For your information, the EPA recently published its review of the results of a delisting petition for ethylene glycol. Although the petition had been withdrawn, the EPA found that, "based on concerns for chronic maternal and developmental effects for the general population following acute inhalation exposure," delisting was not appropriate. The results follow.
Holly Lynch, Director of EHS Programs, IPC
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From: everybody[SMTP:[log in to unmask]]
Sent: Wednesday, May 07, 1997 10:31 AM
To: Multiple recipients of list
Subject: Ethylene Glycol;Toxic Chemical Release Reportin
[Federal Register: May 7, 1997 (Volume 62, Number 88)]
[Notices]
[Page 24919-24924]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr07my97-65]
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ENVIRONMENTAL PROTECTION AGENCY
[OPPTS-400110; FRL-5598-8]
Ethylene Glycol; Toxic Chemical Release Reporting; Community
Right-to-Know
AGENCY: Environmental Protection Agency (EPA).
ACTION: Notice.
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SUMMARY: EPA is issuing the results of its technical review and
evaluation of a petition to delete ethylene glycol from the list of
toxic chemicals subject to the reporting requirements under section 313
of the Emergency Planning and
[[Page 24920]]
Community Right-to-Know Act (EPCRA) and section 6607 of the Pollution
Prevention Act of 1990 (PPA). Since the petition to delete ethylene
glycol was withdrawn on October 28, 1996, there is no need for final
action by the Agency. However, the Agency has decided to issue its
findings in order to make publicly available the technical review and
subsequent scientific conclusion.
FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Acting Petitions
Coordinator, 202-260-3882 or e-mail: [log in to unmask],
for specific information regarding this document. For further
information on EPCRA section 313, contact the Emergency Planning and
Community Right-to-Know Information Hotline, Environmental Protection
Agency, Mail Stop 5101, 401 M St., SW., Washington, DC 20460, Toll
free: 1-800-535-0202, in Virginia and Alaska: 703-412-9877, or Toll
free TDD: 1-800-553-7672.
SUPPLEMENTARY INFORMATION:
I. Introduction
Section 313 of the Emergency Planning and Community Right-to-Know
Act (EPCRA) requires certain facilities manufacturing, processing, or
otherwise using listed toxic chemicals in amounts above reporting
threshold levels, to report their environmental releases of such
chemicals annually. Beginning with the 1991 reporting year, such
facilities also must report pollution prevention and recycling data for
such chemicals, pursuant to section 6607 of the Pollution Prevention
Act of 1990 (PPA), 42 U.S.C. 13106. Section 313 established an initial
list of toxic chemicals that was comprised of more than 300 chemicals
and 20 chemical categories. Ethylene glycol was included on the initial
EPCRA section 313 list of toxic chemicals. Section 313(d) authorizes
EPA to add or delete chemicals from the list, and sets forth criteria
for these actions. EPA has added and deleted chemicals from the
original statutory list. Under section 313(e)(1), any person may
petition EPA to add chemicals to or delete chemicals from the list.
Pursuant to EPCRA section 313(e)(1), EPA must respond to petitions
within 180 days, either by initiating a rulemaking or by publishing an
explanation of why the petition is denied.
EPCRA section 313(d)(2) states that a chemical may be listed if any
of the listing criteria are met. Therefore, in order to add a chemical,
EPA must demonstrate that at least one criterion is met, but does not
need to examine whether all other criteria are also met. Conversely, in
order to remove a chemical from the list, EPA must demonstrate that
none of the criteria are met.
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 compound categories. EPA has also published a
statement clarifying its interpretation of the section 313(d)(2)
criteria for adding and deleting chemical substances from the section
313 list (59 FR 61432, November 30, 1994) (FRL-4922-2).
II. Description of the Petition
On March 21, 1994, Bonded Products, Inc. petitioned the Agency to
delist ethylene glycol from the list of toxic chemicals subject to
reporting under section 313 of EPCRA and section 6607 of PPA. The
Bonded Products petition was based on the contention that: ethylene
glycol is biodegradable, rapidly loses its toxicity and, therefore, is
not expected to cause adverse environmental, or acute or chronic health
effects; and, that releases from the consumer use of ethylene glycol
are likely to be significantly higher compared to releases from
manufacturing facilities. The petitioners argued that ethylene glycol
does not meet any of the EPCRA section 313(d)(2) criteria for listing.
EPA staff reviewed the petition based on information and data that the
Agency retrieved from its own review of the literature, as well as
information supplied by other interested parties. On October 28, 1996,
Bonded Products withdrew their petition.
The review of Bonded Products, Inc.'s petition was complete prior
to their request for withdrawal, and the Agency has determined that it
is in the public's best interest and clearly in keeping with the
Community-Right-to-Know ethic to provide a summary of the chemical
review and conclusion. Bonded Products, Inc. or any other party may re-
petition the Agency on ethylene glycol at any time. The Agency remains
open to receiving and reviewing new information and re-evaluating its
position on this chemical as it relates to section 313 of EPCRA.
III. Technical Review of Ethylene Glycol
The technical review of the petition to delete ethylene glycol from
the EPCRA section 313 list of toxic chemicals included an analysis of
the relevant chemistry, metabolism and absorption, toxicity, and
exposure data available to the Agency for ethylene glycol. Summaries of
the analysis of each of these areas is provided in Units III.A. through
III.F. of this preamble, and a more complete discussion of this
information can be found in the EPA documents prepared for this
assessment (Refs. 1-14), which have been placed in the public docket
for this petition (Docket OPPTS-400110).
A. Chemistry, Use, and Production Profile
Ethylene glycol is a colorless, odorless, syrupy liquid with a
sweet taste. It has a relatively high boiling point (197.6 deg.C),
flash point (116 deg.C), autoignition temperature (412.93 deg.C), and
is relatively non-volatile at room temperature (Ref. 1). Ethylene
glycol absorbs water and can take up twice its weight of water at 100
percent relative humidity. Additionally, the substance reduces the
freezing point of water and is widely used as an antifreeze and deicer.
Ethylene glycol is generally produced by the noncatalytic, liquid
phase hydration of ethylene oxide (Ref. 1). Diethylene glycol,
triethylene glycol and tetraethylene glycol are co-products. Other
processes have been patented such as: (1) oxidation of ethylene in an
aqueous medium using an iron-copper catalyst; and (2) rhodium-catalyzed
production of ethylene glycol from synthesis gas (a mixture of carbon
monoxide and hydrogen from coal gasification) instead of ethylene.
There were 2.3 billion kilograms of ethylene glycol produced in
1992 and production has been fairly steady since the early 1980's (Ref.
2). Domestic consumption was 2.1 billion kilograms. The major end use
of ethylene glycol is in the production of polyethylene terephthalate
(PET), with 30 percent used for fibers and 22 percent used for films,
bottles, and other molded plastics, laminates, and castings (Ref. 2).
An additional 38 percent of ethylene glycol production is used in
antifreeze application, such as the principle ingredient of all-weather
automobile cooling system fluids, deicing solutions for aircraft and
pavement, and in fire extinguishers and sprinkler systems. The
remaining 10 percent of demand is in miscellaneous applications such as
a diluent and coupler in cutting fluids, as a solvent or coupling agent
for stains, dyes, resins, inks, soluble oils, and hydraulic fluids. It
is also used as a component in the manufacture of polyester laminating
resins and other plastics.
[[Page 24921]]
B. Metabolism and Absorption
Ethylene glycol itself appears to have relatively low toxicity, but
it is oxidized to a variety of more toxic metabolites such as
glycolaldehyde, glycolic acid, glyoxalic acid and oxalic acid (Ref. 6).
In general, the accumulation of these acids leads to acidosis (the
state that is characterized by actual or relative decrease of alkali in
body fluids in relation to the acid content). Present information
suggests that glycolic acid is the major toxic metabolite contributing
to metabolic acidosis, which is the underlying cause of systemic
toxicity following exposure to ethylene glycol.
Based on a comparison of metabolism studies, ethylene glycol
appears to be less well absorbed following dermal application than
following administration via oral gavage (Ref. 10). In addition, even
when an ethylene glycol aerosol is generated to maximize the amount
available for inhalation, the body burden remains fairly low. In the
study by Frantz et al. (Ref. 15), ethylene glycol and its metabolites
(glycolic acid and oxalic acid) were excreted in the urine of animals
dosed both orally and dermally. In contrast, the study by Marshall and
Cheng (Ref. 16) showed that after inhalation exposure to
<SUP>14</SUP>C-labeled ethylene glycol, the only <SUP>14</SUP>C-
containing material identified in the plasma and urine (both for the
aerosol and vapor) was unmetabolized ethylene glycol.
C. Human Toxicity Evaluation
The inherent toxicity of ethylene glycol is low relative to several
of its metabolites. The evidence for this comes from clinical studies
and laboratory investigations (Ref. 4). Ethanol is a competitive
inhibitor of alcohol dehydrogenase (ADH), the first enzyme in the
ethylene glycol metabolic pathway, and is very effective in treating
animal and human ethylene glycol poisonings. If treatment is started
early enough, the metabolic acidosis and renal failure discussed below
can be prevented.
1. Inhalation toxicity. Two inhalation developmental toxicity
studies have been conducted by the same group (Refs. 17 and 18). In a
whole body exposure study (Ref. 17), mice and rats were exposed to
ethylene glycol aerosols of 150, 1,000 or 2,500 milligrams per cubic
meter (mg/m<SUP>3</SUP>) for 6 hours/day on gestational days 6 through
15. The actual measured concentrations were 119, 888, or 2,090 mg/
m<SUP>3</SUP>. In rats, maternal toxicity occurred only at the highest
concentration and was indicated by a significant increase in absolute
and relative liver weight. In rats, evidence of prenatal developmental
toxicity (reduced ossification in the humerus, zygomatic arch, and the
metatarsals and proximal phalanges of the hindlimb) was observed at the
two higher concentrations. In mice, incidences of prenatal
developmental toxicity were increased at the two highest concentrations
and included malformations in the head (exencephaly), face (cleft
palate, foreshortened and abnormal face, and abnormal facial bones),
and skeleton (vertebral fusions, and fused, forked, and missing ribs).
The No Observed Adverse Effect Level (NOAEL) for maternal toxicity in
rats was 888 mg/m<SUP>3</SUP> and in mice was 119 mg/m<SUP>3</SUP>. The
NOAEL for developmental toxicity in rats was 119 mg/m<SUP>3</SUP> and
in mice was below this concentration.
A major confounding factor in this study was the deposition of a
detectable quantity of ethylene glycol upon the animals during
exposure. The animals could have received the chemical via the oral
route by preening or by dermal absorption, although much less would be
taken in via the skin. Analysis of the chemical on the fur of rats and
mice after the exposure period at the highest concentration indicated
that much of the chemical dose (65-95 percent) was potentially derived
from ingestion after grooming.
To address the potential confounding factor of multiple exposure
routes cited above, a further study used nose-only exposure of mice to
500, 1,000, and 2,500 mg/m<SUP>3</SUP> of ethylene glycol aerosol for 6
hours/day on gestational days 6 through 15 (Ref. 18). Results from the
positive control (whole body exposure to 2,100 mg/m<SUP>3</SUP>)
confirmed the results from the previous study. In the nose-only
portion, the two higher concentrations produced increased kidney
weights in the dams. At the highest concentration, fetal weights were
reduced and fetal skeletal variations and one fetal skeletal
malformation (fused ribs) were increased. The developmental NOAEL for
nose-only inhalation exposure was 1,000 mg/m<SUP>3</SUP>; the maternal
NOAEL was 500 mg/m<SUP>3</SUP>. The developmental NOAEL in this study
was at least 10 times the whole body value since a NOAEL was not
established in the previous whole body inhalation study but was less
than 119 mg/m<SUP>3</SUP>. The maternal NOAEL was approximately five
times the previous value. This nose-only exposure study indicates that
most of the adverse effects seen in the whole-body exposure study were
due to systemic exposure from noninhalation routes; however, as
discussed above, adverse effects were seen in the nose-only exposure
study.
The toxicity data strongly indicate that ethylene glycol is much
less toxic than its metabolites; however, it is not known if ethylene
glycol might act directly on embryos. The available literature does not
provide adequate data to allow definitive conclusions concerning
ethylene glycol's toxicity to embryos (Ref. 4).
2. Oral toxicity. Ethylene glycol is expected to be absorbed
through the skin and from the lung and the gastrointestinal tract.
After absorption, it is expected to enzymatically oxidize to oxalic
acid, glycolic acid, glycolaldehyde and carbon dioxide. The aldehyde
metabolites are believed to be responsible for neurotoxicity and the
oxalic acid metabolites for renal toxicity (Ref. 8).
a. Renal toxicity. The oral reference dose (RfD) for ethylene
glycol as established by the Agency's RfD/RfC (reference concentration)
working group is 2 milligrams per kilogram per day (mg/kg/day). An RfD
reflects the Agency's estimate of a level of daily exposure to the
human population (including sensitive subgroups) that is likely to be
without an appreciable risk of deleterious effects during a lifetime
(Ref. 19). The RfD for ethylene glycol is based on a feeding study by
DePass et al. (1986, as cited in EPA's Integrated Risk Information
System (IRIS), 1994; Ref. 20) in which the critical effect was kidney
toxicity. Groups of male and female rats (30/sex/group) and male and
female mice (20/sex/group) were fed diets containing ethylene glycol at
doses of 0, 40, 200, or 1,000 mg/kg/day for 2 years. Urinary calcium
oxalate crystals and increased kidney weight were seen in all high-dose
rats. Histopathologic changes in high-dose male rats included tubular
cell hyperplasia, tubular dilation, peritubular nephritis, parathyroid
hyperplasia, and generalized soft tissue mineralization. No adverse
effects were seen in rats of either sex at the mid or the low doses.
There were no adverse effects seen in mice of either sex at any dose
tested. The Lowest Observed Adverse Effect Level (LOAEL) was determined
to be 1,000 mg/kg/day and the NOAEL was 200 mg/kg/day. The RfD was set
with an uncertainty factor of 100, 10 for interspecies extrapolation
and 10 for differences in human sensitivity. Confidence in the study,
the uncertainty factor and the RfD was high.
b. Developmental/reproductive toxicity. IRIS includes a review of
several developmental reproductive studies with LOAELs at or near that
seen in the DePass study which was
[[Page 24922]]
used to set the oral RfD. These studies were not chosen as the basis
for the RfD since the LOAEL from the DePass study was somewhat lower
and the RfD was deemed protective of developmental effects. In a 3-
generation reproduction study, Lamb, as cited in IRIS (Ref. 20),
treated rats with 0, 40, 200, or 1,000 milligrams per kilogram (mg/kg)
in the diet and found no treatment related effects. In another study
cited in IRIS (Ref. 20), ethylene glycol was administered by gavage at
0, 50, 150, 500 or 1,500 mg/kg to 30 pregnant female CD-1 mice/group on
gestation days 6-15. Animals were sacrificed on gestation day 18 and
examined for signs of maternal and developmental toxicity. There was an
increase in skeletal abnormalities at both 500, and 1,500 mg/kg. A No
Observed Effect Level (NOEL) was established at 150 mg/kg for
developmental toxicity with a Lowest Observed Effect Level (LOEL) of
500 mg/kg.
c. Oncogenicity/carcinogenicity/mutagenicity. There is no evidence
that ethylene glycol is oncogenic or that it is a mutagen (Ref. 8).
d. Acute toxicity. Ethylene glycol is acutely toxic to humans; the
minimum lethal ingested dose for adults is approximately 1.4
milliliters per kilogram (ml/kg) or 100 ml for a 70 kg person (Ref. 8).
Signs of ethylene glycol poisoning can be divided into three stages.
Stage one includes central nervous system (CNS) disturbances and
gastrointestinal symptoms. Stage two includes signs of cardiovascular,
pulmonary, and metabolic irregularities and stage three includes renal
failure brought on by the precipitation of calcium oxalate crystals in
renal tubules and from the direct toxic action of oxalic and glycolic
acids upon the kidneys (Ref. 8).
D. Environmental Toxicity
Ethylene glycol appears to represent a low hazard to the
environment (Refs. 8 and 11). The freshwater aquatic toxicity data
range from a median effective concentration (EC<INF>50</INF>) of 4.4
grams per milliliter (g/ml) (duckweed) to a median lethal concentration
(LC<INF>50</INF>) of 111 g/ml (bluegill sunfish). Terrestrial toxicity
data range from a median lethal dose (LD<INF>50</INF>) of 1.65 grams
per kilogram (g/kg) for cats to 5.5 g/kg for dogs and 12 g/kg for mice.
Reports of animal poisonings that were reviewed, were the results
of accidental or intentional releases during consumer use. They were
not the result of environmental exposures that may result from releases
of ethylene glycol that are reasonably likely to come from TRI
reporting facilities under normal operating conditions.
E. Exposure Assessment
Ethylene glycol can be acutely toxic to humans. Therefore, an
assessment was conducted of the potential for adverse acute human
health effects to occur as a result of concentrations of ethylene
glycol that are reasonably likely to exist beyond facility site
boundaries as a result of continuous, or frequently recurring, releases
from facility sites (Refs. 5, 6, and 13). As discussed above in Unit
III.C. of this preamble, ethylene glycol produces adverse chronic
health effects only at relatively high doses and thus has low chronic
toxicity. Therefore, an exposure assessment was also conducted for
chronic health effects (Refs. 5, 6, and 21). For a discussion of the
use of exposure in EPCRA section 313 listing/delisting decisions, refer
to the Federal Register of November 30, 1994.
Ethylene glycol releases reported for 1992 were retrieved from the
Toxic Release Inventory System (TRIS) data base. The TRIAIR model, the
Office of Pollution Prevention and Toxics' (OPPT) program for assessing
releases of TRI chemicals to the atmosphere, was used to estimate
chronic concentrations and exposures resulting from releases of
ethylene glycol. The Point Plume (PTPLU) model was used to derive
estimates of acute concentrations and exposures resulting from
atmospheric releases. The TRIAIR model assumes a 99.9 percent
destruction efficiency for all releases that are reported as sent to
incinerations. A half-life of 22.6 hours in the atmosphere was used for
ethylene glycol in the assessment. Ethylene glycol is quite
biodegradable, but is not readily sorbed, volatilized, or hydrolyzed
(Ref. 6).
According to the 1992 releases obtained from TRIS, over 11.7
million pounds of ethylene glycol are released per year by about 940
facilities nationwide. Data from the Aerometric Information Retrieval
System (AIRS) Facility Subsystem were also considered. Based on review
of AIRS and the type of data available for ethylene glycol, it was
determined that the data for ethylene glycol are not adequate to
support an exposure assessment.
Eighteen states each discharging over 100,000 pounds per year
accounted for 93 percent of the total reported releases of ethylene
glycol to the atmosphere. These releases were used for chronic exposure
estimations. Each of the highest per-site discharges were used to
estimate concentrations and exposures under acute conditions.
Concentrations modeled with the PTPLU model can be expected to
occur up to 250 meters from the source, which may be beyond the
facility fenceline. The PTPLU model provides ground-level
concentrations which are hourly average values. Incorporating wind
conditions, three scenarios were generated: (1) The typical situation;
(2) the stagnation situation; and (3) the maximum situation. The
maximum scenario is anticipate to last for only 2 hours, as compared
with the 24-hour duration of the typical and stagnation scenarios. As
the name implies, the stagnation scenario incorporates relatively
little air movement. Each scenario was run for stack releases and for
fugitive releases. Assumptions made were conservative on the whole.
However, the assumption that releases occur over 365 days and 24 hours
a day is not conservative. If, for example, releases occurred over only
1 month, even with 24-hour a day discharge, the resulting exposure
estimates would increase by a factor of 12 or one order of magnitude.
F. Exposure Evaluation
1. Chronic inhalation exposure. In evaluating chronic inhalation
exposures, ideally, exposure estimates would be compared to an RfC.
However, in this case chronic inhalation information is neither readily
available nor abundant, so an RfC has not been derived for ethylene
glycol. In general, the oral RfD should not be used to evaluate
inhalation exposures to ethylene glycol because it appears that the
metabolism via the two routes is different. Specifically, this is
demonstrated by the lack of toxic metabolites of ethylene glycol found
in the urine and plasma of animals dosed via inhalation. Additionally,
it is believed that the proximate cause for the toxicity seen from
ethylene glycol is not attributed to the chemical itself but rather to
its metabolites. Therefore use of the oral RfD would tend to be overly
protective for inhalation effects from exposure to ethylene glycol. If,
however, the evaluation of the chronic exposure data indicates that
concentrations are below the RfD value, then the likelihood of
concentrations of concern existing for inhalation effects is greatly
diminished. For these reasons, the chronic exposures predicted were
compared to the oral RfD of 2 mg/kg/day. The comparison showed that
even the highest chronic exposures predicted for the chemical are, at a
minimum, an order of magnitude below the RfD. Therefore, it is not
predicted that concentrations of concern will exist for chronic
inhalation exposures to ethylene glycol as a result
[[Page 24923]]
of releases from TRI reporting facilities (Ref. 6).
2. Acute inhalation exposure. Although the oral RfD was used to
assess chronic inhalation exposures it was not used to assess acute
inhalation exposures. This is because oral RfDs are based on the
assumption of lifetime exposure (i.e., long-term exposure) and in most
cases are not appropriately applied to less-than-lifetime exposure
situations such as acute inhalation exposures. In addition, as
discussed above, it appears that ethylene glycol metabolism is
different via the oral and inhalation routes of exposure. Therefore,
instead of using the RfD, the acute inhalation assessment focused on
the generation of Margin of Exposure (MOE) calculations for inhalation
exposures. A MOE calculation is used in instances of non-cancer
endpoints and is essentially a ratio of the NOAEL or LOAEL and the
estimated exposure to the particular chemical, including any modifying
factors on the exposure (absorption, etc.). The resultant value is then
compared to the product of the uncertainty factors which are selected
for the chemical of interest. Uncertainty factors are generally factors
of 10 with each factor representing a specific area of uncertainty in
the available data. For ethylene glycol, a factor of 10 was introduced
to account for the possible differences in responsiveness between
humans and animals in prolonged exposure studies and a second factor of
10 was used to account for variation in susceptibility among
individuals in the human population. The resultant uncertainty factor
of 100 was therefore used in this assessment. This assessment focused
on maternal and developmental toxicity, which EPA believes are the most
significant adverse chronic effects caused by ethylene glycol. For the
generation of MOEs used in this assessment the NOAELs from the Tyl
study (Ref. 18) were utilized.
MOEs calculated from estimated stack emissions were below the
relevant uncertainty factors for the top two releasers for all exposure
scenarios for maternal toxicity. For developmental toxicity, MOEs below
the relevant uncertainty factors were calculated for the stagnant and
maximum exposure scenarios. MOEs calculated from fugitive releases
under the stagnant condition were also below the relevant uncertainty
factors for the top five releasers for both maternal and developmental
toxicity. A similar situation was observed under the maximum scenario
for maternal toxicity. Two things should be noted about the calculated
MOEs. The first is that all exposure estimates were driven by facility
specific data reported as required under EPCRA section 313. These
estimates are considered within the realm of possibility, although are
characterized as ``what if'' scenarios. These ``what if'' scenarios
provide a possible exposure level, without probability and are not
based on bounding or worst-case conditions which fall outside the
exposure curve. Second, there is limited information to suggest that no
metabolites are formed when ethylene glycol is inhaled. Since the
toxicity data indicates that the metabolites of ethylene glycol are
much more toxic than ethylene glycol itself, this normally would
greatly reduce the concern for inhalation exposure to this chemical.
However, adverse effects were noted in the 1995 Tyl study (Ref. 18)
with nose-only exposure in rodents, which indicates that ethylene
glycol is toxic via the inhalation route of exposure. Therefore, the
resultant NOAELs from that study were utilized in this acute inhalation
exposure assessment. Further, 100 percent of the inhaled dose of
ethylene glycol is assumed to be absorbed.
In summary, based on the concentrations likely to exist beyond
facility site boundaries and the resulting MOE calculations, there is a
potential for chronic maternal and developmental effects for the
general population following acute inhalation exposures to ethylene
glycol (Ref. 6).
3. Acute and chronic oral exposures. The potential dose rates
predicted for surface water driven oral exposures are identified as
bounding estimates and are, therefore, likely to be much higher than
actual exposures. Using the highest potential dose rate identified in
the exposure assessment of 80 mg/day and dividing by 70 kg (standard
assumption for body weight), a modified dose of 1.143 mg/kg/day was
calculated. This dose is below the RfD of 2 mg/kg/day indicating that
the exposure estimated is not likely to be associated with adverse
chronic health risks (Refs. 6 and 21).
None of the exposure data indicates that ethylene glycol will be
present beyond facility site boundaries at concentrations that can
reasonably be anticipated to cause the adverse acute human health
effects discussed under Unit III.C.2.d. of this preamble (Refs. 6 and
13). Therefore, it is unlikely that adverse acute human health effects
are reasonably likely to occur as a result of concentrations likely to
exist beyond facility site boundaries as a result of continuous, or
frequently recurring, releases of ethylene glycol.
G. Summary of Technical Review
The data indicate that, based on the doses required to cause
adverse effects, ethylene glycol has low chronic and acute toxicity to
humans both orally and by inhalation. The exposure analysis indicates
that ethylene glycol cannot 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 from facility
sites. The analysis of ethylene glycol's chronic toxicity concluded
that ethylene glycol can reasonably be anticipated to cause chronic
maternal and developmental effects in humans at relatively high doses.
It was also determined that concentrations of ethylene glycol that are
reasonably likely to exist beyond facility site boundaries as a result
of acute exposure scenarios are reasonably likely to be sufficient to
cause these chronic maternal and developmental effects. Based on
available literature, ethylene glycol represents a low hazard to the
environment and is not anticipated to cause environmental toxicity as a
result of reported releases of ethylene glycol from facility sites.
IV. Explanation
Since the petition to delete ethylene glycol has been withdrawn by
Bonded Products, Inc. EPA has no statutory responsibility to deny or
grant the initial request. However, because the technical review and
evaluation of the petition are complete, EPA determined that it is in
the public's best interest, and clearly in keeping with the Community
Right-to-Know ethic, to provide the public with a summary of EPA's
review and conclusion. Based on the technical review discussed above,
EPA concluded that this petition be denied based on concerns for
chronic maternal and developmental effects for the general population
following acute inhalation exposure from reported air releases of
ethylene glycol. EPA believes that ethylene glycol meets the toxicity
criteria of EPCRA section 313(d)(2)(B) based on the available chronic
maternal and developmental toxicity data and the exposure analysis.
V. References
1. USEPA, OPPT. Tou, Jenny; ``Chemistry Report on Ethylene Glycol,
EPCRA Section 313 Delisting Petition.'' (June 1, 1994).
2. USEPA, OPPT. Krueger, Susan; ``Economic Analysis of the Proposed
Delisting of Ethylene Glycol from the
[[Page 24924]]
EPCRA Section 313 Toxic Release Inventory.'' (May 16, 1994).
3. USEPA, OPPT. Memorandum from Pat Jennings, Exposure Assessment
Branch, Economics, Exposure, and Technology Division. Subject: Summary
of the Environmental Fate of Ethylene Glycol. (May 20, 1994).
4. USEPA, OPPT. Memorandum from Mary Henry, Health Effects Branch,
Health and Environmental Review Division. Subject: Ethylene Glycol
Petition. (August 3, 1995).
5. USEPA, OPPT. Memorandum from Patricia Harrigan, Exposure
Assessment Branch, Economics, Exposure, and Technology Division.
Subject: Expanded Exposure Assessment for Ethylene Glycol. (June 19,
1995).
6. USEPA, OPPT. Memorandum from Linda M. Rusak, Hazard Integrator,
Analysis and Information Management Branch, Chemical Screening and Risk
Assessment Division. Subject: Petition to Delist Ethylene Glycol from
TRI. (September 6, 1995).
7. USEPA, OPPT. Memorandum from Leonard C. Keifer, Chemist, Health
Effects Branch, Health and Environmental Review Division. Subject:
Metabolism of Ethylene Glycol. (March 29, 1995).
8. USEPA, OPPT. Memorandum from Angela Auletta, Chief, Health
Effects Branch, Health and Environmental Review Division. Subject:
Petition to Delist Ethylene Glycol from the Toxic Chemical Release
Inventory. (May 23, 1994).
9. USEPA, OPPT. Memorandum from Mary Henry, Health Effects Branch,
Health and Environmental Review Division. Subject: Review of
Developmental Toxicity Studies with Ethylene Glycol. (March 24, 1995).
10. USEPA, OPPT. Memorandum from Leonard C. Keifer, Chemist, Health
Effects Branch, Health and Environmental Review Division. Subject:
Review of Absorption/Metabolism Study for Ethylene Glycol Administered
via Inhalation and Comparison with Results from Dosing via Oral Gavage
and Dermal Administration. (August 1, 1995).
11. USEPA, OPPT. Memorandum from J. V. Nabholz, Health and
Environmental Review Division. Subject: Ethylene Glycol [107-21-1]:
Wildlife Poisoning. (December 5, 1995).
12. USEPA, OPPT. Memorandum from Patricia Harrigan, Exposure
Assessment Branch, Economics, Exposure, and Technology Division.
Subject: Comparison of 1993 Releases of Ethylene Glycol. (August 24,
1995).
13. USEPA, OPPT. Memorandum from Linda M. Rusak, Hazard Integrator,
Analysis and Information Management Branch, Chemical Screening and Risk
Assessment Division. Subject: Ethylene Glycol, Acute Risk Assessment.
(December 16, 1994).
14. USEPA, ORD. Memorandum from Carole Kimmel, National Center for
Environmental Assessment. Subject: Review of Ethylene Glycol Risk
Assessment for EPCRA Section 313 Delisting Petition. (November 2,
1995).
15. Frantz, S.W. et al., ``Ethylene Glycol: Comparison of
Pharmacokinetics and Material Balance Following Single Intravenous,
Oral and Cutaneous Administration to Male and Female Sprague-Dawley
Rats.'' Bushy Run Research Center, Export, PA. Project Report 51-543.
(March 24, 1989).
16. Marshall, Thomas C. and Yung Sung Cheng. ``Deposition and Fate
of Inhaled Ethylene Glycol Vapor and Condensation Aerosol in the Rat.''
Fundamental and Applied Toxicology. v. 3, (1983), pp. 175-181.
17. Tyl, R.W. et al., ``Evaluation of the Developmental Toxicity of
Ethylene Glycol Aerosol in the CD Rat and CD-1 Mouse by Whole-Body
Exposure.'' Fundamental and Applied Toxicology. v. 24, (1995), pp. 57-
75.
18. Tyl R.W. et al., ``Evaluation of the Developmental Toxicity of
Ethylene Glycol Aerosol in CD-1 Mice by Nose-Only Exposure.''
Fundamental and Applied Toxicology. v. 27, (1995), pp. 49-62.
19. IRIS. 1994. ``Glossary of Risk Assessment-Related Terms.'' U.S.
Environmental Protection Agency's Integrated Risk Information System.
(February 1, 1994).
20. IRIS. 1994. U.S. Environmental Protection Agency's Integrated
Risk Information System file pertaining to Ethylene Glycol. (March 8,
1994).
21. USEPA, OPPT. Memorandum from Linda M. Rusak, Hazard Integrator,
Analysis and Information Branch, Chemical Screening and Risk Assessment
Division. Subject: Ethylene Glycol, Chronic Risk Assessment. (August
19, 1996).
VI. Administrative Record
The record supporting this notice is contained in docket control
number OPPTS-400110. All documents, including the references listed in
Unit V. above and an index of the docket, are available to the public
in the TSCA Non-Confidential Information Center (NCIC), also known as
the Public Docket Office, from noon to 4 p.m., Monday through Friday,
excluding legal holidays. The TSCA NCIC is located at EPA Headquarters,
Rm. NE-B607, 401 M St., SW., Washington, DC 20460.
List of Subjects
Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, and Toxic chemicals.
Dated: April 28, 1997.
Lynn R. Goldman,
Assistant Administrator for Prevention, Pesticides and Toxic
Substances.
[FR Doc. 97-11902 Filed 5-7-97; 8:45 am]
BILLING CODE 6560-50-F
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