Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21929

ENVIRONMENTAL PROTECTION

AGENCY

[FRL–6974–2]

RIN 2060–AI72

Hazardous Air Pollutants List

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice of denial of a petition to

delist methanol from the list of

hazardous air pollutants.

SUMMARY: This notice announces EPA’s

decision to deny a petition from the

American Forest and Paper Association

(AF&PA) requesting that EPA remove

the chemical methanol (CAS No. 67–56–

1) from the list of hazardous air

pollutants (HAP) in section 112(b)(1) of

the Clean Air Act (CAA). Petitions to

delist a substance from the HAP list are

permitted under section 112(b)(3) of the

CAA.

The EPA is denying the petition

because we cannot conclude that there

are adequate data to determine that

emissions of methanol may not

reasonably be anticipated to cause any

adverse effects to human health. This

decision is based on our examination of

the available information concerning the

potential hazards of and projected

exposures to methanol emissions. We

have determined that the appropriate

health-based criterion for evaluating the

risks associated with methanol

emissions is the range of 0.3 to 30

milligrams per cubic meter (mg/m3). To

demonstrate that exposures are

reasonably anticipated not to result in

any adverse effects to humans,

including sensitive subpopulations, the

estimated 24-hour exposure

concentrations would need to be 0.3

mg/m3 or lower. Our review of the

petitioner’s exposure assessment leads

us to conclude that maximum 24-hour

exposures could be in the range of 2 to

7 mg/m3, which is well above 0.3

mg/m3. Because the criteria for

removing a substance from the list of

HAP have not been met, EPA must deny

the petition. Moreover, any future

petition for the removal of methanol

from the list of HAP will be denied as

a matter of law unless such future

petition is accompanied by substantial

new information or analysis.

FOR FURTHER INFORMATION CONTACT: Mr.

Chuck French, Emission Standards

Division (MD–13), Office of Air Quality

Planning and Standards, U.S. EPA,

Research Triangle Park, North Carolina

27711, telephone (919) 541–0467,

electronic mail address:

french.chuck@epa.gov.

SUPPLEMENTARY INFORMATION: Docket.

The EPA has compiled a docket, No. A–

99–23, that contains documents relevant

to this notice of denial. The docket

reflects the full administrative record for

this action and includes all the

information relied upon by the EPA in

the development of this notice of denial.

The docket is a dynamic file because

material is added throughout the

decision process. The docketing system

is intended to allow members of the

public and industries to readily identify

and locate documents. It is available for

public review and copying between 8:30

a.m. and 5:30 p.m., Monday through

Friday (except for Federal holidays) at

the following address: U.S. EPA, Air

and Radiation Docket and Information

Center (6102), 401 M Street, SW,

Washington, DC 20460. The docket is

located at the above address in Room

M–1500, Waterside Mall (ground floor).

Alternatively, copies of the docket

index, as well as individual items

contained within the docket, may be

mailed on request from the Air Docket

by calling (202) 260–7548 or (202) 260–

7549. A reasonable fee may be charged

for copying docket materials.

World Wide Web (WWW)

In addition to being available in the

docket, an electronic copy of this notice

will be available on the WWW through

the Technology Transfer Network

(TTN). Following signature, a copy of

the notice will be posted on the TTN’s

policy and guidance page at http://

www.epa.gov/ttn/oarpg. The TTN

provides information and technology

exchange in various areas of air

pollution control. If more information

regarding the TTN is needed, call the

TTN HELP line at (919) 541–5384.

Judicial Review

Today’s final action denying AF&PA’s

petition to remove methanol from the

list of HAP constitutes an order under

section 112 of the CAA that is based on

a determination of nationwide scope

and effect. Pursuant to section 307(b)(1)

of the CAA (42 U.S.C. 7607(b)(1)), a

petition for review of this action may be

filed only in the United States Court of

Appeals for the District of Columbia,

and must be filed within 60 days from

the date of publication of this final

action.

Outline

This notice is organized as follows:

I. Background

II. Criteria for Delisting

III. Evaluation of the Petition and Subsequent

Material

A. Submission of the Petition and

Subsequent Material

B. Uses, Sources, and Chemical

Characteristics of Methanol

C. Methanol Health Effects Analysis

D. Sources of Methanol Emissions and

Maximum Levels of Exposure

E. Risk Characterization

F. Other Elements of the Petition

IV. Denial of the Petition

I. Background

Section 112 of the CAA contains a

mandate for EPA to evaluate and control

emissions of HAP. Section 112(b)(1)

presents the list of HAP which includes

a list of specific chemical compounds

and compound classes used to identify

source categories for which EPA must

promulgate emissions standards. The

EPA is required to periodically review

the list of HAP and, where appropriate,

revise this list by rule. In addition,

under section 112(b)(3), any person may

petition the EPA to modify the list by

adding or deleting one or more

substances. A petition to remove a HAP

from the HAP list must demonstrate that

there are adequate data on the health

and environmental effects of the

substance to determine that emissions,

ambient concentrations,

bioaccumulation, or deposition of the

substance may not reasonably be

anticipated to cause any adverse effects

to human health or the environment.

The petitioner must provide a detailed

evaluation of the available data

concerning the substance’s potential

adverse health and environmental

effects and characterize the potential

human and environmental exposures

resulting from emissions of the

substance.

On March 8, 1996, the AF&PA

submitted a petition to delete the

chemical methanol (methyl alcohol,

methyl hydroxide, wood alcohol, wood

spirit) (CAS No. 67–56–1) from the HAP

list. Following receipt of the petition,

we conducted a preliminary evaluation

to determine whether the petition was

complete according to Agency criteria.

To be deemed complete, a petition must

consider all relevant available health

and environmental effects data. A

petition must also provide

comprehensive emissions data,

including peak and annual average

emissions for each source or for a

representative selection of sources, and

must estimate the resultant exposures of

people living in the vicinity of the

sources. In addition, a petition must

address the environmental impacts

associated with emissions to the

ambient air and impacts associated with

the subsequent cross-media transport of

those emissions. The petitioner

submitted several supplements to the

petition between March 1997 through

February 1999 to address deficiencies

21930 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

1We received eighteen submissions in response

to the request for comments concerning the

methanol petition. The submissions are in the

docket. Fifteen of these were from various industry

groups and supported the removal of methanol from

the HAP list. The other three comments received

were from States opposed to the petition. We

considered all comments during our technical

review.

2A denial with prejudice serves a vital

administrative purpose. It prevents the endless resubmission of essentially identical petitions (with

only peripheral or trivial changes) in the wake of

an EPA decision on the merits of a petition.

Thereby, once EPA has denied a petition to delist

based on a full consideration of the merits, any

future petition to remove the same chemical will

not trigger another full evaluation of the merits

unless it includes substantial data or analyses that

were not present in the earlier petition. Conversely,

EPA may issue a denial without prejudice, for

example, where there has not been a complete

examination of the merits of a petition, and where,

therefore, EPA has not reached a decision on the

petition that is based on a robust evaluation of the

underlying technical data and analyses. For

example, where a petition obviously lacks some

element necessary for EPA to properly evaluate the

petition, EPA may deny such petition without

prejudice and allow the petitioner to re-submit the

petition with the necessary additional information

without a determination that the additional

information constitutes substantial new data or

analysis. See, e.g., Notice of Denial, January 13,

1993 (58 FR 4164) (denying without prejudice a

petition to remove five glycol ethers from the list

of HAP).

identified during the completeness

review. We determined the petition to

delete methanol to be complete, and we

published a notice of receipt of a

complete petition in the Federal

Register on July 19, 1999 (64 FR 38668).

We also requested comment on the

petition, including a request for

additional data relevant to EPA’s

consideration of the petition.1

II. Criteria for Delisting

Section 112(b)(2) of the CAA requires

the EPA to make periodic revisions to

the initial list of HAP, outlines the

criteria to be applied in deciding

whether to add or delete a substance

from the list and identifies pollutants

that should be listed as:

* * * pollutants which present, or may

present, through inhalation or other routes of

exposure, a threat of adverse human health

effects (including, but not limited to,

substances which are known to be, or may

reasonably be anticipated to be, carcinogenic,

mutagenic, teratogenic, neurotoxic, which

cause reproductive dysfunction, or which are

acutely or chronically toxic) or adverse

environmental effects whether through

ambient concentrations, bioaccumulation,

deposition, or otherwise ***.

To assist the EPA in making

judgments about whether a pollutant

causes adverse environmental effects,

section 112(a)(7) defines an ‘‘adverse

environmental effect’’ as:

* * * any significant and widespread

adverse effect, which may reasonably be

anticipated, to wildlife, aquatic life, or other

natural resources, including adverse impacts

on populations of endangered or threatened

species or significant degradation of

environmental quality over broad areas.

Section 112(b)(3) establishes general

requirements for petitioning the Agency

to modify the HAP list by adding or

deleting a substance. Although the

Administrator may add or delete a

substance on his or her own initiative,

when EPA receives a petition to add or

delete a substance from the list, the

burden is on the petitioner to include

sufficient information to support the

request under the substantive criteria set

forth in section 112(b)(3)(B) and (C). The

statute directs the Administrator to

either grant or deny a petition within 18

months of receipt. If the Administrator

decides to grant a petition, the Agency

publishes a written explanation of the

Administrator’s decision, along with a

proposed rule to add or delete the

substance. The proposed rule is open to

public comment and public hearing and

all additional substantive information

received is considered prior to the

issuance of a final rule. If the

Administrator decides to deny the

petition, the Agency publishes a notice

of its denial, along with a written

explanation of the basis for denial. A

decision to deny a petition is a final

Agency action subject to review in the

DC Circuit Court of Appeals under

section 307(b) of the CAA.

To promulgate a final rule deleting a

substance from the HAP list, section

112(b)(3)(C) provides that the

Administrator must determine that:

* * * there is adequate data on the health

and environmental effects of the substance to

determine that emissions, ambient

concentrations, bioaccumulation or

deposition of the substance may not

reasonably be anticipated to cause any

adverse effects to the human health or

adverse environmental effects.

We do not interpret section

112(b)(3)(C) to require absolute certainty

that a pollutant will not cause adverse

effects on human health or the

environment before it may be deleted

from the list. The use of the terms

‘‘adequate’’ and ‘‘reasonably’’ indicate

that the Agency must weigh the

potential uncertainties and their likely

significance. Uncertainties concerning

the risks of adverse health or

environmental effects may be mitigated

if we can determine that projected

exposures are sufficiently low to

provide reasonable assurance that such

adverse effects will not occur. Similarly,

uncertainties concerning the magnitude

of projected exposures may be mitigated

if we can determine that the levels

which might cause adverse health or

environmental effects are sufficiently

high to provide reasonable assurance

that exposures will not reach harmful

levels. However, the burden remains on

a petitioner to demonstrate that the

available data support an affirmative

determination that emissions of a

substance may not be reasonably

anticipated to result in adverse effects

on human health or the environment

(that is, EPA will not remove a

substance from the list of HAP based

merely on the inability to conclude that

emissions of the substance will cause

adverse effects on human health or the

environment). As a part of the requisite

demonstration, a petitioner must resolve

any critical uncertainties associated

with missing information. We will not

grant a petition to delist a substance if

there are major uncertainties which

need to be addressed before we would

have sufficient information to make the

requisite determination.

A denial of a petition may take one of

two forms, it may either be a denial with

prejudice, in which case any future

petition will be denied as a matter of

law unless it is accompanied by

substantial new evidence; or it may be

a denial without prejudice, in which

case EPA will consider future petitions

without the presentation of substantial

new evidence. The EPA will issue a

denial with prejudice when there are

adequate data available which lead EPA

to conclude that emissions of a

substance can be anticipated to result in

adverse effects to human health or the

environment; or when EPA concludes

that the available evidence cannot

support a determination that a

substance may not reasonably be

anticipated to result in adverse effects to

human health or the environment and,

therefore, that substantial new

information or analyses would be

necessary to allow the Agency to make

such a determination. Today’s denial is

a denial with prejudice because EPA

concludes that the available evidence

(the data and analysis upon which the

petitioner relies) cannot support a

determination that methanol emissions

may not reasonably be anticipated to

result in adverse effects to human health

or the environment.2

III. Evaluation of the Petition and

Subsequent Material

A. Submission of the Petition and

Subsequent Material

The original petition submitted on

March 6, 1996, and the supplemental

materials provided by AF&PA up

through February 18, 1999, contain

information on chemical characteristics

Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21931

of methanol, emissions sources, fate and

transport, exposure, toxicity,

atmospheric transformation, and

environmental impacts. We determined

that these materials constituted a

complete petition, and that AF&PA’s

petition was complete as of February 18,

1999. In October 1999, during the

technical review of the complete

petition, a significant new study,

sponsored by the Health Effects Institute

(HEI), titled ‘‘Reproductive and

Offspring Developmental Effects

Following Maternal Inhalation Exposure

to Methanol in Nonhuman Primates’’

(Burbacher, et al., 1999) (hereinafter the

‘‘Burbacher Primate Study’’), was

published in the HEI Research Report

Number 89 (i.e., HEI Report) along with

commentary by the HEI Health Review

Committee. Because of the direct

relevance of this information, we

considered the Burbacher Primate

Study, as well as the entire HEI Report

in our technical review. Moreover, the

petitioner provided EPA with additional

materials on November 13, 1999 and

July 3, 2000, in support of the original

petition. These materials provided

comments, opinions and interpretations

regarding the data presented in the

Burbacher Primate Study.

B. Uses, Sources, and Chemical

Characteristics of Methanol

Methanol is used as a solvent in

various adhesives, cleaners, and inks.

Other sources include wood pulping;

combustion of biomass, refuse, and

plastics; and manufacture of petroleum,

charcoal, and plastics. The petition

describes methanol as a simple alcohol

containing one carbon atom. Methanol

is reported to occur naturally as an

emission resulting from metabolism in

vegetation, microorganisms, and insects.

It has also been found in volcanic gases.

Methanol is produced during the

natural biodegradation of organic wastes

of all kinds, including sewage and

wastewater sludge, by microorganisms

normally found in the environment.

C. Methanol Health Effects Analysis

In the materials submitted between

March 1996 and February 1999, the

petitioner presents an evaluation of the

available health effects data, including

human and laboratory animal studies.

The petition states that there is a

significant amount of data on methanol

toxicity to both animals and humans.

Most of the data relate to acute exposure

through ingestion and, to a lesser

degree, acute inhalation exposures,

although there are also numerous

studies of sub-chronic and chronic

inhalation exposures at low

concentrations. The petition describes

four studies of exposed human workers

and several studies of mice, rats, dogs,

and nonhuman primates.

Based on negative results in

mutagenicity testing, the petition asserts

that methanol is not likely to be

genotoxic. Moreover, based on testing in

mice for 18 months and rats for 24

months, and on an understanding of

methanol’s metabolism and likely mode

of action, the petition states that there

is no evidence to indicate, nor reason to

believe, that methanol is carcinogenic.

The petitioner proposes that the

primary adverse effects of methanol that

occur after acute high exposures are

metabolic acidosis and central nervous

system effects including eye damage.

These acute toxic effects result from

saturation of a metabolic pathway that

results in accumulation of formate.

Other effects reported in four

epidemiology studies of clerical workers

exposed to high concentrations of

methanol include headaches, nausea,

and blurred vision.

The petition states that there are no

reports of reproductive or

developmental effects in humans due to

methanol exposures. However,

laboratory inhalation studies have

shown reproductive and developmental

effects in animals exposed to relatively

high concentrations. The petitioner

determined that the most sensitive toxic

endpoint from the available studies was

developmental effects (ossification of

cervical ribs) in mice exposed in the

womb as identified in a study by Rogers,

et al. 1993. In that study, pregnant mice

were exposed by inhalation to methanol

concentrations ranging from 1,300 to

19,500 mg/m3 for 7 hours per day on

days 6–15 of pregnancy. The noobservable-adverse-effect-level (NOAEL)

reported in the Rogers mouse study is

1,300 mg/m3.

No EPA inhalation reference

concentrations (RfC) are currently

available for methanol to assess the

potential for adverse human health

effects due to inhalation exposure.

Therefore, the petitioner conducted a

dose-response assessment with the

available toxicity data to derive a

similar health-based criterion called a

‘‘safe exposure level’’ (SEL). The

petitioner asserts that exposures at or

below the SEL can be expected to

produce no adverse human health

effects from lifetime inhalation

exposures. The SEL was derived based

on an approach similar to the EPA RfC

methodology, which incorporated the

identification of the most sensitive toxic

endpoint from a critical study and a

corresponding NOAEL, an adjustment of

the NOAEL from an animal exposure

concentration to an equivalent human

exposure concentration, and application

of selected uncertainty factors.

The petitioner identified the Rogers

mouse study as the critical study with

a NOAEL of 1,300 mg/m3. To determine

the human-equivalent concentration

(HEC) of methanol, the petitioner used

this NOAEL and converted it to a

human-equivalent NOAEL by

multiplying the animal species NOAEL

by the ratio of a breathing rate divided

by the body weight of the animal

species to the same parameters for

humans, which resulted in a HEC of

8,300 mg/m3. Application of a standard

10-fold uncertainty factor for

interspecies extrapolation and another

standard 10-fold uncertainty factor for

individual variation in the population

results in a calculated SEL of 83 mg/m3.

To support the claim that the SEL is

safe, the petitioner presents information

on background body levels in humans.

Methanol is found in the body without

exogenous exposures to the chemical in

ambient air. This background body

concentration, which is approximately

1–2 milligrams/liter (mg/l) methanol in

blood, is attributed to both natural

metabolic processes and dietary sources

(such as fresh fruit and vegetables,

fermented beverages, and Aspartamesweetened diet beverages). The

petitioner predicts, using

pharmacokinetic (PK) models, that

steady state blood methanol levels in

humans exposed to 83 mg/m3 are

similar to typical measured background

levels in humans.

The EPA is unconvinced by the

petitioner’s human health effects

assessment and the proposed SEL. We

conclude that the petitioner’s SEL is not

an appropriate criterion for decision

making for this petition. In fact, as

discussed later in today’s notice, we

have derived a range for a health-based

decision criterion that includes values

that are significantly lower than the

petitioner’s SEL. Our concerns about the

health effects assessment and the SEL,

which are explained below, are the basis

for our denial of the petition to remove

methanol from the HAP list.

We agree with the petitioner that the

available evidence does not suggest that

methanol is genotoxic or that it is likely

to be carcinogenic. We agree that

documented adverse effects of methanol

after acute high exposures include

metabolic acidosis and central nervous

system effects, including eye damage.

We also agree that developmental effects

could be one of the most, or the most,

sensitive endpoint and could occur after

acute or chronic exposures. However, as

shown in the Burbacher Primate Study,

reproductive effects could also be

21932 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

considered among the most sensitive

endpoints.

The petitioner derived its proposed

SEL using the available information in

much the same way that EPA might use

this information to derive an RfC. A

specified NOAEL from a critical study

(Rogers et al.) was identified and

adjusted to an HEC yielding a

NOAEL(HEC) of 8,300 mg/m3. This

value was then divided by uncertainty

factors of 10-fold each for interspecies

extrapolation and for intraspecies

variability to produce an SEL of 83 mg/

m3.

In response to suggestions by EPA

scientists in 1996, the petitioner made

no duration adjustment of the NOAEL

in calculating the HEC. However, the

question of whether and how

developmental effects data should be

duration-adjusted has been a matter of

ongoing discussion within the Agency

and the broader scientific community.

Although the specific protocol for

acceptable duration-adjustment remains

to be more fully developed, we believe

the current state of scientific

understanding differs from the

understanding in 1996 and tends to

support incorporating durationadjustment in the petitioner’s derivation

of the SEL for methanol. In order to be

public-health protective, since either the

chemical or its damage may accumulate,

current risk assessment procedures

adjust for duration of exposure, i.e.,

adjust short-term inhalation exposures

associated with adverse effects by a

concentration times time (‘‘c × t’’) factor

in order to derive health risk estimates

for longer-term exposures. To durationadjust the NOAEL, the concentration

would be multiplied by an additional

factor of 7/24 hrs/day (because Rogers et

al. exposed the mice for 7 hrs/day). In

this case, the resulting SEL would be 24

mg/m 3.

We also note that the petitioner’s SEL

analysis did not employ available

techniques such as the benchmark dose

(BMD) method to utilize more of the

data from Rogers et al. to characterize

the dose-response relationship. Current

EPA practice in deriving RfC is to apply

the BMD method whenever the data are

appropriate for its application. This

method has been used relatively

recently in health assessments for

several pollutants (such as

methylmercury, carbon disulfide,

antimony trioxide, manganese, and

diesel exhaust), which are available in

the EPA’s Integrated Risk Information

System (IRIS). We did not require the

petitioner to specifically include a BMD

approach as part of the completeness

review. However, we suggested to the

petitioner (in a letter dated September

30, 1998) that the health hazard

assessment could be strengthened by

utilizing more than one method to

derive the SEL. For example, we stated

that using the EPA’s BMD method

would provide a useful comparison to

the petitioner’s approach.

A BMD analysis was included in the

published paper by Rogers et al. and

yielded 305 parts per million (ppm)

(approximately 400 mg/m 3) as the

BMDL–5 (lower 95 percent confidence

limit on the maximum likelihood

estimate for a 5 percent added risk for

the incidence of cervical ribs). We have

conducted additional but still

preliminary BMD analyses on data from

the study by Rogers et al. using various

mathematical models in conjunction

with the EPA BMD software under

development. By our initial

calculations, a BMDL–5 for excess risk

of cervical ribs could fall in a range from

roughly 195 to 325 mg/m 3. The

difference between this range of

estimates and the value reported by

Rogers et al. is due in part to differences

in the calculation of added risk versus

excess risk, as well as other minor

differences in the treatment of the data.

If the BMDL–5 value we have calculated

were used instead of the NOAEL in the

petitioner’s derivation of their SEL, the

resulting SEL would be roughly 4–7 fold

lower, or on the order of 10–20 mg/m3,

assuming that the BMDL–5 is used as an

alternative for a NOAEL and the same

uncertainty factors are applied.

Incorporating the duration-adjustment

noted above would yield an SEL on the

order of 4–6 mg/m3.

Also in response to our previous

suggestions, the petitioner provided a

supplementary analysis in August 1997

of PK data for experimental animals

exposed to methanol by inhalation. This

analysis involved dosimetric

adjustments of the exposure

concentrations based on either a default

value or data from various publications

(Perkins et al., 1995; Horton et al.,

1992). The petitioner concluded that the

PK data supported their use of the

default dosimetric adjustment and

indicated that the default value

provided a conservative (protective)

SEL. A more refined model of methanol

inhalation pharmacokinetics (Fisher et

al., 1999) has recently become available.

That model appears to suggest that

relative respiratory uptake in monkeys

may be less than previously understood.

To the extent that respiratory uptake in

humans approximates that of nonhuman

primates, this finding may tend to

support the petitioner’s claim that the

default dosimetric adjustment is

conservative in the case of the mouse

data. However, the default adjustment

would still be used and, thus, no change

in the SEL is implied on this basis.

In October 1999, several months after

the petition was determined to be

complete, the Burbacher Primate Study

was released by the HEI. This study was

funded through the HEI and published

after a thorough review by an ad hoc

peer review panel, as well as the

standing HEI Health Review Committee,

both of which comprised wellrecognized, independent, scientific

experts.

In that study, Burbacher et al. exposed

11–12 adult female rhesus macaque

monkeys per group to 0, 200, 600, or

1,800 ppm (0, 260, 780, 2,300 mg/m 3)

methanol vapors for 2.5 hours/day, 7

days/week, prior to and after

conception, but terminating before

parturition. The investigators measured

reproductive performance of the

mothers and also evaluated the offspring

at regular intervals during the first 9

months of life to assess their growth and

neurobehavioral development. They

also conducted PK studies to determine

whether methanol disposition

(absorption, distribution, metabolism,

and excretion) was altered by repeated

methanol exposures.

No significant effects in reproductive

function distinguished the methanolexposed adult groups from the control

group, except for a statistically

significant (p = 0.03) decrease in the

duration of pregnancy. Pregnancies

resulting in live births were about 6–8

days (5 percent) shorter in the

methanol-exposed groups. However, as

described below, there are uncertainties

and ongoing debate as to whether this

decrease is related to methanol

exposures.

With regard to effects on the offspring,

the investigators evaluated growth

measures and various neurological

functions. The only significant effect in

growth measures was a severe wasting

syndrome that became evident in two

female offspring from the 1800 ppm

group at 1–1.5 years of age. Again, as

described below, there is uncertainty

and debate as to whether this wasting

was due to methanol exposure or some

other factors.

Neurobehavioral development was

evaluated in several ways, including

clinical assessments, as well as objective

tests of sensorimotor development,

visual acuity, memory, and social

interaction. Two effects were reported.

First, a concentration-related delay in

sensorimotor development was

measured in male offspring during the

first month of life. As reflected in the

infant’s ability to reach for, grasp, and

retrieve a small object, sensorimotor

development was delayed by

Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21933

3This interpretation is necessary in order to avoid

situations where EPA might otherwise have

insufficient time to adequately review and analyze

substantive information submitted by a petitioner at

or near the end of the statutory time period. See

CAA section 112(b)(3)(D). However, it is entirely

within a petitioner’s discretion to direct EPA to

either proceed with a determination without

looking at such material, or to re-submit the petition

with the new substantive material.

4The five experts were as follows: David G. Hoel,

PhD., from Medical University of Texas; Anthony

R. Scialli, M.D., from Georgetown University;

Thomas B. Starr, PhD., from TBS Associates; and

Alice F. Tarantal, PhD., from University of

California, Davis.

approximately 9 days for the 200 ppm

group to more than 2 weeks for the 600

and 1,800 ppm groups. In addition, the

offspring prenatally exposed to

methanol did not perform as well as

controls on the Fagan Test of Infant

Intelligence. The Fagan test has been

shown to reflect information processing,

attention, and visual memory function

in human and nonhuman primate

infants and has been proven to be

sensitive to the effects of prenatal

exposure to toxic chemicals such as

methylmercury and polychlorinated

biphenyls (PCB), as well as correlating

well with IQ measures in children at

later ages. The test is based on the

ability of an infant to recognize

previously seen visual stimuli and

distinguish them from novel stimuli. A

higher level of cognitive function is

implied by a tendency to attend

preferentially to a novel stimulus. All

three groups of prenatally methanolexposed infants failed to show a

significant preference for novel social

stimuli (pictures of monkey faces),

whereas the control group did show a

significant novelty preference as

expected. However, performance was

not concentration-related, nor was there

a significant overall methanol effect

across the four groups.

As stated by HEI, ‘‘the investigators

reported no systematic effects of

prenatal methanol exposure on most of

the measures used to test infant

neurobehavioral development.’’

Moreover, HEI concludes that ‘‘overall,

the results provide no evidence of a

robust effect of prenatal methanol

exposure on the neurobehavioral

development of nonhuman primate

infants.’’

The petitioner submitted comments

on the Burbacher Primate Study in

November 1999 and July 2000. In the

November 1999 submittal, the petitioner

stated that ‘‘it is doubtful whether this

decrease in gestation period was related

to methanol exposure, as there was no

dose-response and no apparent

differences in the offspring, in terms of

body weight or other physical

parameters, between those animals

exposed in utero and the control group.

The reduced duration of pregnancy

moreover was within the normal range

of gestation periods for this species.’’

The petitioner also stressed that there

was no evidence that the wasting

syndrome observed in two offspring was

related to methanol exposure. In

addition, the petitioner asserted that the

study provides no reliable evidence of

an adverse effect of prenatal exposure

on the neurobehavioral development of

the offspring. Furthermore, the

petitioner stressed that the Burbacher

Primate Study shows that repeated

exposure to concentrations of methanol

vapors as high as 1800 ppm does not

result in accumulation of blood formate

above baseline levels. The petitioner

concludes that overall, the PK data

provide further support for the SEL of

83 mg/m3.

The petitioner submitted additional

comments on the Burbacher Primate

Study in July 2000. The EPA generally

considers substantive augmentation of

an already complete petition late in the

decision-making process to be a petition

amendment that requires withdrawal

and re-submission of the petition,

thereby restarting the statutory clock for

Agency decision making.3 However, in

this case the petitioner requested that

EPA delay its decision on the petition

until after conducting a preliminary

review of the petitioner’s new

submission. The EPA agreed to do so,

and to reserve judgement (pending this

review) as to whether the content of this

submission amounted to substantive

new information or analysis. To the

extent that this material might

constitute a substantive augmentation of

the petition, we are not obligated to

consider it in connection with our

decision on the current petition.

Nevertheless, because we believe that

the arguments and comments presented

in the new submission are merely

extensions of the arguments and

comments previously offered by the

petitioner or presented in the HEI

Report, we have fully considered all of

the petitioner’s submissions as a part of

today’s decision.

In the July 2000 submittal, the

petitioner presented the opinions and

comments of five expert scientists 4 who

had conducted independent reviews of

the HEI Report. The petitioner

summarized the comments of the

experts stating that ‘‘those experts

express strong reservations against

drawing any conclusions about

methanol reproductive or

developmental effects from the HEI

Report, both because the statistical

analyses performed presented a

likelihood that some differences

between controls and exposed groups

would occur just by chance, and

because the observed effects were

inconsistent with the other results of the

study. In particular, the lack of any clear

dose-response relationship; the

inconsistencies between results for

different cohorts, sexes, or tests of

related functions; and the fact that some

of the effects identified were associated

with only a small increase in maternal

blood methanol all caused AF&PA

experts to conclude that the reported

effects on gestation period and

neurobehavioral development are

unlikely to be real.’’ The detailed

comments from the petitioner and

experts are presented in the docket.

The data from the 1999 Burbacher

Primate Study complement and extend

the current understanding of methanol

health effects. As the HEI Health Review

Committee noted in its commentary, the

experiments in this study were ‘‘well

designed and executed with appropriate

quality control and quality assurance

procedures. Thus, one can have

confidence in the data.’’ Moreover,

because nonhuman primates are the best

surrogate to study methanol toxicity and

neurobehavioral development in

humans, the results are highly relevant

for risk assessment. We agree with these

statements by the HEI Health Review

Committee about the relevance of the

Burbacher Primate Study for risk

assessments, and while it is evident that

the results of the study are subject to

multiple interpretation, we believe that,

absent additional data, the observed

effects must be considered in any risk

assessment of methanol emissions.

As mentioned previously in today’s

notice, there was a statistically

significant (p = 0.03) decrease in the

duration of pregnancy. Although no

other adverse reproductive outcomes

(e.g., reduced fertility, spontaneous

abortion, reduced neonatal size or

weight) were statistically significant, it

is noteworthy that cesarian sections (Csections) were performed only on

methanol-exposed females, that is, two

C-sections per group for a total of six in

the methanol-exposed groups versus no

C-sections in the controls. These

operations were performed in response

to signs of difficulty in the pregnancy

(e.g., vaginal bleeding) and, thus, serve

as supporting evidence of reproductive

dysfunction in the methanol-exposed

females.

The HEI Health Review Committee

stated that the pregnancy durations in

both control and methanol-exposed

groups were within the norms of other

colonies. However, the reason for

having a concurrent control is to

provide a more direct comparison with

21934 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

the experimentally treated animals.

Monkeys in other colonies were not

necessarily subjected to the same

conditions or type of handling that

existed in the Burbacher Primate Study.

Moreover, it is not clear what ‘‘norms’’

have been established or how they

should be applied in this case. By

analogy, a reduction of IQ from 102 to

98 is a small percentage change around

a norm of 100, but if this reflects a

population average change, the

reduction is quite meaningful. Although

no one should generalize an effect size

from the small number of monkeys in

the Burbacher Primate Study to an

entire population, neither should the

difference between methanol-exposed

and control groups be dismissed as

inconsequential because it is ‘‘within

the norms.’’

As to the petitioner’s comment that

‘‘vaginal bleeding 1–4 days prior to

delivery of live born-healthy infants is

not that unusual in this species, so

vaginal bleeding does not necessarily

imply an at risk fetus requiring cesariansection delivery,’’ it is noteworthy that

the control animals did not have such

bleeding. No evidence was given by

AF&PA to counter the determination of

the veterinarians conducting the study

that placental separation was occurring

in the methanol-treated animals

requiring C-section. While the exposed

animals that received C-sections were

excluded from the analysis regarding

the determination of gestation length,

this finding, in conjunction with the

shortened gestation length of the other

methanol-exposed animals, would

support the notion of problems with

maintenance of pregnancy. Overall, this

is not a trivial outcome on duration of

pregnancy and may have adverse

consequences on the offspring, even in

the absence of frank effects.

Furthermore, the lack of an increasing

dose-related trend in the pregnancy

duration data does not nullify the fact

that all of the methanol-exposed groups,

both when tested collectively and

separately against controls, had

significantly shorter pregnancy lengths.

In summary, the reduction in pregnancy

duration observed in this study appears

to constitute an adverse reproductive

effect associated with methanol vapor

concentrations of 200–1800 ppm.

As mentioned above, the only

significant effect in growth measures

was a severe wasting syndrome that

became evident in two female offspring

from the 1800 ppm group at 1–1.5 years

of age. In both cases, the animals ate

normally but lost weight and failed to

grow normally, which led to progressive

weakness and ultimately their having to

be euthanized. No infectious agent or

pathogenic factor could be identified.

Thus, it appears that a highly significant

toxicological effect on growth could be

attributed to prenatal methanol

exposure at 1800 ppm.

As noted previously in today’s notice,

two neurobehavioral development

effects were found. A concentrationrelated delay in sensorimotor

development was measured in male

offspring during the first month of life.

Also, the offspring prenatally exposed to

methanol did not perform as well as

controls on the Fagan Test of Infant

Intelligence. The HEI Health Review

Committee recommended that these

neurobehavioral findings should be

interpreted ‘‘cautiously’’ for various

reasons. The first reason for caution was

the small number of animals in each

group. In our view, however, the low

number of animals presumably implies

less statistical power to detect an effect,

not necessarily that an apparent effect

was more likely due to chance. On this

basis, we find the results to be no less

credible and perhaps even more

credible, if anything. The second reason

for caution was that no adjustment was

made for multiple comparisons.

However, it is not clear to us, nor

apparently to the statisticians involved

in either analyzing or reviewing these

data (otherwise, an adjustment would

have been made), what would be the

most appropriate adjustment to make in

this instance, because the concept of

having a battery of tests is to evaluate

different domains of function that are

presumably somewhat, if not entirely,

independent of each other. The third

reason for caution was that ‘‘no dose

response was generally noted’’ in

connection with the observed effects.

Actually, for the sensorimotor effects,

we note that a concentration-related

trend was evident in the data for males

and for both sexes combined (although

not for the females alone); the basis for

the gender-specific nature of this

finding is unknown, but other

developmental neurobehavioral effects,

including the developmental toxicity

effects of ethanol (Osborn et al., 1998;

Rudeen, 1992), are known to differ

between sexes and, thus, cannot be

dismissed as necessarily chance

occurrences. As for the lack of a

concentration-related trend in the Fagan

test results, this could well reflect the

inherent constraints of the measured

endpoint, which typically is an

approximately 60 percent response

preference for novel stimuli vis-a-vis a

50 percent chance response level. If the

control group performs at the 60 percent

level and the most impaired subjects

perform at approximately the 50 percent

chance level (worse than chance

performance would not be expected),

the range over which a concentrationresponse relationship can be expressed

is necessarily quite limited and, thus,

the lack of a clear monotonic trend is

not surprising.

As the fourth reason for caution, the

petitioner and the HEI Committee point

out that a consistent effect was not seen

on other measures of cognitive

performance in the Burbacher Study,

namely, the Nonmatch to Sample Test.

However, the lack of a significant

methanol effect on this test may have

been due in part to the fact that the task

was apparently quite difficult for the

infant monkeys, regardless of their

exposure. Also, other studies suggest

that these particular tests reflect

different neuroanatomical mechanisms

(McKee and Squire, 1993; Clark et al.,

1996) and, therefore, may be

independent of one another. Hence, the

lack of consistency among different tests

does not necessarily imply that the few

significant results are implausible.

Measures of cognition used in the

assessment battery not only measure

different neurobehavioral functions but

also were performed at different ages. A

developmental perturbation would not

be expected to affect all tests of all

endpoints at all times of assessment.

Thus, the tests of visually-directed

reaching and recognition memory

would not necessarily be expected to

give the same results. The supposition

of the AF&PA expert reviewers that

gross effects should be seen on measures

of head circumference and early

measures of growth and development is

an oversimplification of the range of

effects that may follow developmental

exposures to neurotoxic agents.

Consequently, we find that the lack of

concordance among all the tests in the

Burbacher Primate Study is not a cogent

argument for a lack of biological

plausibility for effects of gestational

exposure to methanol.

As the fifth reason for caution, the

HEI Health Review Committee and

petitioner note that maternal blood

methanol levels in the 200 ppm group

were only slightly higher than the

controls (i.e., approximately double).

But as the HEI Health Review

Committee states, ‘‘these results may

indicate sensitivity to even small

increases in maternal blood methanol,

or they may indicate random findings.’’

Without a better understanding of the

fetal PK processes that could have been

involved in these effects, it may be

presumptuous to suppose that the

measured maternal blood methanol

levels are an adequate indicator of fetal

exposure to the responsible toxic agent.

Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21935

In summary, the HEI Health Review

Committee’s notes of caution do not

warrant dismissal of the findings.

Therefore, we conclude that these

findings provide plausible evidence of

developmental neurotoxicity in infant

monkeys that had been exposed

prenatally to methanol via their

mothers’ exposure to concentrations of

600–1800 ppm methanol vapor and

possibly lower.

We also have concerns regarding the

potential background levels of methanol

in human blood resulting from

consumption of fruit. The assertion is

made by the petitioner that foods

(especially fresh fruit) provide

quantities of methanol, as measured in

human breath, that would constitute a

background level similar to that found

from anthropogenic sources. This

assertion is derived from papers by

Taucher et al. (1995) and Lagg et al.

(1994), in which four individuals are fed

either three peaches, three peaches and

one orange, six peaches and one banana,

or five peaches and four bananas. Breath

measurements were taken starting

before, during, and starting immediately

after consuming these fruits. There is no

discussion as to whether these

individuals rinsed their mouths out

after consuming the fruit. Nor is there

any correction for off-gassing of

methanol from the residual mouth

contents or stomach contents.

Additionally, studies by Batterman et al.

(1998) suggest that human breath

concentrations of methanol following

inhalation exposure only achieve

equilibrium with blood concentrations

‘‘if subjects are in a methanol-free

environment for 30 min or more after

exposure’’ due to desorption from the

lining of the respiratory tract. There is

reason to suspect that the same thing

happens with the fruit in the mouth,

esophagus, and stomach, especially

given the tendency of high-fiber foods

such as fruit to leave remnants on teeth

and to stimulate gas release from the

upper GI.

The peak human breath

concentrations reported in the Taucher

et al. and Lagg et al. studies are only 3

ppm (3.9 mg/m3) from the largest

quantity of fruit 2 hours postconsumption and 4 ppm (5.2 mg/m3)

from 100 ml of 48 proof homemade

brandy with 0.19 percent methanol at 4

hours post consumption. The breath

concentration of methanol after brandy

consumption falls off with a half-life of

about 1.5 hr, roughly identical to what

is seen from the Batterman et al. study,

while the concentration after eating fruit

does not decline, strongly suggesting

that the source material is still in the

mouth and upper GI tract. Although a

concentration of 3–4 ppm in exhaled

breath is within the range of human

experience, it is probably an extreme

case. The acute consumption of

sufficient fruit to raise breath

concentrations more than twice that

level most likely involves acute GI

effects sufficient to discourage the

attempt. In summary, based on the

weight of evidence, we think that there

are reproductive and developmental

health consequences following exposure

to methanol in both mice (Rogers et al.)

and primates (Burbacher et al.) and that

these effects should be considered

relevant to potential risks in humans.

Although the findings from Burbacher

et al. provide reasonable qualitative

evidence of reproductive and

developmental toxicity associated with

methanol exposure during pregnancy,

characterizing the dose-response

relationship in these data is more

problematic. It is, therefore, premature

to predict an RfC based on the results of

that study because the process for RfC

development requires a much more

extensive analysis and review than is

possible within the present time

constraints. At a minimum, further

analysis of the primate data using BMD

or other methods needs to be considered

as part of the process to develop an RfC

for methanol. However, some

perspective can be gained by

considering a few of the possible

interpretations and applications of the

data from the Burbacher study. For

example, if 200 ppm (260 mg/m3) were

considered a Lowest Observed Adverse

Effects Level (LOAEL) for reproductive

toxicity (shortened pregnancy length),

adjustment of this value to an HEC,

based on temporal (2.5/24 hours) and

dosimetric (default value of 1) factors,

would yield a LOAEL(HEC) of

approximately 27 mg/m3. Potentially

applicable uncertainty factors include a

factor of as much as 10 for use of a

LOAEL instead of a NOAEL and a factor

of up to 10 for intraspecies variability,

which could result in a reference value

as low as 0.27 mg/m3. As another

example, if 200 ppm were considered a

NOAEL for developmental toxicity

(neurobehavioral effects in infants) and

a temporal adjustment of the HEC were

made, the NOAEL(HEC) would be 27

mg/m3. In this case, an uncertainty

factor of 10 for intraspecies variability

might be applied, resulting in a possible

reference value of 2.7 mg/m3. A rather

wide range of possible values for a

health-based criterion, on the order of

0.3 to 30 mg/m3, can be estimated from

the primate data in this manner,

depending on which type of effect,

effect level, and uncertainty factors are

selected, but this range should not be

construed as bounds on what a fully

developed RfC for methanol vapor

might ultimately be.

Taken together, the studies by Rogers

et al. and Burbacher et al. provide a

pattern of evidence indicative of

reproductive and developmental

toxicity associated with exposure of

mice and monkeys to methanol vapor

during gestation. In our judgment, this

evidence is relevant for evaluating

potential risks of methanol to human

health. The data imply a window of

sensitivity during gestation, which is

supported by other work that has shown

that the critical period for induction of

developmental toxicity by maternal

inhalation of methanol vapor can be at

least as short as 1 day in mice (Rogers

and Mole, 1997). However, the minimal

period of exposure sufficient to induce

such effects has not been determined.

This fact suggests that the potential for

acute exposures, as well as chronic

exposures, must be considered in any

human exposure analysis in connection

with a petition to remove methanol from

the list of HAP.

While we do not believe that the

effects observed in the Burbacher

Primate Study can be dismissed, we are

not prepared at this time to propose a

specific alternative to the petitioner’s

SEL. However, there appears to be some

convergence within the range of

possible reference values that could be

derived from the rodent and primate

studies. As noted above, using BMD

methods and making duration

adjustments of the data from Rogers et

al., it is possible to derive values of

about 4–6 mg/m3, which are at the

approximate midpoint of the values

(0.3–30 mg/m3) that might be derived

from the data of the Burbacher Primate

Study. Although one should not place

too much weight on these specific

numbers, the fact that they converge

suggests greater plausibility than if the

values were widely disparate.

The selection of an appropriate health

effects decision criterion or reference

level is a central component in the

determination of potential risk. For

chronic noncancer risk assessments, the

EPA-verified inhalation RfC values are

the primary quantitative consensus

values used by the Agency. For

assessing potential adverse health

effects due to short-term exposures (e.g.,

24 hours), the Agency utilizes various

acute exposure criteria. Sometimes we

use EPA developmental RfC values to

assess the potential effects to developing

humans due to short-term exposures.

Other benchmarks that we utilize, when

appropriate, may include, among others,

acute minimal risk levels (MRL)

21936 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

produced by the Agency for Toxics

Substances and Disease Registry and

acute reference exposure levels (REL)

produced by the California

Environmental Protection Agency.

For methanol, as discussed

previously, there are no EPA-verified

RfC values available to assess noncancer

risks. Moreover, benchmarks produced

by other agencies have not utilized the

recent results from the Burbacher

Primate Study. Therefore, based on our

review of the available information, we

conclude that a range of 0.3 to 30

mg/m3 represents the most appropriate

criterion for determining whether

methanol emissions may reasonably be

anticipated to cause adverse human

health effects. Furthermore, since the

critical effects are adverse

developmental outcomes that could

occur after short-term exposures, we

judged that, of the available exposure

duration estimates (i.e., 1-hour, 24-hour,

and annual concentrations), 24 hours

would be the most appropriate exposure

duration to compare to the health

criterion range of 0.3 to 30 mg/m3 for

decision-making purposes.

While we conclude, based on

available data, that 24-hour exposures

below 0.3 mg/m3 are not likely to result

in adverse human health effects, we are

unable to make a more precise

determination at this time regarding the

exposure levels at which adverse effects

are likely to occur. The range of values

(0.3 to 30 mg/m3) chosen as a healthbased decision criterion is not presented

as a bright line between safety and

toxicity. There is progressively greater

potential concern about the likelihood

of adverse effects as exposures increase

within, and above, this range, and we

cannot conclude based on the available

evidence that any level of exposure

above 0.3 mg/m3 may not reasonably be

anticipated to cause adverse human

health effects. The comparison of

exposure estimates to the health

criterion is discussed further in the Risk

Characterization section of today’s

notice.

D. Sources of Methanol Emissions and

Maximum Levels of Exposure

In the original petition submittal

(dated March 1996), it is stated that

based on the 1993 Toxic Release

Inventory (TRI), approximately 2,303

facilities reported emissions of

methanol, which resulted in a total

86,155 tons of methanol emitted to the

air in 1993 in the U.S. The 1993 TRI

data indicated that the paper and allied

products industry accounted for about

52 percent of the methanol emissions.

The next largest source category was the

chemical and allied products industry

which accounted for 25 percent of the

methanol emissions. Six facilities

reported emissions over 1,000 tons per

year (tpy), 195 facilities reported

emissions over 100 tpy and 828

facilities reported emissions over 10 tpy.

Subsequent petition submittals present

emissions estimates based on more

recent data sources (e.g., the 1995 TRI)

for sources emitting greater than 500 tpy

of methanol.

In order to focus the exposure

modeling assessment on those sources

that are most likely to present

unacceptable risks, the petitioner

conducted a conservative screening

level exposure assessment to identify an

emissions cut-off for further analysis.

‘‘Conservative’’ refers to the selection of

models and modeling parameters that

are more likely to result in

overestimates, rather than

underestimates, of ambient

concentrations of a pollutant. A

hypothetical plant assumed to have a 10

meter stack with a fenceline 10 meters

from the stack was utilized for the

screening assessment. A very

conservative screening model that

assumes no plume rise and conservative

meteorology was used to model the

emissions dispersion and estimate

maximum offsite concentrations. Using

this approach, the petitioner concludes

that only sources emitting greater than

500 tpy could theoretically result in

offsite concentrations greater than 83

mg/m3. Therefore, most of the emissions

inventory development and exposure

modeling assessment focused on

sources emitting greater than 500 tpy.

In the March 1996 submittal, the

petitioner presented stack and fugitive

emissions estimates for the 15 highest

emitting plants in the U.S. as reported

in the TRI. In the supplements received

between March 1997 and February

1999, the petitioner identified about 55

additional sources of various sizes and

industry types. Overall, the petitioner

identified about 60 sources that emit

greater than 500 tpy of methanol.

In the original submission, the

petitioner also reviewed various

materials developed by EPA for

estimating HAP emissions. Emission

factors found by the petitioner in this

material included such source

categories as ammonia production,

charcoal manufacturing, terephthalic

acid production, formaldehyde

production, glycol ethers productions

and sulfate (kraft) pulping. The

petitioner, however, concluded that the

lack of emission factor data would

preclude the petitioner from compiling

a national inventory using the emissions

factor approach.

The petitioner also obtained

information on methanol’s use as a fuel

for motor vehicles and asserts that

methanol is a promising alternative fuel

for motor vehicles, which could help

reduce emissions of volatile organic

chemicals (VOC) and air toxics such as

benzene. However, the petitioner found

that methanol as a motor fuel is

currently limited to Indianapolis-style

race cars, about 14,000 cars in the

Federal government and private fleets,

and approximately 400 buses in

California. The petitioner claims that

current methanol emissions from motor

vehicles appears to be quite small.

The petitioner concludes in the initial

submittal that the TRI was the most

suitable database for identifying the

most significant industrial categories

and individual sources with large

industrial emissions and would provide

the ‘‘best-estimate’’ of methanol

emissions in the U.S. The petitioner

claims that other potential methanol

sources are comparatively small or

widely dispersed and are unlikely to

cause high ambient concentrations of

methanol.

The petitioner submitted additional

emissions information in March 1997,

January 1998, April 1998, and February

1999. These submittals primarily

contained modeling data for a set of

facilities and did not discuss emissions

inventory development. However, the

petitioner did present some emissions

data and discussed the selection of 500

tpy as a cut-off for the emissions

inventory. The primary focus was to

identify sources that emit greater than

500 tpy of methanol.

The petitioner also contacted various

States and requested data on methanol

emissions. California, Colorado, Kansas,

Louisiana, New York, South Carolina,

Texas, and Wisconsin responded to this

request and provided emission data.

The petitioner’s review of these data

found only one facility that was not

considered in the earlier analyses.

The petitioner also reviewed the 1996

TRI for additional facilities. Two

petroleum refineries reported methanol

emissions in excess of 500 tpy in 1996

that were not considered in the earlier

analyses. The appearance of these

facilities in the 1996 TRI database was

due to new methanol emission estimates

that were developed for a hydrogen

production process.

Finally, the petitioner reviewed

several EPA documents to determine if

any large sources had been left out of

the earlier analyses. The petitioner

could not find any evidence of any large

methanol emissions source that needed

to be considered. Therefore, the

petitioner concluded that all sources

Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21937

above 500 tpy of methanol were

accounted for in the petition.

Based on our review, we believe that

the petitioner’s analysis for establishing

the 500 tpy cutoff for the cited health

benchmark (SEL of 83 mg/m3) is a

reasonable approach and is technically

sound. We confirmed that only sources

emitting more than 500 tpy would have

a theoretical possibility of exceeding an

offsite concentration of 83 mg/m3.

Therefore, assuming an SEL of 83

mg/m3 as a guideline, 500 tpy would be

an appropriate cut-off for emissions

inventory development. Nonetheless, as

discussed above, we have determined

that the appropriate health based

decision criterion is the range of 0.3 to

30 mg/m3. Therefore, the 500 tpy cut-off

may no longer be valid for purposes of

evaluating sources that have the

potential to cause adverse impacts on

human health.

Moreover, while we believe that the

petitioner’s overall methodology for

identifying all the methanol emissions

sources greater than 500 tpy is

technically sound, a comparison with

the EPA’s 1996 National Toxics

Inventory (NTI) shows that the

petitioner may not have found all the

sources emitting more than 500 tpy. A

query of the 1996 NTI database for

methanol resulted in approximately

4,280 facilities reporting methanol

emissions. Of these facilities, 37 had

methanol emissions in excess of 500

tpy. Nineteen of these 37 facilities were

not included in the petitioner’s

inventory. Two of the facilities not

considered in the petitioner’s analysis

are the International Paper Company in

Oregon and the Mead Publishing Paper

Division in Maine. These are the largest

methanol emitting facilities (2,547 and

2,101 tpy, respectively) found in the

NTI. However, the petitioner did

include six of the top ten emitting

sources reported in the NTI, as well as

a few very large sources that were not

found in the NTI. One of these sources

in the petition has higher reported

emissions (2,450 tpy) than all but one

source listed in the NTI. The petition

also included several sources that are

likely to adequately represent the worstcase sources in the U.S., including one

source that emits 829 tpy at ground

level with a relatively close fenceline.

Therefore, the petitioner’s emissions

inventory is generally acceptable for the

purpose of estimating maximum offsite

concentrations.

The petition asserts that inhalation is

the only significant route of human

exposure to methanol emissions. Since

methanol rapidly biodegrades and

volatilizes in water, it is highly unlikely

that humans are exposed to significant

amounts of methanol through fallout

upon soils or water bodies.

The petitioner used the emission

inventory as input in a tiered air

dispersion modeling analysis. A

‘‘tiered’’ analysis applies successive

refinements in model selection and

input data to derive successively less

conservative predictions of the

maximum offsite air concentrations of a

given pollutant. Tier 1 is the simplest

and most conservative approach; tier 2

is somewhat less conservative and more

refined, including some facility-specific

parameter data and less conservative

assumptions; and tier 3 is even more

refined and less conservative than tier 2

and depends on more site-specific

information. For the most part, the

petitioner utilized a mix of tier 2 and

tier 3 approaches from EPA’s three-tier

analysis method (EPA–450/4–92–001).

The petitioner modeled many sources

to estimate maximum annual, maximum

24 hour, and maximum 1-hour

concentrations at the boundaries of the

facilities. Twenty-four hour

concentrations were considered most

relevant for risk assessment since the

critical effect is developmental/

reproductive effects that could occur

after short-term exposures.

In the March 1996 submittal, using

data from the 15 largest emitting

facilities, the petitioner developed ten

model plants representative of the

largest emitters in ten different

industrial categories. When available,

the petitioner used source-specific stack

parameter data (such as stack height,

exit velocity, stack temperature) from

the EPA’s Aerometric Information

Retrieval System (AIRS) database.

Otherwise, the petitioner used industry

average values. The petitioner used a

simple terrain tier 2 modeling approach

and assumed all emissions are from the

same location and the fenceline is 100

meters from the stack. Meteorological

data from each of five cities in the U.S.

were used in the modeling to represent

a variety of meteorological conditions.

This modeling approach predicted

maximum 24-hour ambient methanol

concentrations of 0.1 to 4.5 mg/m3

resulting from the methanol emissions.

To show conservatism of the tier 2

modeling, the petitioner conducted

more refined modeling (tier 3) using

more site-specific data for one of the

largest facilities. The maximum 24-hour

concentration decreased by a factor of 3

for this facility using the tier 3

approach.

In the March 1996 submittal, the

petitioner also included a conservative

screening-level modeling analysis of

complex terrain, whereby a single large

plant (emitting 2,000 tpy) was placed in

a hypothetical location of complex

terrain. This complex terrain analysis

predicted a 24-hour maximum

concentration of 6.9 mg/m3. In addition,

the petitioner assessed the combined

impact of hypothetical co-located

plants, whereby two large plants were

assumed to have emissions being

released from the exact same location.

The results from the combined impact

of co-located sources yielded a

maximum predicted 24-hour ambient

concentration of 6 mg/m3.

In March 1997, the petitioner

submitted a supplement that included

tier 3 modeling for 19 additional

facilities, most of which are among the

largest in the U.S. This modeling

analysis included 12 pulp and paper

mills and seven facilities from other

industries. The maximum 24-hour

offsite concentration from this analysis

was 2.5 mg/m3. This supplement also

included further evaluation and

modeling of potential co-location

situations. The petitioner searched TRI

and found there were no instances

where two large sources were within 2

miles of each other. However, the

petitioner did identify five medium to

small sources along a 1-mile line in

Lexington, NC. Also, the petitioner

found three pulp and paper mills in the

Wisconsin Rapids, WI area and a

number of medium and large sources in

the Mobile, AL area. The petitioner

modeled each of these co-location

scenarios and predicted the maximum

24-hour concentration to be 0.6 mg/m3.

The March 1997 supplement also

presented tier 3 complex terrain

modeling analyses for two actual plants

located in complex terrain, which

predicted a maximum 24-hour

concentration of 0.4 mg/m3. In addition,

data on measured ambient levels of

methanol were presented showing that

background levels of methanol are less

than 0.8 mg/m3 .

In January 1998 and February 1999, in

response to EPA comments, the

petitioner submitted modeling analyses

for 13 additional facilities that included

tier 3 modeling analyses for eight

facilities and tier 2 modeling analyses

for five facilities. These facilities

included all the non-paper sources with

greater than 500 tpy reported in the TRI

for years 1993–95. The range for the

24-hour maximum offsite concentration

for 12 of these plants was 0.1 to 3 mg/

m3. However, there was one facility (the

Missouri Chemical Works), modeled

using tier 3 approach, for which the

maximum 24-hour concentration was

7.6 mg/m3. This source was originally

identified as emitting 829 tpy of fugitive

emissions released at ground level in

the January 1998 submittal based on

21938 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

1995 TRI emissions reporting.

Subsequently, in the July 2000

submittal, the petitioner states that in

1998, this facility initiated several

changes that reduced emissions by

about 70 percent. The petitioner

remodeled this facility using 1999

emissions estimates (253 tpy), which

decreased the maximum offsite

concentration to 3.65 mg/m3.

In the February 1999 submittal, the

petitioner attempted to demonstrate that

the pulp and paper mills modeled in

previous submittals were representative

of the industry and included at least one

worst-case example. The petitioner

stated that the modeling analyses

included the source with the highest

total emissions, the two facilities with

the highest fugitive emissions, as well as

two large sources with low-level

releases. Moreover, the petitioner

creates a very conservative hypothetical

worst-case analysis for a paper plant to

show that the theoretical worst-case

offsite air concentration for a source

emitting 1,815 tpy is 31 mg/m3.

In summary, the petition includes

modeling analyses using a mix of tier 1,

tier 2 and tier 3 approaches for roughly

50 sources in the U.S., including many

of the largest emitting sources.

Moreover, the petition includes

modeling analyses for sources located

near one another (i.e., co-location) and

for a few facilities in complex terrain.

Overall, the maximum modeled

fenceline concentration from any

facility using the tier 2 approach was

about 4.5 mg/m3, and the maximum

concentration of any facility using the

tier 3 approach (with updated emissions

data) was 3.65 mg/m3.

We agree with the petitioner that

inhalation is the primary route of

human exposure to methanol emissions.

The petitioner provides a tiered-based

dispersion modeling analysis of

facilities emitting greater than 500 tpy

methanol. Following generally

acceptable modeling guidelines, the

petitioner estimates maximum 24-hour

modeled fenceline concentrations from

the inventoried facilities using

conservative screening techniques and

more refined (tier 3) modeling

procedures. Further, the petitioner

shows that combined impacts from colocated sources, as well as background

ambient concentrations, are negligible

and will not appreciably contribute to

maximum predicted ambient levels.

Overall, we generally believe that the

petitioner’s conclusions regarding

ambient concentrations of methanol that

are likely to result from facilities

emitting greater than 500 tpy are

technically sound and credible.

Nonetheless, we have a number of

comments regarding the petitioner’s

analyses.

With regard to the March 1996

submittal, we think that some of the

input parameters in the simple terrain

tier 2 analysis were not as conservative

as they should be for a tier 2 analysis.

For example, fugitive emissions were

approximated from a height of 50 feet.

These should have been modeled as

ground-level sources. Also, no basis for

many of the site-parameter assumptions

are provided. However, the rest of the

model assumptions in this tier 2

analysis appear to be conservative,

therefore, the results are most likely

conservative. The tier 3 detailed

modeling of a single large facility also

used the same fugitive source

assumption (50 feet release height).

Therefore, the results from the tier 3

analysis may not result in a conservative

estimation of fenceline concentrations.

The complex terrain modeling of a

single large facility was performed with

an extremely conservative model

(SCREEN2/VALLEY), thus these results

are most likely conservative. Also, the

analysis of combined impact of colocated plants utilized some very

conservative assumptions, thus, these

concentrations are most likely

overpredicted.

With regard to the March 1997

submittal, it appears that the tier 3

modeling of 19 large facilities was

performed following EPA modeling

guidelines. Detailed documentation of

the approach, input data and results are

provided. The results from the complex

terrain analysis appear to be credible.

Also, the reported measured ambient

levels of methanol appear to coincide

well with the data from the EPA’s AIRS

database. Thus, the March 1997

submittal is judged to be technically

sound and appropriate.

With regard to the January 1998 and

February 1999 submittals, it appears

that the modeling of each of the 13

facilities follows EPA modeling

guidance. The one facility (Missouri

Chemical Works) that had a maximum

24-hour modeled concentration of 7.6

mg/m3 (using 1995 TRI emissions data)

seems to be a very good ‘‘worst-case’’

example. Model documentation for this

run was provided and appeared to

justify the results.

The analysis (in the February 1999

submittal) of a hypothetical worst-case

pulp and paper mill is extremely

conservative. The predicted worst-case

air concentration of 31 mg/m3 is clearly

an overestimation for this type of

facility, and fenceline concentration

predictions for a facility of this type

would likely be much lower using a

more realistic approach.

In summary, based on the analyses

presented in all the submittals, the

maximum modeled fenceline

concentration from any facility using

very conservative hypothetical

screening level approaches was 31

mg/m3, the maximum concentration

using tier 2 approaches for actual plants

was about 4.5 mg/m3, and the maximum

concentration of any facility using the

refined tier 3 approach was 7.6 mg/m3

(using 1995 data) and 3.65 mg/m3 (using

1999 data).

Overall, based upon our technical

review of the series of submittals, we

think that the ambient concentrations

predicted by the analysis are technically

sound and credible. However, it is

possible that, using a different facility

source configuration, a different

inventory, or a different model,

predicted concentrations could be

higher or lower than those presented in

the petition. Furthermore, year-to-year

variations in meteorological conditions

could result in different predicted

concentrations. While dispersion

models are generally designed to be

conservative, it is possible that the

models utilized in the analysis are not

as conservative as expected. Also, as

discussed above, the petitioner did not

appear to include all sources greater

than 500 tpy in the modeling analysis.

Thus, the maximum concentration of

3.65 mg/m3 predicted by the refined

(tier 3) model using the updated

emissions data may not accurately

reflect actual worst-case fenceline

concentrations. However, we think it is

unlikely that any existing facility would

present offsite ambient concentrations

that are higher than the maximum

concentration of 7.6 mg/m3 predicted

for the Missouri Chemical Works using

the 1995 TRI data (829 tpy emitted at

ground level).

Moreover, we agree with the

petitioner’s conclusion that background

sources and co-location of facilities are

not significant. Monitoring values of

methanol, primarily measured near

large emitters, are found to generally be

less than 1.0 mg/m3. The worst-case

average methanol concentration in the

AIRS monitoring database was found to

be 0.2 mg/m3. Furthermore, impacts

from individual facilities fall off rapidly

with distance, thus, it is highly unlikely

that coincidental impacts from multiple

facilities would greatly increase

maximum predicted impacts.

Finally, when comparing model

predicted estimates to health criteria,

the petitioner makes a conservative

assumption. Namely, the petitioner does

not apply an inhalation exposure

assessment to the air level predictions,

instead elects to use the maximum

Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices 21939

exposed individual (MEI) approach. The

MEI is the predicted exposure for a

hypothetical person assumed to be

located at the place of maximum

predicted offsite air concentration for 24

hours. If an exposure assessment were

applied, whereby we determine where

actual people are located and account

for daily activities and other exposure

factors, actual maximum individual

inhalation exposures could be

somewhat lower than the MEI

predictions from the dispersion

analysis. Based upon our review of the

petitioner’s analyses, the likely

proximity of inhabitable areas to these

large facilities, and knowledge of human

activity patterns over a 24-hour period,

we conclude that maximum 24-hour

exposures to methanol emissions could

be in the range of 2 to 7 mg/m3, but that

such exposures may not reasonably be

expected to exceed 7 mg/m3. Notably,

this analysis does not address potential

increases in exposures which might

occur should methanol emissions

increase substantially in the future.

E. Risk Characterization

The petitioner states that the

maximum predicted 24-hour

concentration for any of these facilities

was about 3.65 mg/m3. As stated above,

the petitioner proposes a SEL of

83 mg/m3. Thus, the petitioner asserts

that concentrations of methanol

anticipated to occur at the fenceline are

far below the SEL and cannot

reasonably be anticipated to cause either

acute or chronic adverse health effects

to people living nearby these facilities.

The petitioner also asserts, based on

data on PK, that even if a person were

continuously exposed to the maximum

predicted concentration of 3.65 mg/m3,

that individual’s blood methanol level

would increase by about 0.7 mg/l,

which represents only about 3 percent

of the mean baseline level of methanol

that individuals have in their blood as

a result of natural physiological

processes.

Generally, the EPA uses a hazard

quotient (HQ) approach to characterize

the noncancer risk associated with

exposures to pollutants. In this

approach, the HQ is developed by

comparing the level of exposure (and

the appropriate duration of exposure) to

the appropriate health-based decision

criterion that represents a similar

duration of exposure. For example, in

many assessments, the average lifetime

exposures are compared to a chronic

RfC to determine the likelihood of

adverse effects from long-term

exposures. However, for pollutants that

cause developmental effects, such as

methanol, the critical duration of

exposure could be a short duration

(hours or days). Therefore, we conclude

that a 24-hour exposure concentration is

most appropriate for the HQ analysis for

methanol.

Assuming that the estimated exposure

level represents total exposure

(exposure due to the source being

evaluated plus all background

exposures), if the HQ is less than 1, the

reference level is not exceeded, and the

adverse health effect represented by the

health reference level is unlikely.

Usually the RfC is considered protective

of all noncancer adverse health effects.

Therefore, exposures at or below the RfC

are generally not expected to result in

any adverse noncancer health effects. If

on the other hand, the HQ is greater

than 1 (i.e., exposures are greater than

the RfC), we generally are unable to

conclude that adverse effects are not

likely to occur. The risks following

exposures above the RfC are uncertain,

but risk increases as exposures to such

pollutants increase above the RfC.

However, for methanol, at this time,

we do not have a single value criterion,

such as an RfC, that we think is

appropriate for the derivation of an HQ.

Instead, as discussed above, we have

determined that the appropriate healthbased criterion for EPA decision making

for this methanol petition is the range of

0.3 to 30 mg/m3. In other words, at this

time, in order to demonstrate that

exposures are reasonably anticipated

not to result in any adverse effects to

humans, including sensitive

subpopulations, the estimated 24-hour

exposure concentrations would need to

be 0.3 mg/m3 or lower. From the

exposure assessment discussion, we

have determined that maximum 24-hour

exposures could be in the range of 2 to

7 mg/m3, which is well above 0.3

mg/m3. Therefore, at this time, we are

not able to determine that emissions of

methanol may not reasonably be

anticipated to result in any adverse

effects to humans. This means that the

petition has failed to meet the criteria

outlined in section 112(b)(3)(C) of the

CAA. Therefore, EPA must deny

AF&PA’s petition, and methanol will

remain on the list of HAP under section

112(b) of the CAA. Moreover, because

we conclude that the information

submitted in connection with this

petition does not support a

determination that methanol emissions

will not cause adverse human health

effects, any future petition for the

removal of methanol from the list of

HAP will be denied as a matter of law

unless such petition is accompanied by

substantial new information or analysis.

F. Other Elements of the Petition

The petitioner also presented an

evaluation of the potential

environmental impacts of methanol

emissions, and impacts related to

atmospheric transformation of methanol

emissions into formaldehyde. Because

we are denying the petition for the

reasons stated above, we do not find it

necessary to make final determinations

regarding these elements of the petition.

However, we will note a few concerns

with regard to the petitioner’s

environmental impact analysis. First,

the petition contends that methanol has

low inherent toxicity to aquatic biota,

which is a reasonable conclusion based

on available information. However, the

petitioner fails to demonstrate that the

levels emitted from large point sources

would not increase methanol levels in

nearby water bodies (i.e., ponds) to

levels that would cause adverse effects

to sensitive biota. Similarly, with regard

to terrestrial biota, the petitioner has

conservatively estimated ambient

concentrations of methanol near large

emitters, but did not estimate safe levels

for terrestrial receptors with which to

compare these concentrations.

Moreover, there is no methanol-specific

information presented regarding toxicity

to terrestrial plants and invertebrates.

Instead, the petition summarized the

ecological toxicity information by using

broad ranges, which is acceptable as a

preface to a more complete eco-toxicity

assessment, but should be accompanied

by a more detailed description of

sensitive studies (including a discussion

on the quality of the data). Finally,

because small terrestrial mammals (e.g.,

mice) residing near large emitters are

likely to be the most highly exposed

terrestrial biota, due to their relatively

high metabolic rates and small home

ranges, the petition should include an

estimate of safe levels in air and safe

doses for these biota to compare to

estimated exposures near large

methanol emitters.

IV. Denial of the Petition

Based on our review of the petition

submitted by AF&PA and other relevant

material (including the Burbacher

Primate Study and the materials

submitted by the petitioner subsequent

to the release of that study), EPA

concludes that available data do not

support a determination that methanol

emissions may not reasonably be

anticipated to cause any adverse effect

to human health or the environment.

This determination is based on our

conclusions regarding the appropriate

criterion for evaluating the likelihood of

adverse health effects and the maximum

21940 Federal Register / Vol. 66, No. 85 / Wednesday, May 2, 2001 / Notices

24-hour exposures that may reasonably

be anticipated to occur. Accordingly, we

are denying AF&PA’s petition to remove

methanol from the list of HAP under

section 112(b) of the CAA. Moreover,

because we conclude that the

information submitted in connection

with this petition does not support a

determination that methanol emissions

will not cause adverse human health

effects, we are denying this petition

with prejudice, and any future petition

for the removal of methanol from the list

of HAP will be denied as a matter of law

unless such petition is accompanied by

substantial new information or analysis.

Dated: April 27, 2001.

Christine T. Whitman,

Administrator.

[FR Doc. 01–10990 Filed 5–1–01; 8:45 am]

BILLING CODE 6560–50–P

ENVIRONMENTAL PROTECTION

AGENCY

[OPPTS–00312; FRL–6776–3]

National Advisory Committee for Acute

Exposure Guideline Levels (AEGLs) for

Hazardous Substances; Proposed

AEGL Values

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: The National Advisory

Committee for Acute Exposure

Guideline Levels for Hazardous

Substances (NAC/AEGL Committee) is

developing AEGLs on an ongoing basis

to provide Federal, State, and local

agencies with information on short-term

exposures to hazardous chemicals. This

notice provides AEGL values and

Executive Summaries for 18 chemicals

for public review and comment.

Comments are welcome on both the

AEGL values in this notice and the

Technical Support Documents placed in

the public version of the official docket

for these 18 chemicals.

DATES: Comments, identified by the

docket control number OPPTS–00312,

must be received by EPA on or before

June 1, 2001.

ADDRESSES: Comments may be

submitted by mail, electronically, or in

person. Please follow the detailed

instructions for each method as

provided in Unit I. of the

SUPPLEMENTARY INFORMATION. To ensure

proper receipt by EPA, it is imperative

that you identify docket control number

OPPTS–00312 in the subject line on the

first page of your response.

FOR FURTHER INFORMATION CONTACT: For

general information contact: Barbara

Cunningham, Acting Director,

Environmental Assistance Division

(7401), Office of Pollution Prevention

and Toxics, Environmental Protection

Agency, 1200 Pennsylvania Ave., NW.,

Washington, DC 20460; telephone

number: (202) 554–1404; e-mail address:

TSCA-Hotline@epa.gov.

For technical information contact:

Paul S. Tobin, Designated Federal

Officer (DFO), Office of Prevention,

Pesticides and Toxic Substances (7406),

1200 Pennsylvania Ave., NW.,

Washington, DC 20460; telephone

number: (202) 260–1736; e-mail address:

tobin.paul@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

This action is directed to the general

public to provide an opportunity for

review and comment on ‘‘Proposed’’

AEGL values and their supporting

scientific rationale. This action may be

of particular interest to anyone who may

be affected if the AEGL values are

adopted by government agencies for

emergency planning, prevention, or

response programs, such as EPA’s Risk

Management Program under the Clean

Air Act and Amendments Section 112r.

It is possible that other Federal agencies

besides EPA, as well as State and local

agencies and private organizations, may

adopt the AEGL values for their

programs. As such, the Agency has not

attempted to describe all the specific

entities that may be affected by this

action. If you have any questions

regarding the applicability of this action

to a particular entity, consult the DFO

listed under FOR FURTHER INFORMATION

CONTACT.

B. How Can I Get Additional

Information, Including Copies of this

Document or Other Related Documents?

1. Electronically . You may obtain

electronic copies of this document, and

certain other related documents that

might be available electronically, from

the EPA Internet Home Page at http://

www.epa.gov/. To access this

document, on the Home Page select

‘‘Laws and Regulations,’’ ‘‘Proposed

Rules and Regulations,’’ and then look

up the entry for this document under

the ‘‘Federal Register—Environmental

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the Federal Register listings at http://

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2. In person. The Agency has

established an official record for this

action under docket control number

OPPTS–00312. The official record

consists of the documents specifically

referenced in this action, any public

comments received during an applicable

comment period, and other information

related to this action, including any

information claimed as Confidential

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record includes the documents that are

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as the documents that are referenced in

those documents. The public version of

the official record does not include any

information claimed as CBI. The public

version of the official record, which

includes printed, paper versions of any

electronic comments submitted during

an applicable comment period, is

available for inspection in the TSCA

Nonconfidential Information Center,

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Mall, 401 M St., SW., Washington, DC.

The Center is open from noon to 4 p.m.,

Monday through Friday, excluding legal

holidays. The telephone number of the

Center is (202) 260–7099.

3. Fax-on-Demand. You may request

to receive a faxed copy of the

document(s) by using a faxphone to call

(202) 401–0527 and select the item

number 4800 for an index of the items

available by fax-on-demand in this

category, or select the item number for

the document related to the chemical(s)

identified in this document as listed in

the chemical table in Unit III. You may

also follow the automated menu.

C. How and to Whom Do I Submit

Comments?

You may submit comments through

the mail, in person, or electronically. To

ensure proper receipt by EPA, it is

imperative that you identify docket

control number OPPTS–00312 in the

subject line on the first page of your

response.

1. By mail. Submit your comments to:

Document Control Office (7407), Office

of Pollution Prevention and Toxics

(OPPT), Environmental Protection

Agency, 1200 Pennsylvania Ave., NW,

Washington, DC 20460. (Note: for

express delivery, please see ‘‘In person

or by courier’’ in Unit I.C.2.).

2. In person or by courier. Deliver

your comments to: OPPT Document

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telephone number for the DCO is (202)

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