[Federal Register Volume 66, Number 85 (Wednesday, May 2, 2001)]
[Notices]
[Pages 21929-21940]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 01-10990]



[[Page 21929]]

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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.

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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/m\3\). 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/m\3\ 
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/m\3\, which is well above 0.3 
mg/m\3\. 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: [email protected].

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

[[Page 21930]]

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\
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    \1\ We 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.
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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\
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    \2\ A denial with prejudice serves a vital administrative 
purpose. It prevents the endless re-submission 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).
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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

[[Page 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 no-observable-
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 Aspartame-sweetened 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

[[Page 21932]]

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 duration-adjustment 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  x  t'') factor in order to 
derive health risk estimates for longer-term exposures. To duration-
adjust 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/m\3\.
    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 well-recognized, 
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 
methanol-exposed 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

[[Page 21933]]

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 methanol-exposed 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.
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    \3\ This 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.
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    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.
---------------------------------------------------------------------------

    \4\ The 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.
---------------------------------------------------------------------------

    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 (C-sections) 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

[[Page 21934]]

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 cesarian-section 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 concentration-related 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 
concentration-response 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.

[[Page 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 post-consumption 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)

[[Page 21936]]

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/m\3\ 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/m\3\ for decision-making purposes.
    While we conclude, based on available data, that 24-hour exposures 
below 0.3 mg/m\3\ 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/m\3\) chosen as a health-
based 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/m\3\ 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/m\3\. 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

[[Page 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/m\3\) 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/
m\3\. Therefore, assuming an SEL of 83 
mg/m\3\ 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/m\3\. 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 worst-case 
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

[[Page 21938]]

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 co-located 
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 co-located 
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/m\3\, the maximum concentration using tier 2 approaches for actual 
plants was about 4.5 mg/m\3\, and the maximum concentration of any 
facility using the refined tier 3 approach was 7.6 mg/m\3\ (using 1995 
data) and 3.65 mg/m\3\ (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/m\3\ 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/m\3\ 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/m\3\. The worst-case average methanol 
concentration in the AIRS monitoring database was found to be 0.2 mg/
m\3\. 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

[[Page 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/m\3\, but that such exposures may not reasonably be expected to 
exceed 7 mg/m\3\. 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/m\3\. As 
stated above, the petitioner proposes a SEL of 
83 mg/m\3\. 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/m\3\, 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 health-based criterion for EPA decision making for 
this methanol petition is the range of 0.3 to 30 mg/m\3\. 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/m\3\ 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/m\3\, which is well above 
0.3 
mg/m\3\. 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

[[Page 21940]]

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