[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
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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
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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