60818 Federal Register / Vol. 80, No. 195 / Thursday, October 8, 2015 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 372 

[EPA–HQ–TRI–2015–0352; FRL 9935–38– 

OEI] 

Ethylene Glycol Monobutyl Ether; 

Community Right-To-Know Toxic 

Chemical Release Reporting 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Denial of petition. 

SUMMARY: Environmental Protection 

Agency (EPA) is denying a petition to 

remove ethylene glycol monobutyl ether 

(EGBE) from the category Certain Glycol 

Ethers under 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 

EGBE 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 EGBE 

meets the listing criterion of EPCRA 

section 313(d)(2)(B) due to its potential 

to cause serious or irreversible chronic 

health effects in humans, specifically, 

liver toxicity and concerns for 

hematological effects. 

DATES: EPA denied this petition on 

September 24, 2015. 

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 EGBE. 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, 221118, 

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? 

1. Docket. EPA has established a 

docket for this action under Docket ID 

No. EPA–HQ–TRI–2015–0352. 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. 

2. Electronic Access. You may access 

this Federal Register document 

electronically from the Government 

Printing Office under the ‘‘Federal 

Register’’ listings at FDSys (http://

www.gpo.gov/fdsys/browse/

collection.action?collectionCode=FR). 

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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• 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 January 23, 2015, EPA received a 

petition from American Chemistry 

Council (ACC) Ethylene Glycol Ethers 

Panel requesting EPA to delete EGBE 

(Chemical Abstracts Service Registry 

Number (CASRN) 111–76–2) from the 

list of chemicals subject to reporting 

under EPCRA section 313 and PPA 

section 6607 (Reference (Ref. 1)). EGBE 

is not individually listed under EPCRA 

section 313 but rather is reportable 

under the Certain Glycol Ethers 

category. The petitioner contends that 

the available scientific data show that 

EGBE has low potential hazard to 

human health and the environment. 

Therefore, the petitioner believes that 

under EPA’s policy for listing decisions 

under EPCRA section 313, potential 

exposures should be considered. The 

petitioner believes that their analysis 

shows that exposure levels are well 

below the concern levels for human 

health and ecological effects. 

IV. What is EPA’s evaluation of the 

toxicity of EGBE? 

EPA’s evaluation of the toxicity of 

EGBE included a review of the human 

health and ecological effects data. EPA’s 

Integrated Risk Information System 

(IRIS) toxicological review of EBGE (Ref. 

2) was the primary source used to 

determine the human health effects of 

EGBE. EPA also prepared an assessment 

of the chemistry, fate, and ecological 

effects for EGBE (Ref. 3). 

A. What is EPA’s review of the human 

health toxicity data for EGBE? 

EPA’s evaluation of the toxicity of 

EGBE included a review (Ref. 4) of the 

IRIS toxicological review of EGBE (Ref. 

2). EPA also reviewed the findings of 

studies published since the IRIS 

toxicological review of EGBE, but found 

no data relevant to include in this 

evaluation. This Unit outlines the 

evidence of human health toxicity from 

the 2010 IRIS toxicological review of 

EGBE. Unit IV.B. below discusses the 

conclusions regarding EGBE’s potential 

human health toxicity. 

1. Toxicokinetics. In humans, EGBE is 

absorbed and rapidly distributed 

following inhalation, ingestion, or 

dermal exposure (Refs. 5, 6, 7, and 8). 

Several reviews have described the 

metabolism of EGBE in detail (Refs. 9, 

10, and 11). The principal products 

from EGBE metabolism are butoxyacetic 

acid (BAA) (rats and humans) and the 

glutamine or glycine conjugate of BAA 

(humans). BAA is excreted in the urine 

of both rats and humans, which suggests 

that the creation of BAA through the 

formation of butoxyacetaldehyde by 

alcohol dehydrogenase is applicable to 

rats and humans (Refs. 8, 12, and 13). 

The other proposed metabolic 

pathways, however, may only be 

applicable to rats since the metabolites 

of these pathways (i.e., ethylene glycol, 

EGBE glucuronide, and EGBE sulfate) 

have been observed in the urine of rats 

(Refs. 14 and 15), but not in humans 

(Ref. 8). In addition, Corley et al. (Ref. 

8) confirmed the finding from 

Rettenmeier et al. (Ref. 16) that 

approximately two-thirds of the BAA 

formed in humans is conjugated with 

glutamine and glycine. These pathways, 

however, have not been observed in the 

rat. 

Several experimental studies have 

measured the concentration of BAA in 

human serum and urine following 

exposure to EGBE. For humans, the 

elimination kinetics of EGBE and BAA 

appear to be independent of the route of 

exposure with an approximate half-life 

of around one hour for EGBE and an 

approximate half-life of BAA of 3–4 

hours (Refs. 17, 18, and 19). 

Several physiologically based 

pharmacokinetic models for EGBE have 

been developed. Some older models 

have described the kinetics of EGBE for 

acute human exposure and exposure to 

rats via the ingestion, inhalation, and 

dermal routes (Refs. 17 and 20 based on 

data from Refs. 13, 21, and 22). Newer 

models, however, have extended upon 

the work of these previous models. 

Corley et al. (Ref. 7) described the 

kinetics of EGBE and BAA in both rats 

and humans. These authors later 

validated the human dermal exposure 

model (Ref. 8). Lee et al. (Ref. 23) 

modeled the kinetics of EGBE and BAA 

in mice and rats from a National 

Toxicology Program (NTP) 2-year 

inhalation bioassay (based on data from 

Dill et al. (Ref. 24)). Species, gender, 

age, and exposure concentrationdependent differences in the kinetics of 

BAA were observed. Corley et al. (Ref. 

12) built on the Lee et al. (Ref. 23) 

model by replacing some model 

assumptions with experimental data 

(Note: The Corley et al. (Ref. 12) model, 

along with the Lee et al. (Ref. 23) rat and 

mouse model and Corley et al. (Ref. 8) 

human model were used by EPA to 

calculate internal doses of EGBE in the 

2010 IRIS toxicological review of EGBE 

(Ref. 2)). 

2. Effects of Acute and Short-Term 

Exposure. Hematologic and other effects 

have been observed in several acute and 

short-term oral studies of EGBE in rats 

and mice (Refs. 15, 25, 26, 27, 28, 29, 

30, 31, 32, 33, and 34). Varying degrees 

of hematotoxicity have also been 

observed in rats and rabbits following 

dermal application of EGBE (Refs. 14 

and 35). Guinea pigs, however, have not 

demonstrated sensitivity to the 

hematologic effects of EGBE in acute 

studies (Refs. 36 and 37). EGBE has also 

been found to be an ocular irritant when 

instilled in rabbits (Refs. 38 and 39). 

A few in vitro studies have 

investigated EGBE’s potential hemolytic 

effects in human red blood cells after 

acute exposures. Bartnik et al. (Ref. 14) 

reported no hemolysis of human red 


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blood cells exposed for three hours to 

BAA levels up to 15 millimolar (mM). 

Hemolysis was observed in rat red blood 

cells, however, at BAA levels as low as 

1.25 mM. Udden (Ref. 40) incubated 

human red blood cells with up to 2.0 

mM BBA for four hours, and the authors 

observed none of the morphological 

changes observed in rat red blood cells 

at the same concentration. Udden (Ref. 

41) reported a significant change in 

human red blood cell deformability at 

exposure to 7.5 and 10 mM BAA for 4 

hours, whereas deformability in rat red 

blood cells was significantly increased 

at 0.05 mM BAA. Mean cellular volume 

in human blood samples was 

significantly increased at 10 mM BAA 

while mean cellular volume in rats was 

significantly increased at 0.05 mM BAA. 

There are a number of case reports of 

acute ingestion of EGBE with little or no 

hematologic effects observed (Refs. 42, 

43, 44, 45, 46, 47, 48, and 49). Some 

other observed effects were likely not 

directly related to hemolysis; however, 

the cause of the effects cannot be 

explained based on the limited data 

available. Also, hemodialysis was 

employed to remove un-metabolized 

EGBE in many of the cases. 

One experimental study in humans 

(Ref. 50), observed no effects on red 

blood cell fragility after exposure of two 

males and one female to up to 195 part 

per million (ppm) EGBE for 8 hours. 

3. Carcinogenicity and Mutagenicity. 

Under the Guidelines for Carcinogen 

Risk Assessment (Ref. 51), there is 

suggestive evidence of EGBE’s 

carcinogenic potential based on a 2-year 

NTP bioassay in mice and rats (Ref. 52). 

EGBE has been tested for its potential 

for genotoxicity both in vitro and in 

vivo, and the available data do not 

demonstrate that EGBE is mutagenic or 

clastogenic (Refs. 53, 54, 55, 56, 57, and 

58). 

4. Reproductive and Developmental 

Toxicity. The reproductive and 

developmental toxicity of EGBE has 

been investigated in a number of oral 

and inhalation studies in rats, mice, and 

rabbits. In a two-generation 

reproductive toxicity study, fertility was 

reduced in mice at very high maternally 

toxic doses (≤1,000 milligrams/kilogram 

(mg/kg)) (Ref. 59), but no other 

significant reproductive effects were 

reported in any study (Refs. 26, 52, 60, 

61, 62, 63, 64, 65, and 66). Maternal 

toxicity related to the hematologic 

effects of EGBE and relatively minor 

developmental effects have been 

reported in developmental studies (Refs. 

67, 68, 69, and 70). No teratogenic 

effects were noted in any of the studies. 

As such, EGBE is not reasonably 

anticipated to be a reproductive or 

developmental toxicant at moderately 

low to low doses. 

5. Neurotoxicity. There is no evidence 

of neurotoxicity in any animal studies of 

EGBE. One case study patient 

demonstrated neurologic deficits after 

ingesting a product with a high dose of 

EGBE and other chemicals (Ref. 47). 

Given the general limitations of case 

studies and the presence of other 

chemicals, however, EPA cannot draw 

conclusions about EGBE’s potential 

neurotoxicity from this particular study. 

6. Other Subchronic and Chronic 

Toxicity. Hematologic effects and liver 

toxicity have been observed at low 

doses of EGBE in several animal studies. 

The NTP (Ref. 66) conducted a 13- 

week study in F344 rats and B6C3F1 

mice in which groups of 10 animals/

gender/species received EGBE in 

drinking water at doses of 0, 750, 1,500, 

3,000, 4,500, and 6,000 ppm. The 

corresponding doses based on measured 

drinking water consumption were: 0, 69, 

129, 281, 367, or 452 milligrams/

kilogram/day (mg/kg/day) in male rats; 

0, 82, 151, 304, 363, or 470 mg/kg/day 

in female rats; 0, 118, 223, 553, 676, or 

694 mg/kg/day in male mice; and 0, 185, 

370, 676, 861, or 1,306 mg/kg/day in 

female mice. 

Indications of mild to moderate 

anemia were observed in both genders. 

Statistically significant hematologic 

effects in female rats included reduced 

red blood cell counts and hemoglobin 

concentrations at ≥750 ppm and 

increased reticulocytes, decreased 

platelets, and increased bone marrow 

cellularity at 3,000 ppm. Liver effects 

including cytoplasmic alterations, 

hepatocellular degeneration, and 

pigmentation were reported in the midand high-dose groups (≥1,500 ppm for 

males and females; statistics not 

reported). Additionally, cytoplasmic 

alterations of liver hepatocytes were 

observed in the lowest-dose groups (750 

ppm for males and females). The lack of 

cytoplasmic granularity of the 

hepatocytes indicates that this response 

was not due to enzyme induction (Ref. 

71). The NTP (Ref. 66) identified a 

lowest-observed-adverse-effect level 

(LOAEL) for rats of 750 ppm 

(approximately 58.6 mg/kg/day 

calculated using water consumption 

rates and body weights measured during 

the last week of exposure and, therefore, 

slightly different from those reported by 

the study authors (Ref. 2)) based on 

decreased red blood cell count and 

hemoglobin in female rats. A NOAEL 

was not identified. 

A reduction in body weight gain at 

≥3,000 ppm was observed in male and 

female mice. An increase in relative 

kidney weight was also observed at all 

doses in female mice. Body weight 

reductions followed decreased water 

consumption. No histopathologic 

changes were noted at any dose level, 

however, relative kidney weights 

showed a statistically significant 

increase at 750 and 1,500 ppm in the 

absence of reduction in body weight 

gain. The NTP (Ref. 66) identified a 

LOAEL for mice of 3,000 ppm 

(approximately, 553–676 mg/kg/day 

calculated using water consumption 

rates and body weights measured during 

the last week of exposure and, therefore, 

slightly different from those reported by 

the study authors (Ref. 2)) based on 

reduced body weight and body weight 

gain. 

Dodd et al. (Ref. 62) conducted a 90- 

day subchronic inhalation study using 

F344 rats (16/gender/group) exposed to 

EGBE for 6 hours/day, 5 days/week at 

concentrations of 0, 5, 25, and 77 ppm. 

After 6 weeks, the 77 ppm female rats 

had statistically significant decreases in 

red blood cell counts (13%) and 

hemoglobin concentrations, 

accompanied by an 11% increase in 

mean corpuscular hemoglobin. Similar 

results were observed in males. 

However, many of these effects had 

lessened by the end of the study. The 

authors reported a LOAEL of 77 ppm 

based on decreases in red blood cell 

count and hemoglobin concentrations, 

accompanied by an increase in mean 

corpuscular hemoglobin in both 

genders. 

The NTP (Ref. 52) conducted a 

subchronic inhalation study in F344 rats 

and B6C3F1 mice (10/gender). Rats and 

mice were exposed to EGBE 

concentrations of 0, 31, 62.5, 125, 250, 

and 500 ppm (0, 150, 302, 604, 1,208, 

and 2,416 milligrams/cubic meter (mg/ 

m3)) 6 hours/day, 5 days/week for 14 

weeks. The NTP (Ref. 52) identified a 

LOAEL of 31 ppm in female rats based 

on decreases in hematocrit, hemoglobin, 

and red blood cell count and a LOAEL 

of 62.5 ppm in male rats based on a 

decrease in red blood cell count. 

Histopathologic effects were observed in 

male and female rats. Effects reported in 

female rats included liver necrosis at 

250 ppm and centrilobular degeneration 

and renal tubular degeneration at 500 

ppm. Other effects reported in both 

genders included: Excessive splenic 

congestion in the form of 

extramedullary hematopoiesis (at 250 

ppm in male rats and 125 ppm in female 

rats), hemosiderin accumulation in 

Kupffer cells (at 125 ppm in male rats 

and 62.5 ppm in female rats), 

intracytoplasmic hemoglobin (at 125 

ppm in male rats and 31 ppm in female 

rats), hemosiderin deposition (at 125 

ppm in male rats and 62.5 ppm in 


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female rats), and bone marrow 

hyperplasia (at 250 ppm in male rats 

and 62.5 ppm in female rats). The 

authors identified a LOAEL of 62.5 ppm 

for mice based on histopathological 

changes in the forestomach (including: 

Necrosis, ulceration, inflammation, and 

epithelial hyperplasia) in both males 

and females. Signs consistent with the 

hemolytic effects of EGBE (including: 

Decreased red blood cell counts, 

increased reticulocyte counts, and 

increased mean corpuscular volume) 

were also observed at 250 and 500 ppm 

in male and female mice. 

The NTP (Ref. 52) also completed a 2- 

year inhalation study on EGBE in both 

F344 rats and B6C3F1 mice. In this 

study, animals were exposed to EGBE 6 

hours/day, 5 days/week at 

concentrations of 0, 31, 62.5, and 125 

ppm (0, 150, 302, and 604 mg/m3) for 

groups of 50 F344 rats and 0, 62.5, 125, 

and 250 ppm (0, 302, 604, and 1,208 

mg/m3) for groups of 50 B6C3F1 mice. 

The authors identified a LOAEL of 31 

ppm in rats based on decreases in 

hematocrit, hemoglobin, and red blood 

cell count in female rats in a satellite 

group observed at 3 and 6 months. The 

authors identified 62.5 ppm as the 

LOAEL for mice based on hemosiderin 

deposition. 

One long-term occupational study of 

EGBE was identified in the literature. 

Haufroid et al. (Ref. 72) reported a small 

decrease in hematocrit and increase in 

mean corpuscular hemoglobin in a cross 

sectional study of 31 workers exposed to 

an average concentration of 0.6 ppm 

EGBE over 1 to 6 years. The biological 

significance of these findings, however, 

is unclear as they were within normal 

clinical ranges and no other measured 

parameters were affected by EGBE 

exposure. 

B. What are EPA’s conclusions 

regarding the human hazard potential 

of EGBE? 

There is evidence to indicate that the 

human red blood cell response to EGBE 

exposure is less than that of rodents, 

however, this conclusion is based on a 

relatively small number of in vitro and 

short-term human exposure studies with 

supporting evidence from 

pharmacokinetic models (Refs. 7, 8, 14, 

40, 41, and 50). Little is known of the 

long-term or repeated exposure 

responses in humans to EGBE. 

In 2010, EPA concluded in the IRIS 

toxicological review of EGBE that 

human red blood cells do appear 

capable of responding similarly to the 

causative EGBE metabolites, albeit at 

much higher exposures (Ref. 2). The 

IRIS toxicological review of EGBE 

employed an interspecies uncertainty 

factor of 1 to derive the reference values 

for EGBE in part because there was not 

a preponderance of toxicodynamic data 

in both animals and humans describing 

why humans are less sensitive than rats 

to the hematologic effects in question 

(Ref. 2). Also, EPA calculated a human 

equivalent concentration LOAEL 

(LOAELHEC) for hematologic effects of 

271 mg/m3 (approximately 77 mg/kg/

day, assuming constant exposure, an 

inhalation rate of 20 cubic meters/day 

(m3/day), and a 70 kg human) using 

pharmacokinetic model estimates (Refs. 

7 and 8) of the human internal dose 

equivalent of the toxic metabolite BAA 

to that estimated for female rats exposed 

to 31 ppm EGBE in the NTP (Ref. 52) 

study (Ref. 2). In its assessment of 

EGBE, the European Union carried out 

a slightly different calculation based on 

the same underlying data and reported 

a similar, but slightly higher, human 

equivalent LOAEL of 474 mg/m3

(approximately 135 mg/kg/day) (Ref. 

11). 

Additionally, multiple animal studies 

by the NTP reported liver toxicity (e.g., 

cytoplasmic alterations of liver 

hepatocytes at 750 ppm (approximately 

69 mg/kg/day) in male rats and 750 ppm 

(82 mg/kg/day) in female rats (Ref. 66) 

and liver necrosis at 250 ppm 

(approximately 243 mg/kg/day) in 

female rats (Ref. 52)) to which humans 

do not demonstrate decreased 

sensitivity. These findings provide 

further evidence of EGBE’s potential 

toxicity to humans at moderately low to 

low doses. 

Therefore, the available evidence is 

sufficient to conclude that EGBE can be 

reasonably anticipated to demonstrate 

moderately high to high chronic toxicity 

in humans based on the EPCRA Section 

313 listing criteria (59 FR 61432, 

November 30, 1994). 

C. What is EPA’s review of the 

ecological toxicity of EGBE? 

Based on a review of the available 

aquatic ecological toxicity data, EGBE 

does not appear to present a significant 

concern for adverse effects on the 

environment. Experimentally measured 

effects occurred at relatively high 

concentrations indicating low toxicity 

(Ref. 3). Such high concentrations are 

not expected to be observed under 

typical environmental conditions. Table 

1 presents some of the available toxicity 

data for EGBE, the complete listing of 

the available toxicity data and more 

details about the studies can be found 

in the ecological assessment (Ref. 3). 

1. Acute toxicity. Toxicity threshold 

values (duration not specified) of 900 

milligrams/liter (mg/L) and 72-hour 

EC50 values (i.e., the concentration that 

is effective in producing a sublethal 

response in 50% of test organisms) of 

911 and 1,840 mg/L for biomass and 

growth rate, respectively, have been 

reported for green algae (Refs. 73, 74, 

and 75). The corresponding 72-hour NoObserved-Effect-Concentration (NOEC) 

values for biomass and growth rate were 

88 and 286 mg/L (Ref. 76). For water 

fleas (Daphnia magna), 24- or 48-hour 

EC50 values ranged from 835 to 1,815 

mg/L (Refs. 77 and 78). A 48-hour EC50

value of 164 mg/L in rotifers 

(reproduction) has also been reported 

(Refs. 74 and 75). 

Acute toxicity values for freshwater 

fish ranged from an LC50 (i.e., the 

concentration that is lethal to 50% of 

test organisms) of 1,395 mg/L for the 

golden orfe (Leuciscus idus) (duration 

not specified) (Ref. 79) to a 96-hour LC50

of 2,137 mg/L for the fathead minnow 

(Pimephales promelas) (Ref. 80). A 96- 

hour LC50 value of 1,490 mg/L was 

available for bluegill sunfish (Ref. 81) 

and 96-hour LC50 values for rainbow 

trout were 1,474 and 1,700 mg/L (Refs. 

74, 75, and 82). An LC50 value (duration 

not specified) of 1,575 mg/L was also 

available for golden orfe (Leuciscus 

idus) (Ref. 79) and a 24-hour LC50 value 

of 1,700 mg/L was available for goldfish 

(Carassius auratus) (Ref. 83). 

A study of the invertebrate Artemia 

salina (brine shrimp) reported a 24-hour 

LC50 value of 1,000 mg/L (Ref. 84). Also, 

an embryo-larval test in which Japanese 

oyster eggs (Crassostrea gigas) were 

incubated with the test material for 24 

hours and then examined for 

abnormalities indicated an identical 24- 

hour Lowest-Observed-EffectConcentration (LOEC) of 1,000 mg/L 

(Ref. 74). A study of an estuarine/marine 

fish silverside (Menidia beryllina) 

reported a 96-hour LC50 value of 1,250 

mg/L (Ref. 81). 

2. Chronic toxicity. Values for chronic 

toxicity in aquatic plants ranged from an 

8-day LOEC (inhibition of cell division) 

of 35 mg/L for the cyanobacteria 

Microcystis aeruginosa (Refs. 85 and 86) 

to greater than 1,000 mg/L for a 7-day 

EC50 (growth rate) for the green alga 

Selenastrum capricornutum (Ref. 87). 

Experimental data for the freshwater 

invertebrate Daphnia magna include 

values that ranged from 100 mg/L for a 

21-day NOEC (reproduction) (Refs. 74, 

75, and 77) to an EC50 of 297 mg/L 

(endpoint not reported) (Ref. 88). 


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TABLE 1—RANGE OF EXPERIMENTAL ECOLOGICAL TOXICITY VALUES FOR EGBE ON SELECTED TARGET SPECIES

Species Duration and test endpoint Experiment 

type a

Value 

(mg/L) Reference 

Acute aquatic toxicity 

Algae: 

Green algae (Pseudokirchneriella subcapitata) ...... 72-hour EC50 (growth) ....... S, M ............. 1,840 (Refs. 74 and 75). 

Green algae (Pseudokirchneriella subcapitata) ...... 72-hour NOEC (biomass) .. S, M ............ 88 (Ref. 82). 

Freshwater invertebrate: 

Water flea (Daphnia magna) ................................... 48-hour EC50 ..................... S, U, O ........ 1,815 (Ref. 78). 

Rotifer (Brachionus calyciflorus) ............................. 48-hour EC50 (reproduction).S, M ............. 164 (Refs. 74 and 75). 

Freshwater fish: 

Golden orfe (Leuciscus idus) .................................. LC50 ................................... NS ............... 1,395 (Ref. 79). 

Fathead minnow (Pimephales promelas) ............... 96-hour LC50 ...................... S, O ............. 2,137 (Ref. 80). 

Estuarine/marine invertebrate: 

Brine shrimp (Artemia salina) .................................. 24-hour LC50 ...................... S, U, C ........ 1,000 (Ref. 84). 

Japanese oyster eggs (Crassostrea gigas) ............ 24-hr LOEC 

(embryotoxicity).

S .................. 1,000 (Refs. 74 and 75). 

Estuarine/marine fish: 

Silverside (Menidia beryllina) .................................. 96-hour LC50 ...................... S, U ............. 1,250 (Ref. 81). 

Chronic aquatic toxicity 

Algae: 

Blue-green algae (Microcystis aeruginosa) ............. 8-day LOEC (cell multiplication inhibition).S, U ............. 35 (Refs. 85 and 86). 

Green algae (Selenastrum capricornutum) ............. 7-day EC50 (growth rate) ... S, U ............. >1,000 (Ref. 87). 

Freshwater invertebrate: 

Water flea (Daphnia magna) ................................... 21-day NOEC (reproduction).R, M ............ 100 (Refs. 74 and 75). 

Water flea (Daphnia magna) ................................... 21-day NOEC .................... R, M ............ 100 (Ref. 88). 

Water flea (Daphnia magna) ................................... 21-day EC50 ....................... R, M ............ 297 (Ref. 88). 

Freshwater fish: 

Zebrafish (Brachydanio rerio) .................................. 21-day NOEC (mortality) ... NS ............... >100 (Ref. 89). 

aExperiment type: S = static, R = renewal, M = measured, U = unmeasured, O = open test system, NS = not specified 

V. What is EPA’s rationale for the 

denial? 

EPA is denying the petition to delete 

EGBE from the Certain Glycol Ethers 

category which is subject to reporting 

under EPCRA section 313. This denial 

is based on EPA’s conclusion that EGBE 

can reasonably be anticipated to cause 

serious or irreversible chronic health 

effects in humans, specifically, liver 

toxicity and concerns for hematological 

effects. While EPA acknowledges that 

there is evidence to indicate that 

humans are less sensitive than rodents 

to the hematological effects associated 

with acute or short-term exposure to 

EGBE, little is known of the long-term 

or repeated exposure responses in 

humans to EGBE. Thus, some concern 

remains over the potential for 

hematological effects following a 

lifetime of exposure to EGBE. Unlike the 

hematological effects of EGBE, there is 

no evidence of humans’ decreased 

sensitivity to the reported liver effects 

relative to rodents. Therefore, EPA has 

concluded that EGBE meets the EPCRA 

section 313(d)(2)(B) listing criteria based 

on the available human health toxicity 

data. 

Because EPA believes that EGBE has 

moderately high to high chronic 

toxicity, EPA does not believe that an 

exposure assessment is appropriate for 

determining whether EGBE meets the 

criteria of EPCRA section 313(d)(2)(B). 

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–2015–0352. 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. American Chemistry Council. 2014. 

Petition of the American Chemistry 

Council’s Ethylene Glycol Ethers Panel 

To Remove Ethylene Glycol Monobutyl 

Ether From the Toxics Release Inventory 

Under Section 313 Of The Emergency 

Planning and Community Right-ToKnow Act of 1986. December 29, 2014. 

2. U.S. EPA. 2010. Toxicological review of 

Ethylene Glycol Monobutyl Ether 

(CASRN 111–76–2) in support of 

summary information on the Integrated 

Risk Information System (IRIS). U.S. 

Environmental Protection Agency. 

Washington, DC. http://www.epa.gov/

iris/toxreviews/0500tr.pdf. 

3. U.S. EPA. 2009. Technical Review of 

Ethylene Glycol Monobutyl Ether 

(EGBE): Chemistry, Environmental Fate 

and Ecological Toxicity CAS Registry 

Number 111–76–2. Office of 

Environmental Information. September 

9, 2009. 

4. U.S. EPA. 2015. Memorandum from 

Jocelyn Hospital, Toxicologist, 

Environmental Analysis Division to 

Megan Carroll, Acting Division Director 

of the Environmental Analysis Division. 

July 24, 2015. Subject: Review of the 

Data in the 2010 Integrated Risk 

Information System (IRIS) Toxicological 


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Review of Ethylene Glycol Monobutyl 

Ether (EGBE). 

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75. Devillers, J., Chezeau, A., Thybaud, E., 

Poulsen, J.-M., Graff, L., Vasseur, P., 

Chenon, P., Mouchet, F., Ferrier, V., 

Quiniou, F. 2002. Ecotoxicity of ethylene 

glycol monomethyl ether and its acetate. 

Toxicology Mechanisms and Methods. 

12: 241–254. 

76. INERIS. 1999. De ́termination de la 

toxicite ́ chronique du 2-butoxyethanol 

vis-a`-vis de l’algue d’eau douce 

Pseudokirchneriella subcapitata, 

Ba746d-CGR21427. Verneuil-en-Halatte, 

France, 14 december 1999, INERIS: 14. 

As cited in Ref. 77. 

77. ECB (European Chemicals Bureau). 2006. 

European Union Risk Assessment Report 

for 2-Butoxyethanol (EGBE). Vol. 68. 

European Commission. 

78. Bringmann, G., Kuhn, R. 1982. Results of 

the toxic action of water pollutants on 

Daphnia magna in an improved 

standardized procedure. Z. Wasser 

Abwasser Forsch. 15(1): 1–6. (In German) 

79. Juhnke, I., Luedemann, D. 1978. Results 

of the study of 200 chemical compounds 

on acute fish toxicity using the Golden 

Orfe test. Z. Wasser Abwasser Forsch. 

11(5): 161–164. (In German) 

80. Dow Chemical Co. 1979. Toxicity of 

Dowanol EB to freshwater organisms 

(redactor: Bartlett), 31 August 1979. As 

cited in Ref. 77. 

81. Dawson, G.W., Jennings, A.L., 

Drozdowski, D., Rider, E. 1975. The 

acute toxicity of 47 industrial chemicals 


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Federal Register / Vol. 80, No. 195 / Thursday, October 8, 2015 / Proposed Rules 60825 

1See 5 U.S.C. 603. The RFA, see 5 U.S.C. 601– 

612, has been amended by the Small Business 

Regulatory Enforcement Fairness Act of 1996 

(SBREFA), Public Law 104–121, Title II, 110 Stat. 

847 (1996). The SBREFA was enacted as Title II of 

the Contract with America Advancement Act of 

1996 (CWAAA). 

to fresh and saltwater fishes. Journal of 

Hazardous Materials. 1: 303–318. 

82. INERIS. 1999. De ́termination de la 

toxicite ́ aigue ̈ du 2-butoxyethanol vis-a`- 

vis de Oncorhynchus mykiss, 

unpublished, Ba746f-CGR21427. 

Verneuil-en-Halatte, France, 14 

december 1999, INERIS: 10. As cited in 

Ref. 77. 

83. Bridie, A.L., Wolff, C.J.M., Winter, M. 

1979. The acute toxicity of some 

petrochemicals to goldfish. Water Res. 

13(7): 623–626. 

84. Price, K.S., Waggy, G.T., Conway, R.A. 

1974. Brine shrimp bioassay and 

seawater BOD of petrochemicals. Journal 

WPCF. 46(1): 63–76. 

85. Bringmann, G., Kuhn, R. 1978. Threshold 

Values of Substances Harmful to Water 

for Blue Algae (Microcystis aeruginosa) 

and Green Algae (Scenedesmus 

quadricauda) in Tests Measuring the 

Inhibition of Cellular Propagation. Vom 

Wasser. 50:45 60 (in German) (English 

Abstract), Tr 80 0201, Literature 

Research Company: 22 p. 

86. Bringmann, G., Kuhn, R. 1978. Testing of 

Substances for Their Toxicity Threshold: 

Model Organisms Microcystis 

(Diplocystis) aeruginosa and 

Scenedesmus quadricauda. Mitt. Int. 

Ver. Theor. Angew. Limnol. 21: 275 284. 

87. Dill, DC, Milazzo, D.P. 1988. Dowanol PM 

Glycol Ether: Evaluation of the toxicity 

to the green alga, Selenastrum 

capricornutum Printz. Dow Chemical 

Company. EPA Document Control 

Number 86–890001160. 18 pages. 

88. INERIS. 1999. De ́termination de la 

toxicite ́ chronique du 2-butoxyethanol 

vis-a`-vis de Daphnia magna, Ba746a– 

CGR21427. Verneuil-en-Halatte, France, 

15 december 1999, INERIS: 13. As cited 

in Ref. 77. 

89. INERIS. 2001. Essai poisson 21 jours, 

Danio rerio, unpublished report, N° 

22685, 05.11.2001. As cited in Ref. 77. 

List of Subjects in 40 CFR Part 372 

Environmental protection, 

Community right-to-know, Reporting 

and recordkeeping requirements, and 

Toxic chemicals. 

Dated: September 24, 2015. 

Arnold E. Layne, 

Director, Office of Information Analysis and 

Access. 

[FR Doc. 2015–25674 Filed 10–7–15; 8:45 am] 

BILLING CODE 6560–50–P 

FEDERAL COMMUNICATIONS 

COMMISSION 

47 CFR Part 1 

[MD Docket No. 15–121; FCC 15–108] 

Assessment and Collection of 

Regulatory Fees for Fiscal Year 2015 

AGENCY: Federal Communications 

Commission. 

ACTION: Proposed rule. 

SUMMARY: In this document the 

Commission revises its Schedule of 

Regulatory Fees to recover an amount of 

$339,844,000 that Congress has required 

the Commission to collect for fiscal year 

2015. Section 9 of the Communications 

Act of 1934, as amended, provides for 

the annual assessment and collection of 

regulatory fees under sections 9(b)(2) 

and 9(b)(3), respectively, for annual 

‘‘Mandatory Adjustments’’ and 

‘‘Permitted Amendments’’ to the 

Schedule of Regulatory Fees. 

DATES: Comments are due November 9, 

2015 and Reply Comments are due 

December 7, 2015. 

FOR FURTHER INFORMATION CONTACT: 

Roland Helvajian, Office of Managing 

Director at (202) 418–0444. 

SUPPLEMENTARY INFORMATION: This is a 

summary of the Commission’s Further 

Notice of Proposed Rulemaking 

(FNPRM), FCC 15–108, MD Docket No. 

15–121, adopted on September 1, 2015 

and released on September 2, 2015. 

I. Administrative Matters 

A. Initial Regulatory Flexibility Analysis 

1. As required by the Regulatory 

Flexibility Act of 1980 (RFA),1 the 

Commission has prepared an Initial 

Regulatory Flexibility Analysis (FRFA) 

relating to this Further Notice of 

Proposed Rulemaking. 

B. Initial Paperwork Reduction Act of 

1995 Analysis 

2. This document does not contain 

new or modified information collection 

requirements subject to the Paperwork 

Reduction Act of 1995 (PRA), Public 

Law 104–13. In addition, therefore, it 

does not contain any new or modified 

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). 

C. Filing Instructions 

3. Pursuant to sections 1.415 and 

1.419 of the Commission’s rules, 47 CFR 

1.415, 1.419, interested parties may file 

comments and reply comments on or 

before the dates indicated on the first 

page of this document. Comments may 

be filed using the Commission’s 

Electronic Comment Filing System 

(ECFS). See Electronic Filing of 

Documents in Rulemaking Proceedings, 

63 FR 24121 (1998). 

• Electronic Filers: Comments may be 

filed electronically using the Internet by 

accessing the ECFS. 

• Paper Filers: Parties who choose to 

file by paper must file an original and 

one copy of each filing. If more than one 

docket or rulemaking number appears in 

the caption of this proceeding, filers 

must submit two additional copies for 

each additional docket or rulemaking 

number. 

Æ Filings can be sent by hand or 

messenger delivery, by commercial 

overnight courier, or by first-class or 

overnight U.S. Postal Service mail. All 

filings must be addressed to the 

Commission’s Secretary, Office of the 

Secretary, Federal Communications 

Commission. 

Æ All hand-delivered or messengerdelivered paper filings for the 

Commission’s Secretary must be 

delivered to FCC Headquarters at 445 

12th St. SW., Room TW–A325, 

Washington, DC 20554. The filing hours 

are 8:00 a.m. to 7:00 p.m. All hand 

deliveries must be held together with 

rubber bands or fasteners. Any 

envelopes and boxes must be disposed 

of before entering the building. 

Æ Commercial overnight mail (other 

than U.S. Postal Service Express Mail 

and Priority Mail) must be sent to 9300 

East Hampton Drive, Capitol Heights, 

MD 20743. 

Æ U.S. Postal Service first-class, 

Express, and Priority mail must be 

addressed to 445 12th Street SW., 

Washington, DC 20554. 

4. People with Disabilities: To request 

materials in accessible formats for 

people with disabilities (braille, large 

print, electronic files, audio format), 

send an email to fcc504@fcc.gov or call 

the Consumer & Governmental Affairs 

Bureau at 202–418–0530 (voice), 202– 

418–0432 (tty). 

D. Ex Parte Information 

5. This proceeding shall be treated as 

a ‘‘permit-but-disclose’’ proceeding in 

accordance with the Commission’s ex 

parte rules. Persons making ex parte 

presentations must file a copy of any 

written presentation or a memorandum 

summarizing any oral presentation 

within two business days after the 

presentation (unless a different deadline 

applicable to the Sunshine period 

applies). Persons making oral ex parte 

presentations are reminded that 

memoranda summarizing the 

presentation must list all persons 

attending or otherwise participating in 

the meeting at which the ex parte 

presentation was made, and summarize 

all data presented and arguments made 


Lhorne on DSK5TPTVN1PROD with PROPOSALS