994 Federal Register TRI listing 

of chlorsulfuron (59 FR 1788, January 

12, 1994) also cited a slight treatmentrelated decrease in maternal fertility in 

the F3 generation observed in a rat 

chronic toxicity study (Ref. 11), but 

these findings have since been 

questioned. The design of this study is 

briefly summarized in the above 

Carcinogenicity Section (Unit IV.A.3.b.). 

The 2002 Chlorsulfuron Toxicology 

Chapter (Ref. 2) and the Federal 

Register Notice on Chlorsulfuron 

Pesticide Tolerance (67 FR 52866, 

August 14, 2002) concluded that the 

findings of this study are of 

questionable significance due to several 

study deficiencies. This study did not 

satisfy the current guideline (Ref. 14) 

requirements and contains numerous 

deficiencies including but not limited 

to: (1) No assessment of estrous 

cyclicity, (2) no assessment of male 

reproductive performance, (3) no gross 

pathology or histopathology 

examination of parental animals, (4) no 

assessment of developmental 

landmarks, and (5) histopathology 

examinations were conducted only for 

the F3B generation (Ref. 2; 67 FR 52866, 

August 14, 2002). As such, EPA 

classified this study as unacceptable. 

EPA concluded that developmental 

toxicity was observed in both the rabbit 

(Ref. 15) and rat (Ref. 16), as evidenced 

by decreased fetal body weight (Ref. 2). 

However, treatment-related fetal body 

weight decreases in the rabbit study 

(Ref. 15) were slight (10%), occurred at 

a moderately high dose (LOAEL of 400 

mg/kg/day), and were observed in the 

absence of other developmental effects. 

Additionally, decreased fetal body 

weight occurred in the presence of 

decreased maternal body weight. 

Adjusted maternal body weight gains 

throughout the study (days 0–29) in the 

highest treatment groups (original study: 

200, 400 mg/kg/day; supplemental 

study: 400, 1,000 mg/kg/day) were 

substantially lower than those in the 

control group (78%, 54%, 43%, and 

43% of control, respectively). In the 

original and supplemental studies, 

however, the adjusted maternal body 

weight gains in the treatment groups 

appeared to fall within the range of 

normal variation of control group 

animals. Also, the final adjusted 

maternal body weights in both these 

studies were not statistically different 

among treatment and control groups. 

Furthermore, it is not apparent that the 

study authors examined food 

consumption or food efficiency in either 

study. It is important to note that a dose 

of 1,000 mg/kg/day resulted in a high 

percentage of maternal mortality (i.e., 

much greater than 10%), which makes 

the developmental data in this dose 

group unreliable and of limited value 

based on the EPA Developmental Test 

Guidelines (Ref. 17). In the rat study, 

fetal toxicity was limited to decreased 

fetal weight in the highest dose group 

(1,500 mg/kg/day) and there were no 

teratogenic effects observed (Ref. 16). 

Dams in the highest dose group 

exhibited vaginal discharge associated 

with alopecia. Based on these data, the 

authors determined that the maternal 

LOAEL was 500 mg/kg/day and the 

developmental LOAEL was 1,500 mg/

kg/day for rats. 

5. Mutagenicity 

A few mutagenicity studies were 

identified in the 2002 Chlorsulfuron 

Toxicology Chapter (Ref. 2), but none of 

these studies provided evidence of 

mutagenicity. Therefore, EPA concluded 

that there is no concern for mutagenicity 

of chlorsulfuron. 

6. Neurotoxicity 

There is no evidence of neurotoxicity 

in any study of chlorsulfuron. 

7. Other Chronic Toxicity 

In addition to the body weight 

findings from Alvarez (Refs. 15 and 16) 

discussed in the above Reproductive 

and Developmental Toxicity Section 

(Unit IV.A.4), several other chronic 

studies derived chlorsulfuron LOAELs 

based on observed changes in body 

weight and/or body weight gain. Wood 

et al. (Ref. 11) reported a LOAEL of 25 

mg/kg/day based on decreased body 

weight in male rats in the highest dose 

groups (25 and 125 mg/kg/day). The 

reported decrease in body weight, 

however, was slight (4–9% and 5–10%, 

respectively) and decreased body weight 

gain was not significantly different 

between the highest treatment group 

and the control group when measured 

over the entire study. Additionally, no 

changes were reported in female rats 

and no other treatment-related effects 

were reported in the study. Wood et al. 

(Ref. 12) reported a LOAEL of 750 mg/ 

kg/day due to decreased body weight 

and body weight gain in male and 

female mice. This high LOAEL, 

however, is indicative of moderately 

low to low chlorsulfuron toxicity. 

Atkinson et al. (Ref. 18) reported a 

LOAEL of 215 mg/kg/day based on 

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decreased body weight gain in female 

Beagle dogs. While these reported 

changes were observed in the absence of 

decreased food consumption, they were 

not found to be statistically significant. 

Moreover, body weight gains decreased 

in the highest dose group in the first 

half of the study (weeks 1–26), but there 

was no treatment-related effect on 

overall body weight gain over the entire 

study (weeks 1–52). Based on these 

findings, the evidence for body weight 

and body weight changes is not 

sufficient to conclude that chlorsulfuron 

is reasonably anticipated to cause 

serious or irreversible systemic toxicity. 

B. Review of Studies Published Since 

the Reregistration Eligibility Decision for 

Chlorsulfuron 

EPA identified and reviewed all 

relevant studies on chlorsulfuron that 

have been published since the RED for 

Chlorsulfuron (Ref. 3) was issued. After 

review of the recent literature, EPA 

concluded that there were no acceptable 

studies that strongly suggest either acute 

or chronic toxicity of chlorsulfuron (Ref. 

4). Below are brief summaries of the 

findings from these studies identified in 

the recent literature. 

1. Mylchreest Reproductive Study 

In a 2-generation reproduction study, 

Mylchreest (Ref. 19) administered 

chlorsulfuron Crl:CD®(SD)IGS BR rats 

via the diet. The administered dose 

levels were 0, 100, 500, 2,500, and 7,500 

ppm (average daily doses of 0, 6, 30, 

151, 456 mg/kg/day in males and 0, 7, 

39, 188, 591 mg/kg/day in females) 

throughout the 10-week premating 

period and throughout gestation and 

lactation. This study replicated the 

design of the Wood (Ref. 11) study with 

updates to ensure compliance with new 

EPA guidelines (Ref. 14) and good 

laboratory practices. 

No treatment-related effects were 

reported in litter size, live birth index, 

number born dead, viability and 

lactation indices, clinical examinations, 

sex ratio, sexual maturation, organ 

weights, and gross or microscopic 

observations. The first generation (F1) 

sex ratio was significantly higher in the 

highest dose group (55% versus 45% 

males in the control group), but the 

authors did not consider this a 

treatment-related effect because it fell 

within the historical control range (45– 

59%). Lower offspring body weights 

were observed in the highest dose group 

in both generations, but these 

differences were not considered adverse 

because the magnitude of body weight 

changes was slight (5–7%) and the 

potential effect of larger litter size on 

pup weight. The authors reported an 

offspring no-observed-adverse-effect 

level (NOAEL) of 456 mg/kg/day in 

males and 498 mg/kg/day in females 

(note: the administered dose of 591 mg/ 

kg-day was adjusted for decreased 

intake during gestation), the highest 

dose tested. 

There were no treatment-related 

effects on ovarian follicles counts in F1 

females, sperm and estrous cycle 

parameters in parental (P) and F1 

adults, mating, precoital interval, 

fertility, gestation length, number of 

implantation sites, and implantation 

efficiency in either generation. As such, 

the authors reported a reproductive 

NOAEL of 456 mg/kg/day in males and 

498 mg/kg/day in females (note: the 

administered dose of 591 mg/kg-day 

was adjusted for decreased intake 

during gestation), the highest dose 

tested. These results demonstrate that 

chlorsulfuron did not cause any 

treatment-related reproductive toxicity 

and its effects on parental body weight 

and food efficiency indicate moderately 

low to low toxicity. 

2. Other Studies 

In addition to the Mylchreest (Ref. 19) 

study, three other recent chlorsulfuron 

toxicity studies were identified in the 

literature. It is difficult to draw 

conclusions about these studies’ 

findings, however, due to the lack of 

basic information provided by the 

authors. The studies contained 

numerous deficiencies including, no 

details on animal species or strain, the 

body weights of study animals were not 

reported (only an overall range was 

given), the age of the test animals was 

not reported, analytical methods were 

not described nor was their 

methodology for the different tests, etc. 

Given these deficiencies, findings from 

these studies were of very limited use in 

the determination of hazard for 

chlorsulfuron. 

In an acute oral toxicity study, 

Rudaya et al. (Ref. 20) administered 

chlorsulfuron potassium salt 

intragastrically in male and female nonpedigreed white rats, male and female 

mice, and male rabbits of the Chinchilla 

line. The authors concluded that the 

LD50 (i.e., the dose of a chemical that is 

lethal to 50 percent of the test 

organisms) was 5,580 ± 1,002 mg/kg for 

male rats, 5,500 ± 729 mg/kg for female 

rats, 2,050 ± 367 mg/kg for male mice, 

2,460 ± 312 mg/kg for female mice, and 

3,900 ± 451 mg/kg for male rabbits. 

In a chronic oral toxicity study, 

Rudaya et al. (Ref. 21) examined the 

effect of chlorsulfuron potassium salt 

administered intragastrically in male 

white rats. Chlorsulfuron potassium salt 

was administered orally at dose levels of 

0, 0.558, 5.58, and 55.8 mg/kg over 9 

months. The authors reported several 

effects of chlorsulfuron potassium salt 

on the liver, kidneys, heart, and thyroid 

gland, and on behavior, but it is unclear 

from the study whether any of these 

effects were statistically or biologically 

significant. Based on these findings, the 

authors concluded that the no-effect 

dose of chlorsulfuron potassium salt 

was 0.558 mg/kg. 

Rakitsky and Beloyedova (Ref. 22) 

studied the acute and chronic effects of 

several sulfonylurea herbicides, 

including chlorsulfuron, in rats, mice, 

dogs, and rabbits. The authors measured 

central nervous function, liver, kidney, 

and hematologic function up to several 

months after exposure. The authors 

reported an oral LD50 in rats of 5,545– 

6,293 mg/kg in males and females, 

respectively, and a dermal LD50 of 2,500 

mg/kg in rabbits. The authors also 

reported an LC50 (4 hours) of >5,900 mg/ 

m3 in rats. The authors reported a 

chronic no-observed-effect level (NOEL) 

of 0.2–5 mg/kg/day for rats, 108 mg/kg/ 

day for mice, and 60.6 mg/kg/day for 

dogs, but they did not indicate from 

which health endpoints these NOELs 

were derived. 

C. Review of Ecological Effects 

1. Environmental Fate and Degradation 

Chlorsulfuron is likely to be persistent 

and highly mobile in the environment. 

It may be transported to non-target areas 

via runoff and/or spray drift (Ref. 3). 

Degradation in the aquatic environment 

occurs primarily through hydrolysis at 

low pH (23 day half-life at pH 5) but it 

is stable in neutral to basic 

environments (Ref. 23). Aerobic aquatic 

metabolism data are not available; 

however, aerobic soil metabolism data 

suggest that aerobic aquatic metabolism 

may occur. Soil degradation half-lives 

have been reported to vary from 12 to 

183 days (Ref. 24). 

2. Ecological Toxicity and Hazard 

a. Toxicity to aquatic animals. 

Experimental toxicity values are 

reported only for a few surrogate 

species. Estuarine data are limited to a 

crustacean, a mollusk, and a fish. No 

amphibians or reptiles were tested (Ref. 

3). Chlorsulfuron is practically nontoxic 

to both freshwater and marine/estuarine 

fish and slightly toxic to estuarine/ 

marine invertebrates when measured 

under acute conditions (Ref. 3). Chronic 

exposure of rainbow trout 

(Oncorhynchus mykiss) to chlorsulfuron 

resulted in a No Observed Effect 

Concentration (NOEC) of 32 mg/L (Ref. 

25). The observed NOEC for water fleas 

(Daphnia magna) was 20 mg/L (Ref. 26). 

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Federal Register / Vol. 78, No. 236 / Monday, December 9, 2013 / Proposed Rules 73791 

b. Toxicity to aquatic plants. In 

contrast to the data for aquatic animals, 

for some species of aquatic plants the 

toxicity of chlorsulfuron is very high. 

(Ref. 3). Duckweed (Lemna gibba) was 

the most sensitive aquatic vascular plant 

(Refs. 27 and 28). Growth rate studies 

using endpoints for both biomass (dry 

weight) and the number of normal 

fronds found 14 day EC50’s 

(concentration at which 50% of the 

plants are affected) of 3.5 × 10¥4

milligrams per liter (mg/L) and 4.2 × 

10¥4 mg/L respectively (Table I). The 14 

day NOEC for both biomass and the 

number of normal fronds was 0.24 mg/ 

L (micrograms per liter) (Table I). The 

most sensitive nonvascular aquatic 

plant was the green alga 

Pseudokirchneriella subcapitata 

(formerly Skeletonema costatum) (120 

hour (hr) EC50 = 0.05 mg/L; 120 hr 

NOEC = 0.0094 mg/L) (Refs. 29 and 30) 

and measured acute toxicity to the 

freshwater blue-green alga Anabaena 

flos-aquae was also quite high (Refs. 31 

and 32) (Table I). 

TABLE I—SUMMARY OF ACUTE AND CHRONIC TOXICITY DATA OF CHLORSULFURON TO FRESHWATER AQUATIC PLANTS

AND ALGAE

Species Common name Toxicity Citation 

Pseudokirchneriella subcapitata (formerly known as Selenastrum 

capricornutum).

Green Algae ................................................ 120 hr EC50 = 0.05 mg/L (cell density); 120 hr NOEC = 0.0094 mg/ 

L (cell density).

Refs. 29 and 30. 

Lemna gibba .................................... Freshwater Duckweed ................................. 14 day EC50 = 3.5 × 10¥4 mg/L 

(biomass); 14 day EC50 = 4.2 × 

10¥4 mg/L (number of normal 

fronds); 14 day NOEC = 2.4 × 

10¥4 mg/L (for both biomass and 

normal fronds).

Refs. 27 and 28. 

Anabaena flos-aquae ....................... Cyanobacteria ............................................. 120 hr EC50 = 0.609 mg/L (area 

under the growth curve); 120 hr 

EC50 = 1.77 mg/L (mean specific 

growth rate); 120 hr EC50 = 0.807 

mg/L (cell counts); 120 hr NOEC 

= 0.236 mg/L (area under the 

growth curve); 120 hr NOEC = 

0.485 mg/L (mean specific growth 

rate); 120 hr NOEC = 0.236 mg/L 

(cell counts).

Refs. 31 and 32. 

c. Toxicity to terrestrial animals. 

Chlorsulfuron is practically nontoxic to 

birds and mammals in acute exposure 

regimes and chlorsulfuron is also 

practically nontoxic to birds given 

subacute dietary exposures (Refs. 3 and 

33). Chronic toxicity to northern 

bobwhite quail (Colinus virginianus) 

included significant reductions in 

female body weight, decreased 14-day 

old survival, decreased number of 

normal hatchlings, decreased number of 

viable embryos (Ref. 34). 

d. Toxicity to terrestrial plants. 

Chlorsulfuron exposure is known to 

affect nontarget plant fruit or seed 

production and may cause visible 

disease symptoms days or weeks after 

exposure (Ref. 3). Short term symptoms 

include spotting, leaf puckering or 

twisting, as well as chlorosis and 

discolored veins. Developmental and 

reproductive effects of exposure may 

not become apparent until three or four 

months after exposure. Reduced fruit 

development and decreased seed 

production due to chlorsulfuron 

exposure has been observed in canola, 

smartweed, soybean, and sunflower. 

Thus these types of chronic toxicity 

effects may be difficult to recognize in 

the field due to the time lag inherent in 

their expression. 

Available experimental toxicity data 

for terrestrial plants (Refs. 33 and 34) 

reveals EC25 (concentration at which 25 

percent of the organisms are affected) 

values as low as 1.0 × 10¥5 lbs ai/A 

(pounds active ingredient per acre) 

measured for vegetative vigor (shoot dry 

weight) of nontarget plants (sugar beet). 

NOEC values of 5.4 × 10¥6 lbs ai/A for 

vegetative vigor (shoot dry weight) have 

been measured for onion and sugar beet. 

D. Summary of Human Health and 

Ecological Toxicity Evaluation 

Based on previous EPA hazard 

characterizations (Refs. 2 and 3; 67 FR 

52866, August 14, 2002), there is 

sufficient evidence to support a low 

concern for human toxicity from 

exposure to chlorsulfuron. A more 

recent guideline (Ref. 14) study (Ref. 15) 

was not able to replicate findings from 

one of the studies upon which the 

addition of chlorsulfuron to the list of 

toxic chemicals subject to reporting 

requirements of EPCRA section 313 and 

section 6607 of the PPA was based (Ref. 

13). Additionally, recent assessments of 

the studies cited in the listing of 

chlorsulfuron (Refs. 11 and 13) question 

the validity of these studies’ methods 

and conclusions (Ref. 2; 67 FR 52866, 

August 14, 2002). 

Additionally, no studies that strongly 

suggest either acute or chronic toxicity 

of chlorsulfuron were identified in the 

literature since the publication of the 

RED for chlorsulfuron (Ref. 3). A 

relatively recent guideline (Ref. 14) 

study (Ref. 19) was not able to replicate 

findings from another one of the studies 

upon which the addition of 

chlorsulfuron to the EPCRA section 313 

toxic chemical list was based (Ref. 11). 

The reported findings from the other 

additional studies (Refs. 20, 21, and 22) 

were of very limited use in the 

determination of hazard for 

chlorsulfuron due to the study 

deficiencies previously outlined. While 

treatment-related body weight changes 

were observed in the Mylchreest study 

(Ref. 19), these changes were observed 

at a relatively high dose level (close to 

500 mg/kg/day) and were observed in 

the absence of any other treatmentrelated effects. 

Based on EPA’s review of the 

available data, there is no compelling 

evidence of the acute toxicity, 

carcinogenicity, reproductive or 

developmental toxicity, mutagenicity, or 

other serious chronic toxicity of 

chlorsulfuron. While treatment-related 

body weight changes were observed in 

some studies, the evidence for these 

changes is not sufficient to conclude 

maindgalligan on DSK5TPTVN1PROD with PROPOSALS

73792 Federal Register / Vol. 78, No. 236 / Monday, December 9, 2013 / Proposed Rules 

that chlorsulfuron is expected to cause 

serious or irreversible systemic toxicity. 

Therefore, chlorsulfuron is not 

reasonably anticipated to cause acute or 

chronic toxicity in humans. 

Chlorsulfuron has low toxicity to 

most aquatic and terrestrial animals. 

However, chlorsulfuron is highly toxic 

to some species of aquatic plants. 

Toxicity values (EC50s) for aquatic 

plants are as low as 3.5 × 10¥4 mg/L 

indicating very high toxicity (Ref. 3). 

V. What is EPA’s rationale for the 

denial? 

EPA is denying the petition to delete 

chlorsulfuron from the EPCRA section 

313 list of toxic chemicals. This denial 

is based on EPA’s conclusion that 

chlorsulfuron can reasonably be 

anticipated to cause toxicity to aquatic 

plants. Chlorsulfuron has been shown to 

have an adverse effect on aquatic plant 

growth at very low concentrations with 

an EC50 of 3.5 × 10¥4 mg/L for 

duckweed and an EC50 of 0.05 mg/L for 

green algae as well as EC50 of 0.609 mg/ 

L for blue green algae. Therefore, EPA 

has concluded that chlorsulfuron meets 

the EPCRA section 313(d)(2)(C) listing 

criteria based on the available 

environmental toxicity data. 

Because EPA believes that 

chlorsulfuron is highly toxic to aquatic 

plants, EPA does not believe that an 

exposure assessment is appropriate for 

determining whether chlorsulfuron 

meets the criteria of EPCRA section 

313(d)(2)(C). This determination is 

consistent with EPA’s published 

statement clarifying its interpretation of 

the section 313(d)(2) and (d)(3) criteria 

for modifying the section 313 list of 

toxic chemicals (59 FR 61432, 

November 30, 1994). 

VI. References 

EPA has established an official public 

docket for this action under Docket ID 

No. EPA–HQ–TRI–2013–0393. The 

public docket includes information 

considered by EPA in developing this 

action, including the documents listed 

below, which are electronically or 

physically located in the docket. In 

addition, interested parties should 

consult documents that are referenced 

in the documents that EPA has placed 

in the docket, regardless of whether 

these referenced documents are 

electronically or physically located in 

the docket. For assistance in locating 

documents that are referenced in 

documents that EPA has placed in the 

docket, but that are not electronically or 

physically located in the docket, please 

consult the person listed in the above 

FOR FURTHER INFORMATION CONTACT

section. 

1. DuPont Crop Protection. 2012. Petition 

to Delete Chlorsulfuron from TRI List. 

DuPont Crop Protection (DuPont), 

Technology Sciences Group Inc. (TSG). May 

18, 2012. 

2. U.S. EPA. 2002. Toxicology Chapter for 

Chlorsulfuron. Health Effects Division, Office 

of Pesticide Programs. July 17, 2002. 

3. U.S. EPA. 2005. Reregistration Eligibility 

Decision for Chlorsulfuron. Office of 

Pesticide Programs. May 20, 2005. 

4. U.S. EPA, OEI. 2013. Memorandum from 

Jocelyn Hospital, Toxicologist, Analytical 

Support Branch to Daniel Bushman, TRI 

Petitions Coordinator and Chemical List 

Manager, Analytical Support Branch. April 

24, 2013. Subject: Review of Chlorsulfuron 

Studies Published Since Publication of the 

Reregistration Decision for Chlorsulfuron. 

5. Hawking, D., Epsom, L., Garcon, R., et 

al. 1989. The absorption and Disposition of 

o carbon 14–DPX–E9636 in the Rat: Lab 

Project Number: HRC/DPT 190/891138: 

AMR–1197–88. Unpublished study prepared 

by Huntingdon Research Centre Ltd. 76p. As 

cited in Ref. 2. 

6. Edwards, D.F. 1979. Acute Skin 

Absorption Test on Rabbits—LD50: Haskell 

Laboratory Report No. 415–79. (Unpublished 

study received Sep 1, 1981 under 352–EX– 

109; submitted by E.I. du Pont de Nemours 

& Co., Inc., Wilmington, DE; CDL:245879–I). 

As cited in Ref. 2. 

7. Ferenz, R.L. 1980. LC50-Inhalation Test 

for Pesticide Registration—AlbinoHaskell 

Laboratory Report No. 129–80. (Unpublished 

study received Nov 13, 1981 under 352–404; 

submitted by E.I. du Pont de Nemours & Co., 

Inc., Wilmington, DE; CDL:070471–H). As 

cited in Ref. 2. 

8. Trivits, R.L. 1979. Oral LD50 Test in 

Fasted Male and Female Rats; Report No. 

399–79. Unpublished study received Jun 16, 

1980 under 352–EX–105; submitted by E.I. 

du Pont de Nemours & Co., Inc., Wilmington, 

DE; CDL:099460–A). As cited in Ref. 2. 

9. Smith, L.W., Kaplan, A.M., Gibson, J.R. 

et al. 1980. Ninety-Day Range-Finding 

Feeding Study with 2-Chloro-N-o(4-methoxy6-methyl-1,3,5-triazin-2-yl)amino carbonyl 

benzenesulfonamide (INW–4189) in Mice: 

Report No. 69–80. (Unpublished study 

including pathology report no. 55–78, 

received Jun 16, 1980 under 352–EX–105l 

submitted by E.I. du Pont de Nemours & Co., 

Wilmington, DE; CDL: 099461–B). As cited in 

Ref. 2. 

10. Schneider, P.W., Jr., Smith, L.W., 

Barnes, J.R., et al. 1980. Six-Month Feeding 

Study in Dogs with 2-Chloro-N-o(4-methoxy6-methy-1,3,5-triazin–2yl)amino carbonyl 

benzenesulfonamide (INW–4189): Report No. 

108–80. Final rept. (Unpublished study 

including pathology report no. 53–79, 

received Jun 16, 1980 under 352–EX–105; 

submitted by E.I. du Pont de Nemours & Co., 

Wilmington, DE; CDL:099461–A). As cited in 

Ref. 2. 

11. Wood, C.K., Wollenberg, E.J., Turner, 

D.T., et al. 1981a. Long-Term Feeding Study 

with 2-chloro-N-6(4-methoxy-6-methyl-1,3,5- 

triazin-2- 

yl)aminocarbonylbenzenesulfonamide (INW– 

4189) in Rats. E.I. du Pont de Nemours & 

Company, Haskell Laboratory Report No. 

557–81, November 13, 1981. MRID 0086003. 

Unpublished. As cited in Ref. 2. 

12. Wood, C.K., Wollenberg, E.J., Turner, 

D.T., et al. 1981b. Long-Term Feeding Study 

with INW–4189 in Mice. E.I. du Pont de 

Nemours & Company, Haskell Laboratory 

Report No. 836–81, December 28, 1981. 

MRID 0090030. Unpublished. As cited in Ref. 

2. 

13. Hoberman, A.M. 1980. Teratology 

Study in Rabbits. E.I. du Pont de Nemours & 

Company, Haskell Laboratory, Newark, DE, 

Report No. HLO 534–80, July 17, 1980. 

Unpublished. As cited in 59 FR 1788, 

January 12, 1994. 

14. U.S. EPA. 1998. Health Effects Test 

Guidelines OPPTS 870.3800 Reproduction 

and Fertility Effects. Washington, DC. EPA 

712–C–98–208. 

15. Alvarez, L. 1991a. Teratogenicity Study 

of DPX–W4189 (Chlorsulfuron) in Rabbits. 

E.I. du Pont de Nemours & Company, Haskell 

Laboratory for Toxicology and Industrial 

Medicine, Newark, DE, Laboratory Project ID: 

306–390, August 12, 1991. Unpublished. As 

cited in Ref. 2. 

16. Alvarez, L. 1991b. Teratogenicity Study 

of DPX–W4189 (Chlorsulfuron) in Rats. E.I. 

du Pont de Nemours & Company, Haskell 

Laboratory for Toxicology and Industrial 

Medicine, Newark, DE, Laboratory Project ID: 

734–90, February 27, 1991. Unpublished. As 

cited in Ref. 2. 

17. U.S. EPA. 1991. Guidelines for 

Developmental Toxicity Risk Assessment. 

Risk Assessment Forum, Washington, DC. 

EPA/600/FR–91/001. 

18. Atkinson, J. 1991. A Chronic (1 Year) 

Oral Toxicity Study in the Dog with DPX– 

W4189 (Chlorsulfuron) via the Diet: Lab 

Project Number: 89/3501: 163/91. 

Unpublished study prepared by Bio/

dynamics, Inc. 716 p. As cited in Ref. 2. 

19. Mylchreest, E. 2005. Chlorsulfuron 

(DPX–W4189) Technical: Multigeneration 

Reproduction Study in Rats. DuPont Haskell 

Laboratory for Health and Environmental 

Sciences, Newark, DE, Laboratory Project ID: 

DUPONT.13495,14601,904. September 11, 

2003–June 4, 2004. MRID 46493201. 

Unpublished. As cited in Ref. 4. Data 

Evaluation Record: Taylor, Linda (2007), 

MRID 46493201. 

20. Rudaya, P.L., and Zhminko, P.G. 2009. 

Toxic Properties of Chlorsulfuron Potassium 

Salt Herbicide Administered Once Orally to 

Mammals. Modern Problems of Toxicology 2: 

59–65. Translated from Ukrainian. 

21. Rudaya, P.L., Zhminko, P.G., Povyakel, 

L.I., and Reshavska, O.V. 2010. 

Toxicodynamics of Chlorsulfuron Potassium 

Salt Given Orally In Long-Term Experiment 

on White Rats. Modern Problems of 

Toxicology 1: 59–63. Translated from 

Ukrainian. 

22. Rakitsky, V.N. and Beloyedova, N.S. 

2009. Toxicity and Hazardousness of 

Sulfonylurea Herbicides. Toxicology Herald 

4: 25–30. Translated from Russian. 

23. Dietrich, R. and McAleer, N. (1989) 

Hydrolysis of Phenyl(U)-C14-Chlorsulfuron 

and Triazine-2-C14-Chlorsulfuron: Lab 

Project Number: AMR–1455–89. 161–1. 

Unpublished study prepared by E.I. du Pont 

de Nemours & Co., Inc. 61 pp. MRID: 

42156701. As cited in Ref. 3. 

24. Hawkins, D., Kirkpatrick, D., Dean, G., 

et al. (1990) The Photodegradation of C14- 

maindgalligan on DSK5TPTVN1PROD with PROPOSALS

Federal Register / Vol. 78, No. 236 / Monday, December 9, 2013 / Proposed Rules 73793 

Chlorsulfuron on a Silty Clay Loam Soil: Lab 

Project Number: HRC/DPT 205/90571: AMR– 

1563–89. Unpublished study prepared by 

Huntingdon Research Centre Ltd. 58 pp. 

MRID: 42156703. As cited in Ref. 3. 

25. Pierson, K. (1991) Flow-Through 77 

Day Toxicity of DPX–W4189–170 to Embryo 

and Larval Rainbow Trout, Oncorhynchus 

mykiss. Lab Project Number 494–91: MR– 

4581–866. Unpublished study prepared by 

E.I. du Pont de Nemours and Co. 471 pp. 

MRID: 41976405. As cited in Ref. 3. 

26. Hutton, D. (1991) Chronic Toxicity of 

DPX–W4189–94 to Daphnia magna. Lab 

Project Number: 4581–655: 87–89. 

Unpublished study prepared by E.I. du Pont 

de Nemours and Co. 92 pp. MRID: 41976408. 

As cited in Ref. 3. 

27. Boeri, R., Wyskiel, D., Ward, T. (2002) 

Chlorsulfuron (DPX–W4189) Technical: 

Influence on Growth and Growth Rate of the 

Duckweed, Lemna gibba: Lab Project 

Number: 2042–DU: DUPONT–4468: ASTM 

E1415–91. Unpublished study prepared by 

T.R. Wilbury Laboratories. 38 pp. MRID: 

45832901. As cited in Refs. 3 and 28. 

28. Bryan, R., Worcester, D., Brichfield, N., 

Ballaff, D. (2003a) Data Evaluation Report on 

the acute toxicity of Chlorsulfuron to aquatic 

vascular plants Lemna gibba. 12 pp. MRID: 

45832901. 

29. Blasberg, J., Hicks, S., Stratton, J. (1991) 

Acute Toxicity of Chlorsulfuron to 

Selenastrum capricornutum Printz,: Final 

Report: Lab Project Number: AMR–2081–91: 

39427. Unpublished study prepared by ABC 

Laboratories, Inc., 33 pp. MRID: 42186801. 

As cited in Ref. 30. 

30. Levy, B., Myers, T., Behl, E., Ballaff, D. 

(2003) Data Evaluation Report on the acute 

toxicity of Chlorsulfuron to algae 

Selenastrum capricornutum Printz. 12 pp. 

MRID: 42186801. 

31. Boeri, R., Wyskiel, D., Ward, T. (2001b) 

Chlorsulfuron (DPX–W4189) Technical: 

Influence on Growth and Growth Rate of the 

Alga, Anabaena flos-aquae: Lab Project 

Number: DU: DUPONT–4466:2044DU. 

Unpublished study prepared by T.R. Wilbury 

Laboratories. 38 pp. MRID: 45832903. As 

cited in Refs. 3 and 32. 

32. Bryan, R., Worcester, D., Brichfield, N., 

Ballaff, D. (2003b) Data Evaluation Report on 

the acute toxicity of Chlorsulfuron to the 

freshwater algae Anabaena flos-aquae. 14 pp. 

MRID: 45832903. 

33. Hinkle, S. (1979) Final Report—Avian 

Dietary Toxicity (LC50) Study in Bobwhite 

Quail: Project No. 201–523 (Unpublished 

study received June 16, 1980 under 352–105; 

prepared by Hazelton Laboratories America, 

Inc., submitted by E.I. du Pont de Nemours 

& Co., Wilmington, DE; CDL:099462–K). 

MRID: 00035265. As cited in Ref. 3. 

34. Beavers, J., Foster, J., Lynn, S. et al. 

(1992) H–18,053 (Chlorsulfuron): A Onegeneration Reproduction Study with the 

Northern Bobwhite (Colinus virginianus): Lab 

Project Number: 112–266: 564–92. 

Unpublished study prepared by Wildlife 

International Ltd. 185 pp. MRID: 42634001. 

As cited in Ref. 3. 

35. Porch, J. and Martin, K. (2004a) 

Chlorsulfuron (DPX–W4189) 75WG: A 

Greenhouse to investigate the Effects on 

Vegetative Vigor of Ten Terrestrial Plants 

Following Foliar Exposure. Project Number: 

112/542, DUPONT/13552, 14901. 

Unpublished study prepared by Wildlife 

International, Ltd.. 191 pp. MRID: 46326801. 

As cited in Ref. 3. 

36. Porch, J. and Martin, K. (2004b) 

Chlorsulfuron (DPX–W4189) 75WG: A 

Greenhouse to investigate the Effects on 

Vegetative Vigor of Ten Terrestrial Plants 

Following Soil Exposure. Project Number: 

112/541, 14901, 1495. Unpublished study 

prepared by Wildlife International, Ltd. 264 

pp. MRID: 46361801. As cited in Ref. 3. 

List of Subjects in 40 CFR Part 372 

Environmental protection, 

Community right-to-know, Reporting 

and recordkeeping requirements, and 

Toxic chemicals. 

Dated: November 18, 2013. 

Arnold E. Layne, 

Director, Office of Information Analysis and 

Access. 

[FR Doc. 2013–28365 Filed 12–6–13; 8:45 am] 

BILLING CODE 6560–50–P 

FEDERAL COMMUNICATIONS 

COMMISSION 

47 CFR Part 73 

[MB Docket No. 13–284; RM–11704; DA 13– 

2241] 

Radio Broadcasting Services; Evart 

and Ludington, Michigan 

AGENCY: Federal Communications 

Commission. 

ACTION: Proposed rule. 

SUMMARY: This document proposes, at 

the request of Synergy Lakeshore 

Licenses, LLC (‘‘Synergy’’), licensee of 

Station WMLQ(FM), Manistee, 

Michigan, the deletion of vacant FM 

Channel 274A at Evart, Michigan. The 

document also proposes the return of 

Stations WMLQ(FM), Manistee, and 

WMOM(FM), Pentwater, Michigan, to 

the channels that they previously 

occupied, and the modification of the 

construction permit for a new FM 

station at Ludington, Michigan. See 

SUPPLEMENTARY INFORMATION, supra. 

DATES: Comments must be filed on or 

before January 13, 2014, and reply 

comments on or before January 28, 

2014. 

ADDRESSES: Secretary, Federal 

Communications Commission, 445 12th 

Street SW., Washington, DC 20554. In 

addition to filing comments with the 

FCC, interested parties should serve the 

petitioner as follows: David D. 

Oxenford, Esq., Wilkinson Barker 

Knauer, LLP, 2300 N Street NW., Suite 

700, Washington, DC 20037–1128. 

FOR FURTHER INFORMATION CONTACT: 

Andrew J. Rhodes or Rolanda F. Smith, 

Media Bureau, (202) 418–2700. 

SUPPLEMENTARY INFORMATION: This is a 

synopsis of the Commission’s Notice of 

Proposed Rule Making, MB Docket 

No.13–284, adopted November 21, 2013, 

and released November 22, 2013. The 

full text of this Commission decision is 

available for inspection and copying 

during normal business hours in the 

FCC’s Reference Information Center at 

Portals II, CY–A257, 445 12th Street 

SW., Washington, DC 20554. This 

document may also be purchased from 

the Commission’s duplicating 

contractors, Best Copy and Printing, 

Inc., 445 12th Street SW., Room CY– 

B402, Washington, DC 20554, telephone 

1–800–378–3160 or via email 

www.BCPIWEB.com. This document 

does not contain proposed information 

collection requirements subject to the 

Paperwork Reduction Act of 1995, 

Public Law 104–13. In addition, 

therefore, it does not contain any 

proposed information collection burden 

‘‘for small business concerns with fewer 

than 25 employees,’’ pursuant to the 

Small Business Paperwork Relief Act of 

2002, Public Law 107–198, see 44 U.S.C. 

3506(c)(4). 

Previously, we allotted Channel 274A 

at Evart, Michigan. In order to 

accommodate this new allotment, we 

modified the licenses for Station 

WMOM(FM), Pentwater, from Channel 

274A to Channel 242A, and Station 

WMLQ(FM), Manistee, from Channel 

249A to Channel 282A. We required the 

ultimate permittee of Channel 274A at 

Evart to reimburse Stations WMOM(FM) 

and WMLQ(FM) for their reasonable 

costs in changing channels. We also 

substituted Channel 249A for vacant 

Channel 242A at Ludington, Michigan. 

See 74 FR 13125, March 26, 2009. 

The document solicits comment on 

whether vacant Channel 274A at Evart 

should be deleted because it went 

unsold in Auction 94. Interested parties 

should file comments expressing an 

interest in this vacant allotment to 

prevent its removal and provide an 

explanation as to why they did not 

participate in our competitive bidding 

process. 

We issue an Order to Show Cause to 

the licensee of Station WMOM(FM), 

Pentwater, to show cause as to why its 

license should not be modified to 

specify Channel 274A in lieu of Channel 

242A. We also propose to modify the 

construction permit for a new FM 

station at Ludington, Michigan, from 

Channel 249A to Channel 242A in order 

to accommodate the previously 

discussed channel changes. It is not 

maindgalligan on DSK5TPTVN1PROD with PROPOSALS