to increased medication use, increased school and work absences,
increased visits to doctors’ offices and emergency departments, and
increased hospital admissions, especially in people with lung disease.
These physiological effects are all indicators of potential adverse
O3-related morbidity effects, which are consistent with and lend
plausibility to the associations observed between O3 and adverse
morbidity effects and mortality effects in epidemiological studies.

With regard to epidemiological studies, the Administrator observes that
statistically significant associations between ambient O3 levels and a
wide array of respiratory symptoms and other morbidity outcomes
including school absences, emergency department visits, and hospital
admissions have been reported in a large number of studies.  More
specifically, positive and robust associations were found between
ambient O3 concentrations and respiratory hospital admissions and
emergency department visits, when focusing particularly on the results
of warm season analyses.  Taken together, the overall body of evidence
from controlled human exposure, toxicological, and epidemiological
studies supports the inference of a causal relationship between acute
ambient O3 exposures and increased respiratory morbidity outcomes
resulting in increased emergency department visits and hospitalizations
during the warm season.  Further, the Administrator notes that recent
epidemiological evidence is highly suggestive that O3 directly or
indirectly contributes to non-accidental and cardiopulmonary-related
mortality.

The Administrator also considered the epidemiological evidence with
regard to considering potential effects thresholds at the population
level for morbidity and mortality effects.  As discussed above, while
some studies provide some indication of possible 8-hour average
threshold levels from below about 0.025 to 0.035 ppm (within the range
of background concentrations) up to approximately 0.050 ppm, other
studies observe linear concentration-response functions suggesting that
there may be no effects thresholds at the population level above
background concentrations.  In addition, other studies conducted subset
analyses that included only days with ambient O3 concentrations below
the level of the then current standard, or below even lower O3
concentrations, including a level as low as 0.061 ppm, and continue to
report statistically significant associations.  The Administrator notes
that the relationships between ambient O3 concentrations and lung
function decrements, respiratory symptoms, indicators of respiratory
morbidity including increased respiratory-related emergency department
visits and hospital admissions, and possibly mortality reported in a
large number of studies likely extend down to ambient O3 concentrations
well below the level of the standard set in 2008 (0.075 ppm), in that
the highest level at which there is any indication of a threshold is
approximately 0.050 ppm.  The Administrator notes as well that toward
the lower end of the range of O3 concentrations observed in such
studies, ranging down to background levels (i.e., 0.035 to 0.015 ppm),
there is increasing uncertainty as to whether the observed associations
remain plausibly related to exposures to ambient O3, rather than to the
broader mix of air pollutants present in the ambient atmosphere.  She
also notes that there are limitations in epidemiological studies that
make discerning population thresholds difficult, as discussed above,
such that there is the possibility that thresholds for individuals may
exist in reported associations at fairly low levels within the range of
air quality observed in the studies but not be detectable as population
thresholds in epidemiological analyses.

In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the
Administrator finds substantial evidence, newly available for
consideration in the 2008 rulemaking, that people with asthma and other
preexisting pulmonary diseases are among those at increased risk from O3
exposure.  As discussed above, altered physiological, morphological, and
biochemical states typical of respiratory diseases like asthma, COPD,
and chronic bronchitis may render people sensitive to additional
oxidative burden induced by O3 exposure.  Children and adults with
asthma are the group that has been studied most extensively.  Evidence
from controlled human exposure studies indicates that asthmatics and
people with allergic rhinitis may exhibit larger lung function
decrements in response to O3 exposure than healthy subjects and that
they can have larger inflammatory responses.  The Administrator also
notes that two large U.S. epidemiological studies, as well as several
smaller U.S. and international studies, have reported fairly robust
associations between ambient O3 concentrations and measures of lung
function and daily symptoms (e.g., chest tightness, wheeze, shortness of
breath) in children with moderate to severe asthma and between O3 and
increased asthma medication use.  These more serious responses in
asthmatics and others with lung disease provide biological plausibility
for the respiratory morbidity effects observed in epidemiological
studies, such as respiratory-related emergency department visits and
hospital admissions.

The Administrator also observes that a substantial body of evidence from
controlled human exposure and epidemiological studies indicates that
relative to the healthy, non-asthmatic subjects used in most controlled
human exposure studies, a greater proportion of people with asthma may
be affected, and those who are affected may have as large or larger lung
function and symptomatic responses to O3 exposures.  Thus, the
Administrator concludes that controlled human exposure studies of lung
function decrements and respiratory symptoms that evaluate only healthy,
non-asthmatic subjects likely underestimate the effects of O3 exposure
on asthmatics and other susceptible populations.

In addition to the evidence-based considerations discussed above, the
Administrator also considered quantitative exposures and health risks
estimated to occur associated with air quality simulated to just meet
various standard levels to help inform judgments about a range of
standard levels for consideration that could provide an appropriate
degree of public health protection.  In so doing, she is mindful of the
important uncertainties and limitations that are associated with the
exposure and risk assessments, as discussed in more detail in the 2007
Staff Paper, and above in sections II.B and II.C.1.b.  Beyond these
uncertainties, the Administrator also recognized important limitations
related to the exposure and risk analyses.  For example, EPA did not
have sufficient information to evaluate all relevant at-risk groups
(e.g., outdoor workers) or all O3-related health outcomes (e.g.,
increased medication use, school absences, emergency department visits),
and the scope of the analyses was generally limited to estimating
exposures and risks in 12 urban areas across the U.S., and to only five
or just one area for some health effects.  Thus, it is clear that
national-scale public health impacts of ambient O3 exposures are much
larger than the quantitative estimates of O3-related incidences of
adverse health effects and the numbers of children likely to experience
exposures of concern associated with meeting the then current standard
or alternative standards.  Taking these limitations into account, the
CASAC advised EPA not to rely solely on the results of the exposure and
risk assessments in considering alternative standards, but also to place
significant weight on the body of evidence of O3-related health effects
in drawing conclusions about an appropriate range of levels for
consideration.  The Administrator agrees with this advice.

Turning first to the results of the exposure assessment, the
Administrator focused on the extent to which alternative standard
levels, approximately at and below the 0.075 ppm O3 standard set in the
2008 final rule, are estimated to reduce exposures over the 0.060 and
0.070 ppm health effects benchmark levels, for all and asthmatic school
age children in the 12 urban areas included in the assessment.  The
Administrator also took note that the lowest standard level included in
the exposure and health risk assessments was 0.064 ppm and that
additional reductions in exposures over the selected health benchmark
levels would be anticipated for just meeting a 0.060 ppm standard.

As an initial matter, the Administrator recognized that the concept of
“exposures of concern” is more appropriately viewed as a continuum,
with greater confidence and less uncertainty about the existence of
health effects at the upper end and less confidence and greater
uncertainty as one considers increasingly lower O3 exposure levels.  In
considering the concept of exposures of concern, the Administrator also
noted that it is important to balance concerns about the potential for
health effects and their severity with the increasing uncertainty
associated with our understanding of the likelihood of such effects at
lower O3 levels.  Within the context of this continuum, estimates of
exposures of concern at discrete benchmark levels provide some
perspective on the public health impacts of O3-related physiological
effects that have been demonstrated in controlled human exposure and
toxicological studies but cannot be evaluated in quantitative risk
assessments, such as lung inflammation, increased airway responsiveness,
and changes in host defenses.  They also help in understanding the
extent to which such impacts have the potential to be reduced by meeting
alternative standards.  As discussed in II.C.1.a above, these O3-related
physiological effects are plausibly linked to the increased morbidity
seen in epidemiological studies (e.g., as indicated by increased
medication use in asthmatics, school absences in all children, and
emergency department visits and hospital admissions in people with lung
disease).

Estimates of the number of people likely to experience exposures of
concern cannot be directly translated into quantitative estimates of the
number of people likely to experience specific health effects, since
sufficient information to draw such comparisons is not available -- if
such information were available, these health outcomes would have been
included in the quantitative risk assessment.  Due to individual
variability in responsiveness, only a subset of individuals who have
exposures at and above a specific benchmark level are expected to
experience such adverse health effects, and susceptible population
groups such as those with asthma are expected to be affected more by
such exposures than healthy individuals.

For the reasons discussed in section II.C.1.b above, the Administrator
has concluded that it is appropriate to focus on both the 0.060 and
0.070 ppm health effect benchmarks for her decision on the primary
standard.  In summary, the focus on these two benchmark levels reflects
the following evidence-based considerations, discussed above in section
II.C.1.a, that raise concerns about adverse health effects likely
occurring at levels below 0.080 ppm:  (1) that there is limited, but
important, new evidence from controlled human exposure studies showing
lung function decrements and respiratory symptoms in some healthy
subjects at 0.060 ppm; (2)  that asthmatics are likely to have more
serious responses than healthy individuals; (3) that lung function is
not likely to be as sensitive a marker for O3 effects as lung
inflammation; and (4) that there is epidemiological evidence which
reports associations between ambient O3 concentrations and respiratory
symptoms, ED visits, hospital admissions, and premature mortality in
areas with O3 levels that extend well below 0.080 ppm.

Based on the exposure and risk considerations discussed in detail in the
2007 Staff Paper and presented in sections II.B and II.C.1.b above, the
Administrator notes the following important observations from these
assessments:  1) there is a similar pattern for all children and
asthmatic school age children in terms of exposures of concern over
selected benchmark levels when estimates are expressed in terms of
percentage of the population; 2) the aggregate estimates of exposures of
concern reflecting estimates for the 12 urban areas included in the
assessment are considerably larger for the benchmark level of 0.060 ppm
compared to the 0.070 ppm benchmark; 3) there is notable year-to-year
variability in exposure and risk estimates with higher exposure and risk
estimates occurring in simulations involving a year with generally
poorer air quality in most areas (2002) compared to a year with
generally better air quality (2004); and 4) there is significant
city-to-city variability in exposure and risk estimates, with some
cities receiving considerably less protection associated with air
quality just meeting the same standard.  As discussed above, the
Administrator believes that it is appropriate to consider not just the
aggregate estimates across all cities, but also to consider the public
health impacts in cities that receive relatively less protection from
alternative standards under consideration.  Similarly, the Administrator
believes that year-to-year variability should also be considered in
making judgments about which standards will protect public health with
an adequate margin of safety.

In addition, significant reductions in exposures of concern and risk
have been estimated to occur across standard levels analyzed.  The
magnitudes of exposure and risk reductions estimated to occur in going
from a 0.074 ppm standard to a 0.064 ppm standard are as large as those
estimated to occur in going from the then current 0.084 ppm standard to
a 0.074 ppm standard.  Consequently, the reduction in risk that can be
achieved by going from a standard of 0.074 ppm to a standard of 0.064
ppm is  comparable to the risk reduction that can be achieved by moving
from the 1997 O3 standard, effectively a 0.084 ppm standard, to a
standard very close to the 2008 standard of 0.075 ppm.

The Administrator also observes that estimates of exposures of concern
associated with air quality just meeting the alternative standards below
0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm, the levels included in the
assessment) are notably lower than estimates for alternative standards
set at and above 0.080 ppm.  As shown in Table 6-8 in the 2007 Staff
Paper, just meeting a 0.080 ppm standard is associated with an aggregate
estimate of exposures of concern of about 13% of asthmatic children at
the 0.070 ppm benchmark level, ranging up to 31% in the city with the
least degree of protection in a year with generally poorer air quality,
and an aggregate estimate of exposures of concern of about 40% of
asthmatic children, ranging up to 63% in the city with the least degree
of protection at the 0.060 ppm benchmark level.  Based on the exposure
estimates presented in Table 3 in this notice, she observes that
standards included in the assessment below 0.080 ppm (i.e., 0.074,
0.070, and 0.064 ppm), are estimated to have substantially lower
estimates of exposures of concern at the 0.070 ppm benchmark level.
Similarly, she notes that exposures of concern at the 0.060 ppm
benchmark associated with alternative standards below 0.080 ppm are
appreciably lower than exposures associated with standards at or above
0.080 ppm, especially for standards set at 0.064 and 0.070 ppm.

As noted previously, the Administrator also recognizes that the risk
estimates for health outcomes included in the risk assessment are
limited and that the overall health effects evidence is indicative of a
much broader array of O3-related health effects that are part of a
“pyramid of effects” that include various indicators of morbidity
that could not be included in the risk assessment (e.g., school
absences, increased medication use, doctor’s visits, and emergency
department visits), some of which have a greater impact on at-risk
groups.  Consideration of such unquantified risks for this array of
health effects, taken together with the estimates of exposures of
concern and the quantified health risks discussed above, supports the
Administrator’s evidence-based conclusion that revising the standard
level to a level well below 0.080 ppm will provide important increased
public health protection, especially for at-risk groups such as people
with asthma or other lung disease, as well as children and older adults,
particularly those active outdoors, and outdoor workers

Based on the evidence- and exposure/risk-based considerations discussed
above, the Administrator concludes that it is appropriate to set the
level of the primary O3 standard to a level well below 0.080 ppm, a
level at which the evidence provides a high degree of certainty about
the adverse effects of O3 exposure in healthy people, to provide an
adequate margin of safety for at-risk groups.  In selecting a proposed
range of levels, the Administrator believes it is appropriate to
consider the following information:  (1) the strong body of evidence
from controlled human exposure studies evaluating healthy people at
exposure levels of 0.080 ppm and above that demonstrated lung function
decrements, respiratory symptoms, pulmonary inflammation, and other
medically significant airway responses, as well as limited but important
evidence of lung function decrements and respiratory symptoms in healthy
people down to O3 exposure levels of 0.060 ppm; (2) the substantial body
of evidence from controlled human exposure and epidemiological studies
indicating that people with asthma are likely to experience larger and
more serious effects than healthy people; (3) the body of
epidemiological evidence indicating associations are observed for a wide
range of serious health effects, including respiratory-related emergency
department visits and hospital admissions and premature mortality,
across distributions of ambient O3 concentrations that extend below the
current standard level of 0.075 ppm, as well as questions of biological
plausibility in attributing the observed effects to O3 alone at the
lower end of the concentration ranges extending down to background
levels; and (4) the estimates of exposures of concern and risks for a
range of health effects that indicate that important improvements in
public health are very likely associated with O3 levels just meeting
alternative standards, especially for standards set at 0.070 and 0.064
ppm (the lowest levels included in the assessment), relative to
standards set at and above 0.080 ppm.

The Administrator next considered what standard level well below 0.080
ppm would be requisite to protect public health, including the health of
at-risk groups, with an adequate margin of safety that is sufficient but
not more than necessary to achieve that result.  The assessment of a
standard level calls for consideration of both the degree of risk to
public health at alternative levels of the standard as well as the
certainty that such risk will occur at any specific level.  Based on the
information available in the 2008 rulemaking, there is no evidence-based
bright line that indicates a single appropriate level.  Instead there is
a combination of scientific evidence and other information that needs to
be considered as a whole in making this public health policy judgment,
and selecting a standard level from a range of potentially reasonable
values.

As an initial matter, the Administrator considered whether the standard
level of 0.075 ppm set in the 2008 final rule is sufficiently below
0.080 ppm to be requisite to protect public health with an adequate
margin of safety.  In considering this standard level, the Administrator
looked to the rationale for selecting this level presented in the 2008
final rule, as summarized above in section II.C.3.  In that rationale,
EPA observed that a level of 0.075 ppm is above the range of 0.060 to
0.070 ppm recommended by CASAC, and that the CASAC Panel appeared to
place greater weight on the evidence from the Adams studies and on the
results of the exposure and risk assessments, whereas EPA placed greater
weight on the limitations and uncertainties associated with that
evidence and the quantitative exposure and risk assessments.
Additionally, EPA’s rationale did not discuss and thus
placedapparently gave no weight at all toon exposures of concern
relative to the 0.060 ppm benchmark which reflected the
lowest-observed-effects level for lung function effects observed in
healthy adults in the Adams studies.  Further, EPA concluded that “[a]
standard set at a lower level than 0.075 ppm would only result in
significant further public health protection if, in fact, there is a
continuum of health risks in areas with 8-hour average O3 concentrations
that are well below the concentrations observed in the key controlled
human exposure studies and if the reported associations observed in
epidemiological studies are, in fact, causally related to O3 at those
lower levels.  Based on the available evidence, [EPA] is not prepared to
make these assumptions” (73 FR 16483).

In reconsidering the entire body of evidence available in the 2008
rulemaking, including the Agency’s own assessment of the
epidemiological evidence in the 2006 Criteria Document, and placing
significant weight on the views of CASAC, the Administrator now finds a
compelling basis for concludesing that important and significant risks
to public health are likely to occur at a standard level of 0.075 ppm
based on the controlled human exposure, toxicological, and
epidemiological evidence.  She judges that a standard level of 0.075 ppm
is not sufficient to provide protection with an adequate margin of
safety.  In support of this conclusion, the Administrator finds that
setting a standard that would protect public health, including the
health of at-risk populations, with an adequate margin of safety should
reasonably depend upon giving some weight to the results of the Adams
studies and EPA's reanalysis of the Adams's data, and to how effectively
alternative standard levels would serve to limit exposures of concern
relative to the 0.060 ppm benchmark level as well as to the 0.070 ppm
benchmark level.  The Administrator notes that EPA’s risk assessment
estimates comparable risk reductions in going from a 0.074 ppm standard
to a 0.064 ppm standard as were estimated in going from the then current
0.084 ppm standard down to a 0.074 ppm standard for an array of health
effects analyzed.  These estimates include reductions in risk for lung
function decrements in all and asthmatic school age children,
respiratory symptoms in asthmatic children, respiratory-related hospital
admissions, and non-accidental mortality.

Further, based on the exposure assessment estimates discussed above, the
Administrator notes that for air quality just meeting a 0.074 ppm
standard, approximately 27% of asthmatic school age children and 25% of
all school age children are estimated to experience one or more
exposures of concern over the 0.060 ppm benchmark level based on
simulations for a year with generally poorer air quality; this estimate
increases to about 50% of asthmatic and all children in the city with
the least degree of protection.  The Administrator judges that these
estimates are large and strongly suggest significant public health
impacts would likely remain in many areas with air quality just meeting
a 0.075 ppm O3 standard.

In light of these estimates and the available evidence, the
Administrator agrees with CASAC’s conclusion that important public
health protections can be achieved by a standard set below 0.075 ppm,
within the range of 0.060 to 0.070 ppm.  In addition, based on both the
evidence- and exposure/risk-based considerations summarized above, the
Administrator concludes that a standard set as high as 0.075 would not
be considered requisite to protect public health with an adequate margin
of safety, and that consideration of lower levels is warranted.  In
considering such lower levels, the Administrator recognizes that the CAA
requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical assessments
that have inherent uncertainties and limitations.  This judgment
requires making reasoned decisions as to what weight to place on various
types of evidence and assessments and on the related uncertainties and
limitations.

In selecting a level below 0.075 ppm that would serve as an appropriate
upper end for a range of levels to propose, the Administrator has
considered a more cautious approach to interpreting the available
evidence and exposure/risk-based information – that is, an approach
that places significant weight on uncertainties and limitations in the
information so as to avoid potentially overestimating public health
risks and protection likely to be associated with just meeting a
particular standard level.   In so doing, she notes that the most
certain evidence of adverse health effects from exposure to O3 comes
from the controlled human exposure studies, and that the large bulk of
this evidence derives from studies of exposures at levels of 0.080 ppm
and above.  At those levels, there is consistent evidence of lung
function decrements and respiratory symptoms in healthy young adults, as
well as evidence of inflammation and other medically significant airway
responses.  Further, she takes note of the limited but important
evidence from controlled human exposure studies indicating that lung
function decrements and symptoms can occur in healthy people at levels
as low as 0.060 ppm, while also recognizing the limitations in that
evidence, as discussed above in sections II.A.1 and II.C.1.a.  She also
notes that some people with asthma are likely to experience larger and
more serious effects than the healthy subjects evaluated in the
controlled exposure studies, while recognizing that there is uncertainty
about the magnitude of such differences.  In considering the available
epidemiological studies, she recognizes that they provide evidence of
serious respiratory morbidity effects, including respiratory-related
emergency department visits and hospital admissions, and non-accidental
mortality at levels well below 0.080 ppm, while also recognizing that
there is increasing uncertainty associated with the likelihood that such
effects occur at decreasing O3 levels down to background levels.
Considering the exposure/risk information, as shown in Table 3, the
Administrator observes that a standard set at 0.070 ppm would likely
substantially limit exposures of concern relative to the 0.070 ppm
benchmark level, while affording far less protection against exposures
of concern relative to the 0.060 ppm benchmark level.  To the extent
that more weight is placed on protection relative to the higher
benchmark level, and more weight is placed on the uncertainties
associated with the epidemiological evidence, a standard set at 0.070
ppm might be considered to be adequately protective.  Taken together,
this type of cautious approach to interpreting the evidence and the
exposure/risk information serves as the basis for the Administrator’s
conclusion that the upper end of the proposed range should be set at
0.070 ppm O3.

In selecting a level that would serve as an appropriate lower end for a
range of levels to propose, the Administrator has considered a more
precautionary approach to interpreting the available evidence and
exposure/risk-based information – that is, an approach that places
less weight on uncertainties and limitations in the information so as to
avoid potentially underestimating public health improvements likely to
be associated with just meeting a particular standard level.  In so
doing, the Administrator notes the limited, but important evidence of a
lowest-observed-effects level at 0.060 ppm O3 from controlled human
exposure studies reporting lung function decrements and respiratory
symptoms in healthy subjects.  Notably, these studies also report that a
small percentage of subjects (7 to 20 percent) experienced moderate lung
function decrements (> 10 percent) at the 0.060 ppm exposure level,
recognizing that for people with lung disease, such moderate functional
or symptomatic responses would likely interfere with normal activity for
many individuals, and would likely result in more frequent use of
medication.  In addition, a substantial body of evidence indicates that
people with asthma are likely to experience larger and more serious
effects than healthy people and therefore controlled human exposure
studies done with healthy subjects likely underestimate effects in this
at-risk population.

Moreover, epidemiological studies provide evidence of serious
respiratory morbidity effects, including respiratory-related emergency
department visits and hospital admissions, and non-accidental mortality
at O3 levels that may plausibly extend down to at least 0.060 ppm even
when considering the uncertainties inherent in such studies.  The
Administrator notes that the controlled human exposure studies conducted
at 0.060 ppm provide some biological plausibility for associations
between respiratory morbidity and mortality effects found in
epidemiological studies and O3 exposures down to 0.060 ppm.  Considering
the exposure information, as shown in Table 3, the Administrator
observes that a standard set at 0.064 ppm would likely essentially
eliminate exposures of concern relative to the 0.070 ppm benchmark
level, while appreciably limiting exposures of concern relative to the
0.060 ppm benchmark level to approximately 6 percent of asthmatic
children in the aggregate across 12 cities and up to 16 percent in the
city that would receive the least protection.  While not addressed in
the exposure assessment done as part of the 2008 rulemaking, a standard
set at 0.060 ppm would be expected to provide somewhat greater
protection from such exposures, which is important to the extent that
more weight is placed on providing protection relative to the lower
benchmark level.  Taken together, the Administrator concludes that this
precautionary approach to interpreting the evidence and the
exposure/risk information supports a level of 0.060 ppm as the lower end
of the proposed range.

The Administrator has also concluded that the lower end of the proposed
range should not extend below 0.060 ppm O3.  In reaching this
conclusion, she gives significant weight to the recommendation of the
CASAC panel that 0.060 ppm should be the lower end of the range for
consideration (Henderson, 2006c).  In the Administrator's view, the
evidence from controlled human exposure studies at the 0.060 ppm
exposure level, the lowest level tested, is not robust enough to support
consideration of a lower level.  While some epidemiological studies
provide evidence of serious respiratory morbidity effects and
non-accidental mortality with no evidence of a threshold, the
Administrator notes that other studies provide evidence of a potential
threshold somewhat below 0.060 ppm.  Moreover, there are limitations in
epidemiological studies that make discerning population thresholds
difficult, including fewer observations in the range of lower
concentrations, concerns related to exposure measurement error, the
possible role of copollutants and effects modifiers, and interindividual
differences in susceptibility to O3-related effects.  In the
Administrator’s judgment, these limitations in epidemiological
studies, including the limitations in judging the causality of observed
associations at lower O3 levels, and the lack of robust controlled human
exposure data at 0.060 ppm make it difficult to interpret this evidence
as a basis for a standard level set below 0.060 ppm.  Thus, in selecting
0.060 ppm as the lower end of the range for the proposed level of the O3
standard, the Administrator has taken into account information on the
lowest-observed-effects levels in controlled human exposure studies,
indications of possible thresholds reported in some epidemiological
studies, the increasing uncertainty in the epidemiological evidence at
even lower levels, as well as evidence about increased susceptibility of
people with asthma and also other lung diseases.  In so doing, she
concludes that a primary O3 standard set below 0.060 ppm would be more
than is necessary to protect public health with an adequate margin of
safety for at-risk groups.

In reaching her proposed decision, the Administrator has also considered
the public comments that were received on the 2007 proposed rule (72 FR
37818).  The Administrator notes that there were sharply divergent views
expressed by two general sets of commenters with regard to considering
the health effects evidence, results of exposure and risk assessments,
and the advice of the CASAC panel.  On one hand, medical groups, health
effects researchers, public health organizations, environmental groups,
and some state, tribal and local air pollution control agencies strongly
supported a standard set within the range recommended by the CASAC.
These commenters generally placed significant weight on the more recent
evidence from controlled human exposure studies, down to the 0.060 ppm
exposure level, as well as on the epidemiological studies and the
results of the exposure and risk assessment conducted for the 2008
rulemaking.  Many of these commenters took a more precautionary view and
supported a standard set at 0.060 ppm O3, the lower end of the CASAC
recommended range.  The Administrator notes that these views are
generally consistent with her proposed conclusions.  On the other hand,
another group of commenters primarily representing industry associations
and businesses and some state environmental agencies, primarily
expressed the view that the more recent evidence from controlled human
exposure, the epidemiological studies, and the results of exposure and
human health risk assessments were so uncertain that they did not
provide a basis for making any changes to the then current 0.084 ppm O3
standard set in 1997.  This group of commenters generally argued that
the health effects evidence newly available in the 2008 rulemaking, the
results of the exposure and health risk assessments, and the advice of
the CASAC were flawed.  For the reasons discussed above, the
Administrator does not agree with the later group of commenters that
essentially no weight should be placed on any of the new evidence or
assessments that were available for consideration in the 2008
rulemaking.

Based on consideration of the entire body of evidence and information
available in the 2008 rulemaking, including exposure and risk estimates,
as well as the recommendations of CASAC, the Administrator proposes to
set the level of the primary 8-hour O3 standard to a level within the
range of 0.060 to 0.070 ppm.  A standard level within this range would
reduce the risk of a variety of health effects associated with exposure
to O3, including the respiratory symptoms and lung function effects
demonstrated in the controlled human exposure studies, and the
respiratory-related emergency department visits, hospital admissions and
mortality effects observed in the epidemiological studies.  All of these
effects are indicative of a much broader array of O3-related health
endpoints, such as school absences and increased medication use, that
are plausibly linked to these observed effects.  Depending on the weight
placed on the evidence and information available in the 2008 rulemaking,
as well as the uncertainties and limitations in the evidence and
information, a standard could be set within this range  at a level that
would be requisite to protect public health with an adequate margin of
safety.

In reaching this proposed decision, as discussed above, the
Administrator has focused on the nature of the increased public health
protection that would be afforded by a standard set within the proposed
range of levels relative to the protection afforded by the standard set
in 2008.  Having considered the public comments received on the 2007
proposed rule in reaching this proposed decision that reconsiders the
2008 final rule, the Administrator is interested in again receiving
public comment on the benefits to public health associated with a
standard set at specific levels within the proposed range relative to
the benefits associated with the standard set in 2008.

D.	Proposed Decision on the Level of the Primary Standard

For the reasons discussed above, and taking into account information and
assessments presented in the 2006 Criteria Document and 2007 Staff
Paper, the advice and recommendations of CASAC, and public comments
received during the 2008 rulemaking, the Administrator proposes to set a
new level for the 8-hour primary O3 standard.  Specifically, the
Administrator proposes to set the level of the 8-hour primary O3
standard to within a range of 0.060 to 0.070 ppm.  The proposed 8-hour
primary standard would be met at an ambient air monitoring site when the
3-year average of the annual forth-highest daily maximum 8-hour average
O3 concentration is less than or equal to the level of the standard that
is promulgated.  Thus, the Administrator proposes to set a standard with
a level within this range.  She solicits comment on this range and on
the appropriate weight to place on the various types of available
evidence, the exposure and risk assessment results, and the
uncertainties and limitations related to this information, as well as on
the benefits to public health associated with a standard set within this
range relative to the benefits associated with the standard set in 2008.

III.	Communication of Public Health Information

	Information on the public health implications of ambient concentrations
of criteria pollutants is currently made available primarily through
EPA's Air Quality Index (AQI) program.  The current Air Quality Index
has been in use since its inception in 1999 (64 FR 42530).  It provides
accurate, timely, and easily understandable information about daily
levels of pollution (40 CFR 58.50).  The AQI establishes a nationally
uniform system of indexing pollution levels for O3, carbon monoxide,
nitrogen dioxide, particulate matter and sulfur dioxide.  The AQI
converts pollutant concentrations in a community's air to a number on a
scale from 0 to 500.  Reported AQI values enable the public to know
whether air pollution levels in a particular location are characterized
as good (0 - 50), moderate (51 - 100), unhealthy for sensitive groups
(101 - 150), unhealthy (151 - 200), very unhealthy (201 - 300), or
hazardous (300 - 500).  The AQI index value of 100 typically corresponds
to the level of the short-term NAAQS for each pollutant.  An AQI value
greater than 100 means that a pollutant is in one of the unhealthy
categories (i.e., unhealthy for sensitive groups, unhealthy, very
unhealthy, or hazardous) on a given day; whereas an AQI value at or
below 100 means that a pollutant concentration is in one of the
satisfactory categories (i.e., moderate or good).  Decisions about the
pollutant concentrations at which to set the various AQI breakpoints,
that delineate the various AQI categories, draw directly from the
underlying health information that supports the NAAQS review.

	In the 2008 rulemaking, the AQI for O3 was revised by setting an AQI
value of 100 equal to 0.075 ppm, 8-hour average, the level of the
revised primary O3 standard.  The other AQI breakpoints were also
revised as follows:  An AQI value of 50 is set at 0.059 ppm; an AQI
value of 150 was set at 0.095 ppm; and an AQI value of 200 was set at
0.115 ppm.  All these levels are averaged over 8 hours.  These levels
were developed by making proportional adjustments to the other AQI
breakpoints (i.e., AQI values of 50, 150 and 200).

The Agency recognizes the importance of revising the AQI in a timely
manner to be consistent with any revisions to the NAAQS.  Therefore,
having proposed to set a new level for the 2008 primary 8-hour O3
standard in this action, EPA also proposes to finalize conforming
changes to the AQI in connection with the Agency's final decision on the
level of the primary O3 standard.  These conforming changes would
include setting the 100 level of the AQI at the same level as that set
for the primary O3 standard resulting from this rulemaking, and also
making proportional adjustments to AQI breakpoints at the lower end of
the range (i.e., AQI values of 50, 150 and 200).  EPA does not propose
to change breakpoints at the higher end of the range (from 300 to 500),
which would apply to state contingency plans or the Significant Harm
Level (40 CFR 51.16), because the information from this reconsideration
of the 2008 final rule does not inform decisions about breakpoints at
those higher levels.

With respect to reporting requirements (40 CFR Part 58, §58.50), EPA
proposes to require that the AQI be reported in all metropolitan and
micropolitan statistical areas where O3 monitoring is required, as
discussed below in section VI.  The Agency solicits comments on our
proposed approach to AQI reporting requirements.  We are also revising
40 CFR Part 58, §58.50 (c) to require the reporting requirements to be
based on the latest available census figures, rather than the most
recent decennial U.S. census.  This change is consistent with our
current practice of using the latest population figures to make
monitoring requirements more responsive to changes in population.

IV. 	Rationale for Proposed Decision on the Secondary Standard

	As an initial matter, the Administrator notes that the 2008 final rule
concluded that (1) the protection afforded by the 1997 secondary O3
standard was “not sufficient and that the standard needs to be revised
to provide additional protection from known and anticipated adverse
effects on sensitive natural vegetation and sensitive ecosystems, and
that such a revised standard could also be expected to provide
additional protection to sensitive ornamental vegetation” and (2)
“that there is not adequate information to establish a separate
secondary standard based on other effects of O3 on public welfare” (73
FR 16497).  The Administrator is not reconsidering these aspects of the
2008 decision, which are based on the reasons discussed in section IV.B
of the 2008 final rule (73 FR 16489-16497).  The Administrator also
notes that the 2008 final rule concluded that it was appropriate to
retain the O3 indicator for the secondary O3 standard.   The
Administrator is not reconsidering this aspect of the 2008 decision,
which was based on the reasons discussed in sections IV.B and IV.C of
the 2008 final rule (73 FR 16489-16497).  For these reasons, the
Administrator is not reopening the 2008 decision with regard to the need
to revise the 1997 secondary O3 standard to provide additional
protection from known and anticipated adverse effects on sensitive
natural vegetation and sensitive ecosystems, nor with regard to the
appropriate indicator for the secondary standard.  Thus, the information
that follows in this section specifically focuses on a reconsideration
of the 8-hour secondary O3 standard set in the 2008 final rule for the
purpose of determining whether and, if so, how to revise the form,
averaging time, and level of the standard to provide appropriate
protection from known and anticipated adverse effects on sensitive
natural vegetation and sensitive ecosystems.

	This section presents the rationale for the Administrator’s proposed
decision that the secondary O3 standard, which was set identical to the
revised primary standard in the 2008 final rule, should instead be a new
cumulative, seasonal standard.  This standard is expressed in terms of a
concentration-weighted form commonly called W126, which uses a sigmoidal
weighting function to assign a weight to each hourly O3 concentration
within the 12 hour daylight period (8:00 am to 8:00 pm).   This daily
ozone index is defined as follows:

 .

 The daily index values are then summed over each month within the O3
season, and the annual highest consecutive three month sum is
determined.  The proposed standard consists of the three-year average of
this highest three-month statistic, set at a level within the range of 7
to 15 ppm-hours.

	As discussed more fully below, the rationale for this proposed new
standard is based on a thorough review, in the 2006 Criteria Document,
of the latest scientific information on vegetation, ecological and other
public welfare effects associated with the presence of O3 in the ambient
air.  This rationale also takes into account and is consistent with:
(1) staff assessments of the most policy-relevant information in the
2006 Criteria Document and staff analyses of air quality, vegetation
effects evidence, exposure, and risks, presented in the 2007 Staff
Paper, upon which staff recommendations for revisions to the secondary
O3 standard are based; (2) CASAC advice and recommendations as reflected
in discussions of drafts of the 2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate written comments, and in CASAC's
letters to the Administrator, both before and after the 2008 rulemaking,
and (3) public comments received during development of these documents,
either in conjunction with CASAC meetings or separately; and on the 2007
proposed rule, and (4) consideration of the degree of protection to
vegetation potentially afforded by the 2008 8-hour standard.

	In developing this rationale, the Administrator has again focused on
direct O3 effects on vegetation, specifically drawing upon an
integrative synthesis of the entire body of evidence (EPA, 2006a,
chapter 9), published through early 2006, on the broad array of
vegetation effects associated with the presence of O3 in the ambient
air.  In addition, because O3 can also indirectly affect other ecosystem
components such as soils, water, and wildlife, and their associated
ecosystem goods and services, through its effects on vegetation, a
qualitative discussion of these other indirect impacts is also included,
though these effects were not quantifiable at the time of the 2008
rulemaking.  As discussed below in section IV.A, the peer-reviewed
literature includes studies conducted in the U.S., Canada, Europe, and
many other countries around the world.  In reconsidering this evidence,
as was concluded in the 2008 rulemaking, and based on the body of
scientific literature assessed in the 2006 Criteria Document, the
Administrator continues to believes that it is reasonable to conclude
that a secondary standard protecting the public welfare from known or
anticipated adverse effects to trees and native vegetation would also
afford increased protection from adverse effects to other environmental
components relevant to the public welfare, including ecosystem services
and function.  Section IV.B focuses on considerations related to
biologically relevant exposure indices.  This rationale also draws upon
the results of quantitative exposure and risk assessments, discussed
below in section IV.C.  Section IV.D focuses on the considerations upon
which the Administrator’s proposed conclusions are based.
Considerations regarding a cumulative seasonal standard as well as an
8-hour standard are discussed, and the rationale for the 2008 decision
on the secondary standard and CASAC advice, given both prior to the
development of the 2007 proposed rule and following the 2008 final rule,
are summarized.  Finally, the Administrator’s proposed conclusions on
the secondary standard are presented.  Section IV.E summarizes the
proposed decision on the secondary O3 standard and the solicitation of
public comments.

	As with virtually any policy-relevant vegetation effects research,
there is uncertainty in the characterization of vegetation effects
attributable to exposure to ambient O3.  As discussed below, however,
research conducted since the 1997 review provides important information
coming from field-based exposure studies, including free air, gradient,
and biomonitoring surveys, in addition to the more traditional open top
chamber (OTC) studies. Moreover, the newly available studies evaluated
in the 2006 Criteria Document have undergone intensive scrutiny through
multiple layers of peer review and many opportunities for public review
and comment.  While important uncertainties remain, the review of the
vegetation effects information has been extensive and deliberate.  In
the judgment of the Administrator, the intensive evaluation of the
scientific evidence that has occurred provides an adequate basis for
this reconsideration of the 2008 rulemaking.

A.	Vegetation Effects Information

	This section outlines key information contained in the 2006 Criteria
Document (chapter 9) and in the 2007 Staff Paper (chapter 7) on known or
anticipated effects on public welfare associated with the presence of O3
in ambient air.  The information highlighted here summarizes: (1) new
information available in the 2008 rulemaking on potential mechanisms for
vegetation effects associated with exposure to O3; (2) the nature of
effects on vegetation that have been associated with exposure to O3 and
consequent potential impacts on ecosystems; and (3) considerations in
characterizing what constitutes an adverse welfare impact of O3.

	Exposures to O3 have been associated quantitatively and qualitatively
with a wide range of vegetation effects.  The decision in the 1997
review to set a more protective secondary standard primarily reflected
consideration of the quantitative information on vegetation effects
available at that time, particularly growth impairment (e.g., biomass
loss) in sensitive forest tree species during the seedling growth stage
and yield loss in important commercial crops.  This information, derived
mainly using the open top chamber (OTC) exposure method, found
cumulative, seasonal O3 exposures were most strongly associated with
observed vegetation response.  The 2006 Criteria Document discusses a
number of additional studies that support and strengthen key conclusions
regarding O3 effects on vegetation and ecosystems found in the previous
Criteria Document (EPA, 1996a, 2006a), including further clarification
of the underlying mechanistic and physiological processes at the
sub-cellular, cellular, and whole system levels within the plant.  More
importantly, however, in the context of this review, new quantitative
information is now available across a broader array of vegetation
effects (e.g., growth impairment during seedlings, saplings and mature
tree growth stages, visible foliar injury, and yield loss in annual
crops) and across a more diverse set of exposure methods, including
chamber, free air, gradient, model, and field-based observation.  The
non-chambered, field-based study results begin to address one of the key
data gaps cited by EPA in the 1997 review.

	The following discussion of the policy-relevant science regarding
vegetation effects associated with cumulative, seasonal exposures to
ambient levels of O3 integrates information from the 2006 Criteria
Document (chapter 9) and the 2007 Staff Paper (chapter 7).

1.	Mechanisms

Scientific understanding regarding O3 impacts at the genetic,
physiological, and mechanistic levels helps to explain the biological
plausibility and coherence of the evidence for O3-induced vegetation
effects and informs the interpretation of predictions of risk associated
with vegetation response at ambient O3 exposure levels.  In most cases,
the mechanisms of response are similar regardless of the degree of
sensitivity of the species.  The evidence assessed in the 2006 Criteria
Document (EPA, 2006a) regarding the O3-induced changes in physiology
continues to support the information discussed in the 1997 review (EPA,
1996a, 2006a).  In addition, during the last decade understanding of the
cellular processes within plants has been further clarified and
enhanced.  This section reviews the key scientific conclusions
identified in 1996 Criteria Document (EPA, 1996a), and incorporates
recent information from the Criteria Document (EPA, 2006a).  This
section describes: (1) plant uptake of O3, (2) O3-induced cellular to
systemic response, (3) plant compensation and detoxification mechanisms,
(4) O3-induced changes to plant metabolism, and (5) plant response to
chronic O3 exposures.

a.	Plant Uptake of Ozone

To cause injury, O3 must first enter the plant through openings in the
leaves called stomata.  Leaves exist in a three dimensional environment
called the plant canopy, where each leaf has a unique orientation and
receives a different exposure to ambient air, microclimatological
conditions, and sunlight.  In addition, a plant may be located within a
stand of other plants which further modifies ambient air exchange with
individual leaves.  Not all O3 entering a plant canopy is absorbed into
the leaf stomata, but may be adsorbed to other surfaces e.g., leaf
cuticles, stems, and soil (termed non-stomatal deposition) or scavenged
by reactions with intra-canopy biogenic VOCs and naturally occurring NOx
emissions from soils.  Because O3 does not typically penetrate the
leaf’s cuticle, it must reach the stomatal openings in the leaf for
absorption to occur.  The movement of O3 and other gases such as CO2
into and out of leaves is controlled by stomatal guard cells that
regulate the size of the stomatal apertures.  These guard cells respond
to a variety of internal species-specific factors as well as external
site specific environmental factors such as light, temperature,
humidity, CO2 concentration, soil fertility, water status, and in some
cases, the presence of air pollutants, including O3.  These modifying
factors produce stomatal conductances that vary between leaves of the
same plant, individuals and genotypes within a species as well as
diurnally and seasonally.

b.	Cellular to Systemic Response

Once inside the leaf, O3 can react with a variety of biochemical
compounds that are exposed to the air spaces within the leaf or it can
be dissolved into the water lining the cell wall of the air spaces.
Once in the aqueous phase, O3 can be rapidly altered to form oxidative
products that can diffuse more readily into and through the cell and
react with many biochemical compounds.  Early steps in a series of
O3-induced events that can lead to leaf injury seems to involve
alteration in cell membrane function, including membrane transport
properties (EPA, 2006a) and/or reactions with organic molecules that in
certain circumstances result in the generation of signaling compounds.
The generation of such signaling compounds can lead to a cascade of
events.  One such signaling molecule is hydrogen peroxide (H2O2). The
presence of higher-than-normal levels of H2O2 within the leaf is a
potential trigger for a set of metabolic reactions that include those
typical of the well documented “wounding” response or pathogen
defense pathway generated by cutting of the leaf or by pathogen/insect
attack.  Ethylene is another compound produced when plants are subjected
to biotic or abiotic stressors. Increased ethylene production by plants
exposed to O3 stress was identified as a consistent marker for O3
exposure in studies conducted decades ago (Tingey et al., 1976).

c.	Compensation and Detoxification

Ozone injury will not occur if (1) the rate and amount of O3 uptake is
small enough for the plant to detoxify or metabolize O3 or its
metabolites or (2) the plant is able to repair or compensate for the O3
impacts (Tingey and Taylor, 1982; U.S. EPA, 1996a).  With regard to the
first, a few studies have documented direct stomatal closure or
restriction in the presence of O3 in some species, which limits O3
uptake and potential subsequent injury.  This response may be initiated
ranging from within minutes to hours or days of exposure (Moldau et al.,
1990; Dann and Pell, 1989; Weber et al., 1993).  However, exclusion of
O3 simultaneously restricts the uptake of CO2, which also limits
photosynthesis and growth.  In addition, antioxidants present in plants
can effectively protect tissue against damage from low levels of
oxidants by dissipating excess oxidizing power.  Since 1996, the role of
detoxification in providing a level of resistance to O3 has been further
investigated.  A number of antioxidants have been found in plants.
However, the pattern of changes in the amounts of these antioxidants
varies greatly among different species and conditions.  Most recent
reports indicate that ascorbate within the cell wall provides the first
significant opportunity for detoxification to occur.  In spite of the
new research, however, it is still not clear as to what extent
detoxification protects against O3 injury.  Specifically, data are
needed on potential rates of antioxidant production, sub-cellular
location(s) of antioxidants, and whether generation of these
antioxidants in response to O3-induced stress potentially diverts
resources and energy away from other vital uses.  Thus, the 2006
Criteria Document concludes that scientific understanding of the
detoxification mechanisms is not yet complete and requires further
investigation (EPA, 2006a).

Regarding the second, once O3 injury has occurred in leaf tissue, some
plants are able to repair or compensate for the impacts.  In general,
plants have a variety of compensatory mechanisms for low levels of
stress including reallocation of resources, changes in root/shoot ratio,
production of new tissue, and/or biochemical shifts, such as increased
photosynthetic capacity in new foliage and changes in respiration rates,
indicating possible repair or replacement of damaged membranes or
enzymes.  Since these mechanisms are genetically determined, not all
plants have the same complement of compensatory mechanisms or degree of
tolerance, and these may vary over the life of the plant as not all
stages of a plant’s development are equally sensitive to O3.  At
higher levels or over longer periods of O3 stress, some of these
compensatory mechanisms, such as a reallocation of resources away from
storage in the roots in favor of leaves or shoots, could occur at a cost
to the overall health of the plant.  However, it is not yet clear to
what degree or how the use of plant resources for repair or compensatory
processes affects the overall carbohydrate budget or subsequent plant
response to O3 or other stresses (EPA, 1996a, EPA, 2006a).

d.	 Changes to Plant Metabolism

Ozone inhibits photosynthesis, the process by which plants produce
energy rich compounds (e.g., carbohydrates) in the leaves.  This
impairment can result from direct impact to chloroplast function and/or
O3-induced stomatal closure resulting in reduced uptake of CO2.  A large
body of literature published since 1996 has further elucidated the
mechanism of effect of O3 within the chloroplast.  Pell et al. (1997)
showed that O3 exposure results in a loss of the central carboxylating
enzyme that plays an important role in the production of carbohydrates.
Due to its central importance, any decrease in this enzyme may have
severe consequences for the plant’s productivity.  Several recent
studies have found that O3 has a greater effect as leaves age, with the
greatest impact of O3 occurring on the oldest leaves (Fiscus et al.,
1997; Reid and Fiscus, 1998; Noormets et al., 2001; Morgan et al.,
2004).  The loss of this key enzyme as a function of increasing O3
exposure is also linked to an early senescence or a speeding up of
normal development leading to senescence.  If total plant photosynthesis
is sufficiently reduced, the plant will respond by reallocating the
remaining carbohydrate at the level of the whole organism (EPA, 1996a,
2006a).  This reallocation of carbohydrate away from the roots into
above ground vegetative components can have serious implications for
perennial species, as discussed below.

e.	Plant Response to Chronic Ozone Exposures

Though many changes that occur with O3 exposure can be observed within
hours, or perhaps days, of the exposure, including those connected with
wounding, other effects take longer to occur and tend to become most
obvious after chronic seasonal exposures to low O3 concentrations.
These lower chronic exposures have been linked to senescence or some
other physiological response very closely linked to senescence.  In
perennial plant species, a reduction in carbohydrate storage in one year
may result in the limitation of growth the following year (Andersen et
al., 1997).  Such “carry-over” effects have been documented in the
growth of tree seedlings (Hogsett et al., 1989; Sasek et al., 1991;
Temple et al., 1993; EPA, 1996a) and in roots (Andersen et al., 1991;
EPA, 1996a).  Though it is not fully understood how chronic seasonal O3
exposure affects long-term growth and resistance to other biotic and
abiotic insults in long-lived trees, accumulation of these carry-over
effects over time could affect survival and reproduction.

2.	Nature of Effects

Ozone injury at the cellular level can accumulate sufficiently to induce
effects at the level of a whole leaf or plant.  These larger scale
effects can include: reduced carbohydrate production and/or
reallocation; reduced growth and/or reproduction; visible foliar injury
and/or premature senescence; and reduced plant vigor.  Much of what is
now known about these O3-related effects, as summarized below, is based
on research that was available in the 1997 review.  Studies available in
the 2008 rulemaking continue to support and expand this knowledge (EPA,
2006a).

a.	 Carbohydrate Production and Allocation

	When total plant photosynthesis is sufficiently reduced, the plant will
respond by reallocating the remaining carbohydrate at the level of the
whole organism.  Many studies have demonstrated that root growth is more
sensitive to O3 exposure than stem or leaf growth (EPA, 2006a). When
fewer carbohydrates are present in the roots, less energy is available
for root-related functions such as acquisition of water and nutrients.
In addition, by inhibiting photosynthesis and the amount of
carbohydrates available for transfer to the roots, O3 can disrupt the
association between soil fungi and host plants.  Fungi in the soil form
a symbiotic relationship with many terrestrial plants.  For host plants,
these fungi improve the uptake of nutrients, protect the roots against
pathogens, produce plant growth hormones, and may transport
carbohydrates from one plant to another (EPA, 1996a).  These below
ground effects have recently been documented in the field (Grulke et
al., 1998; Grulke and Balduman, 1999).  Data from a long-studied
pollution gradient in the San Bernardino Mountains of southern
California suggest that O3 substantially reduces root growth in natural
stands of Ponderosa pine (Pinus ponderosa).  Root growth in mature trees
was decreased at least 87 percent in a high-pollution site as compared
to a low-pollution site (Grulke et al., 1998), and a similar pattern was
found in a separate study with whole-tree harvest along this gradient
(Grulke and Balduman, 1999).  Though effects on other ecosystem
components were not examined, a reduction of root growth of this
magnitude could have significant implications for the below-ground
communities at those sites.  Because effects on leaf and needle
carbohydrate content under O3 stress can range from a reduction (Barnes
et al., 1990; Miller et al., 1989), to no effect (Alscher et al., 1989),
to an increase (Luethy-Krause and Landolt, 1990), studies that examine
only above-ground vegetative components may miss important O3-induced
changes below ground.  These below-ground changes could signal a shift
in nutrient cycling with significance at the ecosystem level (Young and
Sanzone, 2002).

b.	Growth Effects on Trees

	Studies comparing the O3-related growth response of different
vegetation types (coniferous and deciduous) and growth stages (e.g.,
seedling and mature) have established that on average, individual
coniferous trees are less sensitive than deciduous trees, and deciduous
trees are generally less sensitive to O3 than most annual plants, with
the exception of a few fast growing deciduous tree species (e.g.,
quaking aspen, black cherry, and cottonwood), which are highly sensitive
and, in some cases, as much or more sensitive to O3 than sensitive
annual plants.  In addition, studies have shown that the relationship
between O3 sensitivity in seedling and mature growth stages of trees can
vary widely, with seedling growth being more sensitive to O3 exposures
in some species, while in others, the mature growth stage is the more O3
sensitive.  In general, mature deciduous trees are likely to be more
sensitive to O3 than deciduous seedlings, and mature evergreen trees are
likely to be less sensitive to O3 than their seedling counterparts.
Based on these results, stomatal conductance, O3 uptake, and O3 effects
cannot be assumed to be equivalent in seedlings and mature trees.

In the 1997 review (EPA, 1996b), analyses of the effects of O3 on trees
were limited to 11 tree species for which concentration-response (C-R)
functions for the seedling growth stage had been developed from OTC
studies conducted by the National Health and Environmental Effects
Research Lab, Western Ecology Division (NHEERL-WED).  A number of
replicate studies were conducted on these species, leading to a total of
49 experimental cases.  The 2007 Staff Paper presented a graph of the
composite regression equation that combines the results of the C-R
functions developed for each of the 49 cases.  The NHEERL-WED study
predicted relative biomass loss at various exposure levels in terms of a
12-hour W126.  For example, 50 percent of the tree seedling cases would
be protected from greater than 10 percent biomass loss at a 3-month,
12-hour W126 of approximately 24 ppm-hour, while 75 percent of cases
would be protected from 10 percent biomass loss at a 3-month, 12-hour
W126 level of approximately 16 ppm-hour.

Since the 1997 review, only a few studies have developed C-R functions
for additional tree seedling species (EPA, 2006a).  One such study is of
particular importance because it documented growth effects in the field
of a similar magnitude as those previously seen in OTC studies but
without the use of chambers or other fumigation methods (Gregg et al.,
2003).  This study placed eastern cottonwood (Populus deltoides)
saplings at sites along a continuum of ambient O3 exposures that
gradually increased from urban to rural areas in the New York City area
(Gregg et al., 2003).  Eastern cottonwood is a fast growing O3 sensitive
tree species that is important ecologically along streams and
commercially for pulpwood, furniture manufacturing, and as a possible
new source for energy biomass (Burns and Hankola, 1990).  Gregg et al.
(2003) found that the cottonwood saplings grown in urban New York City
grew faster than saplings grown in downwind rural areas.  Because these
saplings were grown in pots with carefully controlled soil nutrient and
moisture levels, the authors were able to control for most of the
differences between sites. After carefully considering these and other
factors, the authors concluded the primary explanation for the
difference in growth was the gradient of cumulative O3 exposures that
increased as one moved downwind from urban to less urban and more rural
sites.  It was determined that the lower O3 exposure within the city
center was due to NOx titration reactions which removed O3 from the
ambient air.  The authors were able to reproduce the growth responses
observed in the field in a companion OTC experiment, confirming O3 as
the stressor inducing the growth loss response (Gregg et al., 2003).

Another recent set of studies employed a modified Free Air CO2
Enrichment (FACE) methodology to expose vegetation to elevated O3
without the use of chambers.  This exposure method was originally
developed to expose vegetation to elevated levels of CO2, but was later
modified to include O3 exposure in Illinois (SoyFACE) and Wisconsin
(AspenFACE) for soybean and deciduous trees, respectively (Dickson et
al., 2000; Morgan et al., 2004).  The FACE method releases gas (e.g.,
CO2, O3) from a series of orifices placed along the length of the
vertical pipes surrounding a circular field plot and uses the prevailing
wind to distribute it. This exposure method has many characteristics
that differ from those associated with the OTC.  Most significantly,
this exposure method more closely replicates conditions in the field
than do OTCs.  This is because, except for O3 levels which are varied
across co-located plots, plants are exposed to the same ambient growing
conditions that occur naturally in the field (e.g., location-specific
pollutant mixtures; climate conditions such as light, temperature and
precipitation; insect pests, pathogens).  By using one of several
co-located plots as a control (e.g., receives no additional O3), and by
exposing the other rings to differing levels of elevated O3, the growth
response signal that is due solely to the change in O3 exposure can be
clearly determined.  Furthermore, the FACE system can expand vertically
with the growth of trees, allowing for exposure experiments to span
numerous years, an especially useful capability in forest research.

On the other hand, the FACE methodology also has the undesirable
characteristic of potentially creating hotspots near O3 gas release
orifices or gradients of exposure in the outer ring of trees within the
plots, such that averaging results across the entire ring potentially
overestimates the response.  In recognition of this possibility,
researchers at the AspenFACE experimental site only measured trees in
the center core of each ring, (e.g., at least 5-6 meters away from the
emission sites of O3) (Dickson et al 2000, Karnosky et al. 2005).  By
taking this precaution, it is unlikely that their measurements were
influenced by any potential hotspots or gradients of exposure within the
FACE rings.  Taking all of the above into account, results from the
Wisconsin FACE site on quaking aspen appear to demonstrate that the
detrimental effects of O3 exposure seen on tree growth and symptom
expression in OTCs can be observed in the field using this exposure
method (Karnosky et al., 1999; 2005).

The 2007 Staff Paper thus concluded that the combined evidence from the
AspenFACE and Gregg et al. (2003) field studies provide compelling and
important support for the appropriateness of continued use of the C-R
functions derived using OTC from the NHEERL-WED studies to estimate risk
to these tree seedlings under ambient field exposure conditions.  These
studies make a significant contribution to the coherence of the weight
of evidence available in this review and provide additional evidence
that O3-induced effects observed in chambers also occur in the field.

Trees and other perennials, in addition to cumulating the effects of O3
exposures over the annual growing season, can also cumulate effects
across multiple years.  It has been reported that effects can “carry
over” from one year to another (EPA, 2006a).  Growth affected by a
reduction in carbohydrate storage in one year may result in the
limitation of growth in the following year (Andersen, et al., 1997).
Carry-over effects have been documented in the growth of some tree
seedlings (Hogsett et al. 1989; Simini et al., 1992; Temple et al.,
1993) and in roots (Andersen et al., 1991; EPA, 1996a).  On the basis of
past and recent OTC and field study data, ambient O3 exposures that
occur during the growing season in the United States are sufficient to
potentially affect the annual growth of a number of sensitive seedling
tree species.  However, because most studies do not take into account
the possibility of carry over effects on growth in subsequent years, the
true implication of these annual biomass losses may be missed.  It is
likely that under ambient exposure conditions, some sensitive trees and
perennial plants could experience compounded impacts that result from
multiple year exposures.

c.	Visible Foliar Injury

Cellular injury to leaves due to exposure to O3 can and often does
become visible.  Acute injury usually appears within 24 hours after
exposure to O3 and, depending on species, can occur under a range of
exposures and durations from 0.040 ppm for a period of 4 hours to 0.410
ppm for 0.5 hours for crops and 0.060 ppm for 4 hours to 0.510 ppm for 1
hour for trees and shrubs (Jacobson, 1977). Chronic injury may be mild
to severe. In some cases, cell death or premature leaf senescence may
occur.  The significance of O3 injury at the leaf and whole plant levels
depends on how much of the total leaf area of the plant has been
affected, as well as the plant’s age, size, developmental stage, and
degree of functional redundancy among the existing leaf area.  As a
result, it is not presently possible to determine, with consistency
across species and environments, what degree of injury at the leaf level
has significance to the vigor of the whole plant.

The presence of visible symptoms due to O3 exposures can, however, by
itself, represent an adverse impact to the public welfare.
Specifically, it can reduce the market value of certain leafy crops
(such as spinach, lettuce), impact the aesthetic value of ornamentals
(such as petunia, geranium, and poinsettia) in urban landscapes, and
affect the aesthetic value of scenic vistas in protected natural areas
such as national parks and wilderness areas.  Many businesses rely on
healthy looking vegetation for their livelihoods (e.g.,
horticulturalists, landscapers, Christmas tree growers, farmers of leafy
crops) and a variety of ornamental species have been listed as sensitive
to O3 (Abt Associates Inc, 1995).  Though not quantified, there is
likely some level of economic impact to businesses and homeowners from
O3-related injury on sensitive ornamental species due to the cost
associated with more frequent replacement and/or increased maintenance
(fertilizer or pesticide application).  In addition, because O3 not only
results in discoloration of leaves but can lead to more rapid senescence
(early shedding of leaves) there potentially could be some lost tourist
dollars at sites where fall foliage is less available or attractive.

T  SEQ CHAPTER \h \r 1 he use of sensitive plants as biological
indicators to detect phytotoxic levels of O3 is a longstanding and
effective methodology (Chappelka and Samuelson, 1998; Manning and Krupa,
1992).  Each bioindicator exhibits typical O3 injury symptoms when
exposed under appropriate conditions.  These symptoms are considered
diagnostic as they have been verified in exposure-response studies under
experimental conditions.  In recent years, field surveys of visible
foliar injury symptoms have become more common, with greater attention
to the standardization of methods and the use of reliable indicator
species (Campbell et al., 2000; Smith et al., 2003). Specifically, the
Unites States Forest Service (USFS) through the Forest Health Monitoring
Program (FHM) (1990 - 2001) and currently the Forest Inventory and
Analysis (FIA) Program collects data regarding the incidence and
severity of visible foliar injury on a variety of O3 sensitive plant
species throughout the U.S. (Coulston et al. 2003, 2004; Smith et al.
2003).

	Since the conclusion of the 1997 review, the FIA monitoring program
network and database has continued to expand.  This network continues to
document foliar injury symptoms in the field under ambient exposure
conditions.  Recent survey results show that O3-induced foliar injury
incidence is widespread across the country.  The visible foliar injury
indicator has been identified as a means to track O3 exposure stress
trends in the nation’s natural plant communities as highlighted in
EPA’s most recent Report on the Environment (EPA, 2003a;
http://www.epa.gov/indicators/roe).

Previous Criteria Documents have noted the difficulty in relating
visible foliar injury symptoms to other vegetation effects such as
individual tree growth, stand growth, or ecosystem characteristics (EPA,
1996a) and this difficulty remains to the present day (EPA, 2006a).  It
is important to note that direct links between O3 induced visible foliar
injury symptoms and other adverse effects are not always found.
Therefore, visible foliar injury cannot serve as a reliable surrogate
measure for other O3-related vegetation effects because other effects
(e.g., biomass loss) have been reported with and without visible injury.
 In some cases, visible foliar symptoms have been correlated with
decreased vegetative growth (Karnosky et al., 1996; Peterson et al.,
1987; Somers et al., 1998) and with impaired reproductive function
(Black et al., 2000; Chappelka, 2002).  Therefore, the lack of visible
injury should not be construed to indicate a lack of phytotoxic
concentrations of O3 nor absence of other non-visible O3 effects.

d.	Reduced Plant Vigor

Though O3 levels over most of the U.S. are not high enough to kill
vegetation directly, current levels have been shown to reduce the
ability of many sensitive species and genotypes within species to adapt
to or withstand other environmental stresses.  These O3 effects may
include increased susceptibility to freezing temperatures, increased
vulnerability to pest infestations and/or root disease, and compromised
ability to compete for available resources.  As an example of the
latter, when species with differing O3-sensitivities occur together,
O3-sensitive species may experience a greater reduction in growth than
more O3-tolerant species, which then can better compete for available
resources.  The result of such above effects can produce a loss in plant
vigor in O3-sensitive species that over time may lead to premature plant
death.

Ecosystems

Ecosystems are comprised of complex assemblages of organisms and the
physical environment with which they interact.  Each level of
organization within an ecosystem has functional and structural
characteristics.  At the ecosystem level, functional characteristics
include, but are not limited to, energy flow; nutrient, hydrologic, and
biogeochemical cycling; and maintenance of food chains.  The sum of the
functions carried out by ecosystem components provides many benefits to
humankind, as in the case of forest ecosystems (Smith, 1992).  Some of
these benefits, also termed “ecosystem goods and services”, include
food, fiber production, aesthetics, genetic diversity, maintenance of
water quality, air quality, and climate, and energy exchange.  A
conceptual framework for discussing the effects of stressors, including
air pollutants such as O3, on ecosystems was developed by the EPA
Science Advisory Board (Young and Sanzone, 2002).  In this report, the
authors identify six essential ecological attributes (EEAs) of
ecosystems including landscape condition, biotic condition,
chemical/physical condition, ecological processes,
hydrology/geomorphology, and natural disturbance regime.  Each EEA is
depicted as one of six triangles that together build a hexagon.  On the
outside of each triangle is a list of stressors that can act on the EEA.
 Tropospheric O3 is listed as a stressor of both biotic condition and
the chemical/physical condition of ecosystems.  As each EEA is linked to
all the others, it is clearly envisioned in this framework that O3 could
either directly or indirectly impact all of the EEAs associated with an
ecosystem that is being stressed by O3.

Vegetation often plays an influential role in defining the structure and
function of an ecosystem, as evidenced by the use of dominant vegetation
forms to classify many types of natural ecosystems, e.g., tundra,
wetland, deciduous forest, and conifer forest.  Plants simultaneously
inhabit both above-and below-ground environments, integrating and
influencing key ecosystem cycles of energy, water, and nutrients.  When
a sufficient number of individual plants within a community have been
affected, O3-related effects can be propagated up to ecosystem-level
effects.  Thus, through its impact on vegetation, O3 can be an important
ecosystem stressor.

i.	Potential Ozone Alteration of Ecosystem Structure and Function

	The 2006 Criteria Document outlines seven case studies where O3 effects
on ecosystems have either been documented or are suspected.  The oldest
and clearest example involves the San Bernardino Mountain forest
ecosystem in California.  This system experienced chronic high O3
exposures over a period of 50 or more years.  The O3-sensitive and
co-dominant species of ponderosa and Jeffrey pine demonstrated severe
levels of foliar injury, premature senescence, and needle fall that
decreased the photosynthetic capacity of stressed pines and reduced the
production of carbohydrates resulting in a decrease in radial growth and
in the height of stressed trees.  It was also observed that ponderosa
and Jeffrey pines with slight to severe crown injury lost basal area in
relation to competing species that are more tolerant to O3.  Due to a
loss of vigor, these trees eventually succumbed to the bark beetle,
leading to elevated levels of tree death.  Increased mortality of
susceptible trees shifted the community composition towards white fir
and incense cedar, effectively reversing the development of the normal
fire climax mixture dominated by ponderosa and Jeffrey pines, and
leading to increased fire susceptibility.  At the same time, numerous
other organisms and processes were also affected either directly or
indirectly, including successional patterns of fungal microflora and
their relationship to the decomposer community.  Nutrient availability
was influenced by the heavy litter and thick needle layer under stands
with the most severe needle injury and defoliation.  In this example, O3
appeared to be a predisposing factor that led to increased drought
stress, windthrow, root diseases, and insect infestation (Takemoto et
al., 2001).  Thus, through its effects on tree water balance, cold
hardiness, tolerance to wind, and susceptibility to insect and disease
pests, O3 potentially impacted the ecosystem-related EEA of natural
disturbance regime (e.g., fire, erosion).  Although the role of O3 was
extremely difficult to separate from other confounding factors, such as
high nitrogen deposition, there is evidence that this shift in species
composition has altered the structure and dynamics of associated food
webs (Pronos et al., 1999) and carbon (C) and nitrogen (N) cycling
(Arbaugh et al., 2003).  Ongoing and new research in this important
ecosystem is needed to reveal the extent to which ecosystem services
have been affected and to what extent strong causal linkages between
historic and/or current ambient O3 exposures and observed
ecosystem-level effects can be made.

	Ozone has also been reported to be a selective pressure among sensitive
tree species (e.g., eastern white pine) in the east.  The nature of
community dynamics in eastern forests is different, however, than in the
west, consisting of a wider diversity of species and uneven aged stands,
and the O3 levels are less severe.  Therefore, lower level chronic O3
stress in the east is more likely to produce subtle long-term forest
responses such as shifts in species composition, rather than wide-spread
community degradation.

	Some of the best-documented studies of population and community
response to O3 effects are the long-term studies of common plantain
(Plantago major) in native plant communities in the United Kingdom
(Davison and Reiling, 1995; Lyons et al., 1997; Reiling and Davison,
1992c).  Elevated O3 significantly decreased the growth of sensitive
populations of common plantain (Pearson et al., 1996; Reiling and
Davison, 1992a, b; Whitfield et al., 1997) and reduced its fitness as
determined by decreased reproductive success (Pearson et al., 1996;
Reiling and Davison, 1992a).  While spatial comparisons of population
responses to O3 are complicated by other environmental factors, rapid
changes in O3 resistance were imposed by ambient levels and variations
in O3 exposure (Davison and Reiling, 1995).  Specifically, in this case
study, it appeared that O3-sensitive individuals are being removed by O3
stress and the genetic variation represented in the population could be
declining.  If genetic diversity and variation is lost in ecosystems,
there may be increased vulnerability of the system to other biotic and
abiotic stressors, and ultimately a change in the EEAs and associated
services provided by those ecosystems.

	Recent free-air exposure experiments have also provided new insight
into how O3 may be altering ecosystem structure and function (Karnosky
et al., 2005).  For example, a field O3 exposure experiment at the
AspenFACE site in Wisconsin (described in section IV.A.2.b. above) was
designed to examine the effects of both elevated CO2 and O3  on mixed
stands of aspen (Populus tremuloides), birch (Betula papyrifera), and
sugar maple (Acer saccharum) that are characteristic of Great Lakes
aspen-dominated forests (Karnosky et al., 2003; Karnosky et al., 1999).
They found evidence that the effects on above- and below-ground growth
and physiological processes have cascaded through the ecosystem, even
affecting microbial communities (Larson et al., 2002; Phillips et al.,
2002).  This study also confirmed earlier observations of O3-induced
changes in trophic interactions involving keystone tree species, as well
as important insect pests and their natural enemies (Awmack et al.,
2004; Holton et al., 2003; Percy et al., 2002).

	Collectively these examples suggest that O3 is an important stressor in
natural ecosystems, but it is difficult to quantify the contribution of
O3 due to the combination of other stresses present in ecosystems.  In
most cases, because only a few components in each of these ecosystems
have been examined and characterized for O3 effects, the full extent of
ecosystem changes in these example ecosystems is not fully understood.
Clearly, there is a need for highly integrated ecosystem studies that
specifically investigate the effect of O3 on ecosystem structure and
function in order to fully determine the extent to which O3 is altering
ecosystem services.  Continued research, employing new approaches, will
be necessary to fully understand the extent to which O3 is affecting
ecosystem services.

ii.	Effects on Ecosystem Services and Carbon Sequestration

Since it has been established that O3 affects photosynthesis and growth
of plants, O3 is most likely affecting the productivity of forest
ecosystems.  Therefore, it is desirable to link effects on growth and
productivity to essential ecosystem services.  However, it is very
difficult to quantify ecosystem-level productivity losses because of the
amount of complexity in scaling from the leaf-level or individual plant
to the ecosystem level, and because not all organisms in an ecosystem
are equally affected by O3.

	Terrestrial ecosystems are important in the Earth's carbon (C) balance
and could help offset emissions of CO2 by humans if anthropogenic C is
sequestered in vegetation and soils.  The annual increase in atmospheric
CO2 is less than the total inputs from fossil fuel burning and land use
changes (Prentice et al., 2001), and much of this discrepancy is thought
to be attributable to CO2 uptake by plant photosynthesis (Tans & White,
1998).  Temperate forests of the northern hemisphere have been estimated
to be a net sink of about 0.6 to 0.7 petagrams (Pg) C per year (Goodale
et al. 2002).  Ozone interferes with photosynthesis, causes some plants
to senesce leaves prematurely, and in some cases, reduces allocation to
stem and root tissue.  Thus, O3 decreases the potential for C
sequestration.  For the purposes of this discussion, C sequestration is
defined as the net exchange of carbon by the terrestrial biosphere.
However, long-term storage in the soil organic matter is considered to
be the most stable form of C storage in ecosystems.

	In a study including all ecosystem types, Felzer et al. (2004),
estimated that U.S. net primary production (net flux of C into an
ecosystem) was decreased by 2.6-6.8 percent due to O3 pollution in the
late 1980's to early 1990's.  Ozone not only reduces C sequestration in
existing forests, it can also affect reforestation projects (Beedlow et
al. 2004).  This effect, in turn, has been found to ultimately inhibit C
sequestration in forest soils which act as long-term C storage (Loya et
al., 2003; Beedlow et al. 2004).  The interaction of rising O3 pollution
and rising CO2 concentrations in the coming decades complicates
predictions of future sequestration potential.  Models generally predict
that, in the future, C sequestration will increase with increasing CO2,
but often do not account for the decrease in productivity due to the
local effects of current or potentially increasing levels of
tropospheric O3.  In the presence of high O3 levels, the stimulatory
effect of rising CO2 concentrations on forest productivity has been
estimated to be reduced by more that 20 percent (Tingey et al., 2001;
Ollinger et al. 2002; Karnosky et al., 2003).

	In summary, it would be anticipated that meeting lower O3 standards
would increase the amount of CO2 uptake by many ecosystems in the U.S.
However, the amount of this improvement would be heavily dependent on
the species composition of those ecosystems.  Many ecosystems in the
U.S. do have O3 sensitive plants.  For, example forest ecosystems with
dominant species such as aspen or ponderosa pine would be expected to
increase CO2 uptake more with lower O3 than forests with more O3
tolerant species.

	A recent critique of the secondary NAAQS review process published in
the report by the National Academy of Sciences on Air Quality Management
in the United States (NRC, 2004) stated that “EPA’s current practice
for setting secondary standards for most criteria pollutants does not
appear to be sufficiently protective of sensitive crops and
ecosystems...”  This report made several specific recommendations for
improving the secondary NAAQS process and concluded that “There is
growing evidence that tighter standards to protect sensitive ecosystems
in the United States are needed....”  An effort has been recently
initiated within the Agency to identify indicators of ecological
condition whose responses can be clearly linked to changes in air
quality that are attributable to Agency environmental programs.  Using a
single indicator to represent the complex linkages and dynamic cycles
that define ecosystem condition will always have limitations.  With
respect to O3-related impacts on ecosystem condition, only two candidate
indicators, foliar injury (as described above) and radial growth in
trees, have been suggested.  Thus, while at the present time, most
O3-related effects on ecosystems must be inferred from observed or
predicted O3-related effects on individual plants, additional research
at the ecosystem level could identify new indicators and/or establish
stronger causal linkages between O3-induced plant effects and ecosystem
condition.

f.	Yield Reductions in Crops

	Ozone can interfere with carbon gain (photosynthesis) and allocation of
carbon with or without the presence of visible foliar injury.  As a
result of decreased carbohydrate availability, fewer carbohydrates are
available for plant growth, reproduction, and/or yield.  Recent studies
have further confirmed and demonstrated O3 effects on different stages
of plant reproduction, including pollen germination, pollen tube growth,
fertilization, and abortion of reproductive structures, as reviewed by
Black et al. (2000).  For seed-bearing plants, these reproductive
effects will culminate in reduced seed production or yield.

	As described in the 1997 review and again in the 2006 Criteria Document
and 2007 Staff Paper, the National Crop Loss Assessment Network (NCLAN)
studies undertaken in the early to mid-1980's provide the largest, most
uniform database on the effects of O3 on agricultural crop yields.  The
NCLAN protocol was designed to produce crop exposure-response data
representative of the areas in the U.S. where the crops were typically
grown.  In total, 15 species (e.g., corn, soybean, winter wheat,
tobacco, sorghum, cotton, barley, peanuts, dry beans, potato, lettuce,
turnip, and hay [alfalfa, clover, and fescue]), accounting for greater
than 85 percent of U.S. agricultural acreage planted at that time, were
studied.  Of these 15 species, 13 species including 38 different
cultivars were combined in 54 cases representing unique combinations of
cultivars, sites, water regimes, and exposure conditions.  Crops were
grown under typical farm conditions and exposed in open-top chambers to
ambient O3, sub-ambient O3, and above ambient O3.  Robust C-R functions
were developed for each of these crop species.  These results showed
that 50 percent of the studied cases would be protected from greater
than 10 percent yield loss at a W126 level of 21 ppm-hour, while a W126
of 13 ppm-hour would provide protection for 75 percent of the cases
studied from greater than 10 percent yield loss.

	Recent studies continue to find yield loss levels in crop species
studied previously under NCLAN that reflect the earlier findings.  In
other words, there has been no evidence that crops are becoming more
tolerant of O3 (EPA, 2006a).  For cotton, some newer varieties have been
found to have higher yield loss due to O3 compared to older varieties
(Olszyk et al., 1993, Grantz and McCool, 1992).  In a meta-analysis of
53 studies, Morgan et al. (2003) found consistent deleterious effects of
O3 exposures on soybean from studies published between 1973 and 2001.
Further, early results from the field-based exposure experiment SoyFACE
in Illinois indicate a lack of any apparent difference in the O3
tolerance of old and recent cultivars of soybean in a study of 22
soybean varieties (Long et al., 2002).  Thus, the 2007 Staff Paper
concluded that the recent scientific literature continues to support the
conclusions of the 1996 Criteria Document that ambient O3 concentrations
are reducing the yield of major crops in the U.S.

	In addition to the effects described on annual crop species, several
studies published since the 1997 review have focused on perennial forage
crops (EPA, 2006a).  These recent results confirm that O3 is also
impacting yields and quality of multiple-year forage crops at sufficient
magnitude to have nutritional and possibly economic implications to
their use as ruminant animal feed at O3 exposures that occur in some
years over large areas of the U.S.

3.	Adversity of Effects

The 2007 Staff Paper recognized that the statute requires that a
secondary standard be protective against “adverse” O3 effects, not
all identifiable O3-induced effects.  In considering what constitutes a
vegetation effect that is adverse to the public welfare, the 2007 Staff
Paper recognizes that O3 can cause a variety of vegetation effects,
beginning at the level of the individual cell and accumulating up to the
level of whole leaves, plants, plant populations, communities and whole
ecosystems, not all of which have been classified in past reviews as
“adverse” to public welfare.

Previous reviews have classified O3 vegetation effects as either
“injury” or “damage” to help in determining adversity.
Specifically, “injury” is defined as encompassing all plant
reactions, including reversible changes or changes in plant metabolism
(e.g., altered photosynthetic rate), altered plant quality, or reduced
growth, that does not impair the intended use or value of the plant
(Guderian, 1977).  In contrast, “damage” has been defined to include
those injury effects that reach sufficient magnitude as to also reduce
or impair the intended use or value of the plant.  Examples of effects
that are classified as damage include reductions in aesthetic values
(e.g., foliar injury in ornamental species) as well as losses in terms
of weight, number, or size of the plant part that is harvested (reduced
yield or biomass production).  Yield loss also may include changes in
crop quality, i.e., physical appearance, chemical composition, or the
ability to withstand storage, while biomass loss includes slower growth
in species harvested for timber or other fiber uses.  While this
construct has proved useful in the past, it appears to be most useful in
the context of evaluating effects on single plants or species grown in
monocultures such as agricultural crops or managed forests.  It is less
clear how it might apply to potential effects on natural forests or
entire ecosystems when O3-induced species level impacts lead to shifts
in species composition and/or associated ecosystem services such as
nutrient cycling or hydrologic cycles, where the intended use or value
of the system has not been specifically identified.

	A more recent construct for assessing risks to forests described in
Hogsett et al. (1997) suggests that “adverse effects could be
classified into one or more of the following categories: (1) economic
production, (2) ecological structure, (3) genetic resources, and (4)
cultural values.”  This approach expands the context for evaluating
the adversity of O3-related effects beyond the species level.  Another
recent publication, A Framework for Assessing and Reporting on
Ecological Condition: an SAB report (Young and Sanzone, 2002), provides
additional support for  expanding the consideration of adversity beyond
the species level by making explicit the linkages between stress-
related effects (e.g., O3 exposure) at the species level and at higher
levels within an ecosystem hierarchy.  Taking this recent literature
into account, the 2007 Staff Paper concludes that a determination of
what constitutes an “adverse” welfare effect in the context of the
secondary NAAQS review can appropriately occur within this broader
paradigm.

B.	Biologically Relevant Exposure Indices

	The 2006 Criteria Document concluded that O3 exposure indices that
cumulate differentially weighted hourly concentrations are the best
candidates for relating exposure to plant growth responses.  This
conclusion follows from the extensive evaluation of the relevant studies
in the 1996 Criteria Document (EPA, 1996a) and the recent evaluation of
studies that have been published since that time.  The following
selections, taken from the 1996 Criteria Document (EPA, 1996a, section
5.5), further elucidate the depth and strength of these conclusions.
Specifically, with respect to the importance of taking into account
exposure duration, the 1996 Criteria Document stated, “when O3 effects
are the primary cause of variation in plant response, plants from
replicate studies of varying duration showed greater reductions in yield
or growth when exposed for the longer duration” and “the mean
exposure index of unspecified duration could not account for the
year-to-year variation in response” (EPA, 1996a, pg. 5-96).  Further,
“because the mean exposure index treats all concentrations equally and
does not specifically include an exposure duration component, the use of
a mean exposure index for characterizing plant exposures appears
inappropriate for relating exposure with vegetation effects” (EPA,
1996a, pg. 5-88).  Regarding the relative importance of higher
concentrations than lower in determining plant response, the 1996
Criteria Document concluded that “the ultimate impact of long-term
exposures to O3 on crops and seedling biomass response depends on the
integration of repeated peak concentrations during the growth of the
plant” (EPA, 1996a, pg. 5-104).  Further, “at this time, exposure
indices that weight the hourly O3 concentrations differentially appear
to be the best candidates for relating exposure with predicted plant
response” (EPA, 1996a, pgs. 5-136).

	At the conclusion of the 1997 review, the biological basis for a
cumulative, seasonal form was not in dispute.  There was general
agreement between EPA and CASAC, based on their review of the air
quality criteria, that a cumulative, seasonal form was more biologically
based than the then current 1-hour and newly proposed 8-hour average
form.  However, in selecting a specific form appropriate for a secondary
standard, there was less agreement.  An evaluation of the performance of
several  cumulative seasonal forms in predicting plant response data
taken from OTC experiments had found that all performed about equally
well and was unable to distinguish between them (EPA, 1996a).  In
selecting between two of these cumulative forms, the SUM06 and W126, in
the absence of biological evidence to distinguish between them, EPA
based its decision on both science and policy considerations.
Specifically, these were: (1) all cumulative, peak-weighted exposure
indices considered, including W126 and SUM06, were about equally good as
exposure measures to predict exposure-response relationships reported in
the NCLAN crop studies; and (2) the SUM06 form would not be influenced
by PRB O3 concentrations (defined at the time as 0.03 to 0.05 ppm) under
many typical air quality distributions.  On the basis of these
considerations, EPA chose the SUM06 as the most appropriate cumulative,
seasonal form to consider when proposing an alternative secondary
standard form (61 FR 65716).

	Though the scientific justification for a cumulative, seasonal form was
generally accepted in the 1997 review, an analysis undertaken by EPA at
that time had shown that there was considerable overlap between areas
that would be expected not to meet the range of alternative 8-hour
standards being considered for the primary NAAQS and those expected not
to meet the range of values (expressed in terms of the seasonal SUM06
index) of concern for vegetation.  This result suggested that
improvements in national air quality expected to result from attaining
an 8-hour primary standard within the recommended range of levels would
also be expected to significantly reduce levels of concern for
vegetation in those same areas.  Thus, in the 1996 proposed rule, EPA
proposed two alternatives for consideration:  one alternative was to
make the secondary standard equal in every way to the proposed 8-hour,
0.08 ppm primary standard; and the second was to establish a cumulative,
seasonal secondary standard in terms of a SUM06 form as also appropriate
to protect public welfare from known or anticipated adverse effects
given the available scientific knowledge and that such a seasonal
standard “…is more biologically relevant…” (61 FR 65716).

In the 1997 final rule, EPA decided to make the secondary standard
identical to the primary standard.  The EPA acknowledged, however, that
“it remained uncertain as to the extent to which air quality
improvements designed to reduce 8-hr average O3 concentrations averaged
over a 3-year period would reduce O3 exposures measured by a seasonal
SUM06 index.” (62 FR 38876)  In other words, it was uncertain as to
whether the 8-hour average form would, in practice, provide sufficient
protection for vegetation from the cumulative, seasonal and
concentration-weighted exposures described in the scientific literature
as of concern.

	On the basis of that history, the 2007 Staff Paper (chapter 7)
revisited the issue of whether the SUM06 was still the most appropriate
choice of cumulative, seasonal form for a secondary standard to protect
the public welfare from known and anticipated adverse vegetation effects
in light of the new information available in this review.  Specifically,
the 2007 Staff Paper considered: (1) the continued lack of evidence
within the vegetation effects literature of a biological threshold for
vegetation exposures of concern; and (2) new estimates of PRB that were
lower than in the 1997 review.  The W126 form, also evaluated in the
1997 review, was again selected for comparison with the SUM06 form.
Regarding the first consideration, the 2007 Staff Paper noted that the
W126 form, by its incorporation of a continuous sigmoidal weighting
scheme, does not create an artificially imposed concentration threshold,
yet also gives proportionally more weight to the higher and typically
more biologically potent concentrations, as supported by the scientific
evidence.  Second, the index value is not significantly influenced by O3
concentrations within the range of estimated PRB, as the weights
assigned by the sigmoidal weighting scheme to concentrations in this
range are near zero.  Thus, it would also provide a more appropriate
target for air quality management programs designed to reduce emissions
from anthropogenic sources contributing to O3 formation.  On the basis
of these considerations, the 2007 Staff Paper concluded that the W126
form was the most biologically-relevant cumulative, seasonal form
appropriate to consider in the context of the 2008 rulemaking.

C.	Vegetation Exposure and Impact Assessment

	The vegetation exposure and impact assessment conducted for the 2008
rulemaking and described in the 2007 Staff paper, consisted of exposure,
risk and benefits analyses and improved and built upon similar analyses
performed in the 1997 review (EPA 1996b).  The vegetation exposure
assessment was performed using interpolation and included information
from ambient monitoring networks and results from air quality modeling.
The vegetation risk assessment included both tree and crop analyses.
The tree risk analysis includes three distinct lines of evidence:  (1)
observations of visible foliar injury in the field linked to monitored
O3 air quality for the years 2001 – 2004;  (2) estimates of seedling
growth loss under then current and alternative O3 exposure conditions;
and (3) simulated mature tree growth reductions using the TREGRO model
to simulate the effect of meeting alternative air quality standards on
the predicted annual growth of a single western species (ponderosa pine)
and two eastern species (red maple and tulip poplar).  The crop analysis
includes estimates of the risks to crop yields from then current and
alternative O3 exposure conditions and the associated change in economic
benefits expected to accrue in the agriculture sector upon meeting the
levels of various alternative standards.  Each element of the assessment
is described below, including discussions of known sources and ranges of
uncertainties associated with the elements of this assessment.

1.	Exposure Characterization

	Though numerous effects of O3 on vegetation have been documented as
discussed above, it is important in considering risk to examine O3 air
quality patterns in the U.S. relative to the location of O3 sensitive
species that have a known concentration-response in order to predict
whether adverse effects are occurring at current levels of air quality,
and whether they are likely to occur under alternative standard forms
and levels.

	The most important information about exposure to vegetation comes from
the O3 monitoring data that are available from two national networks:
(1) Air Quality System (AQS;   HYPERLINK
"http://www.epa.gov/ttn/airs/airsaqs"
http://www.epa.gov/ttn/airs/airsaqs ) and (2) Clean Air Status and
Trends Network (CASTNET;   HYPERLINK "http://www.epa.gov/castnet/"
http://www.epa.gov/castnet/ ).  The AQS monitoring network currently has
over 1100 active O3 monitors which are generally sited near population
centers.  However, this network also includes approximately 36 monitors
located in national parks.  CASTNET is the nation's primary source for
data on dry acidic deposition and rural, ground-level O3.  It consists
of over 80 sites across the eastern and western U.S. and is
cooperatively operated and funded with the National Park Service.  In
the 1997 O3 NAAQS final rule, it was acknowledged that because the
national air quality surveillance network for O3 was designed
principally to monitor O3 exposure in populated areas, there was limited
measured data available to characterize O3 air quality in rural and
remote sites.  Since the 1997 review, there has been a small increase in
the number of CASTNET sites (from approximately 52 sites in 1992 to 84
sites in 2004), however these monitors are not used for attainment
designations.

	National parks represent areas of nationally recognized ecological and
public welfare significance, which have been afforded a high level of
protection by Congress.  Two recent reports presented some discussion of
O3 trends in a subset of national parks:  The Ozone Report: Measuring
Progress Through 2003 (EPA, 2004), and 2005 Annual Performance and
Progress Report: Air Quality in National Parks (NPS, 2005).
Unfortunately, much of this information is presented only in terms of
the current 8-hr average form.  The 2007 Staff Paper analyzed available
air quality data in terms of the cumulative 12-hour W126 form from 2001
to 2005 for a subset of national parks and other significant natural
areas representing 4 general regions of the U.S.  Many of these national
parks and natural areas have monitored O3 levels above concentrations
that have been shown to decrease plant growth and above the 12-hour W126
levels analyzed in this review.  For example, the Great Smokey Mountain,
Rocky Mountain, Grand Canyon, Yosemite and Sequoia National Parks all
had more than one year within the 2001-2005 period with a 12-hour W126
above 21 ppm-hour.  This level of exposure has been associated with
approximately no more than 10 percent biomass loss in 50 percent of the
49 tree seedling cases studied in the NHEERL-WED experiments (Lee and
Hogsett, 1996).  Black cherry (Prunus serotina), an important
O3-sensitive tree species in the eastern U.S., occurs in the Great Smoky
Mountain National Park and is estimated to have O3-related seedling
biomass loss of approximately 40 percent when exposed to a 3 month,
12-hour W126 O3 level greater than 21 ppm-hour.  Ponderosa pine (Pinus
ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia
National Parks has been reported to have approximately 10 percent
biomass losses at 3 month, 12 hour W126 O3 levels as low as 17 ppm-hour
(Lee and Hogsett, 1996).  Impacts on seedlings may potentially affect
long-term tree growth and survival, ultimately affecting the
competitiveness of O3-sensitive tree species and genotypes within forest
stands.

In order to characterize exposures to vegetation at the national scale,
however, the 2007 Staff Paper concluded that it could not rely solely on
limited site-specific monitoring data, and that it was necessary to
select an interpolation method that could be used to characterize O3 air
quality over broad geographic areas.  The 2007 Staff Paper therefore
investigated the appropriateness of using the O3 outputs from the
EPA/NOAA Community Multi-scale Air Quality (CMAQ) model system (
HYPERLINK "http://www.epa.gov/asmdnerl/CMAQ"
http://www.epa.gov/asmdnerl/CMAQ , Byun and Ching, 1999; Arnold et al.
2003, Eder and Yu, 2005) to improve spatial interpolations based solely
on existing monitoring networks.  Due to the significant resources
required to run CMAQ, model outputs were only available for a limited
number of years.  For the 2008 rulemaking, the most recent outputs
available at the time from CMAQ version 4.5 were for the year 2001.

	Based on the significant difference in monitor network density between
the eastern and western U.S., the 2007 Staff Paper concluded that it was
appropriate to use separate interpolation techniques in these two
regions.  Only AQS and CASTNET monitoring data were used for the eastern
interpolation, since it was determined that enhancing the interpolation
with CMAQ data did not add much information to the eastern U.S.
interpolation.  In the western U.S., however, where rural monitoring is
more sparse, O3 values generated by the CMAQ model were used to develop
scaling factors to augment the interpolation.

In order to characterize uncertainties associated with the interpolation
method, monitored O3 concentrations were systematically compared to
interpolated O3 concentrations in areas where monitors were located.  In
general, the interpolation method used in the current review performed
well in many areas in the U.S., although it under-predicted higher
12-hour W126 exposures in rural areas.  Due to the important influence
of higher exposures in determining risks to plants, this feature of the
interpolated surface could result in an under-estimation of risks to
vegetation in some areas.  Taking these uncertainties into account, and
given the absence of more complete rural monitoring data, this approach
was used in developing national vegetation exposure and risk assessments
that estimate relative changes in risk for the various alternative
standards analyzed.

	To evaluate changing vegetation exposures and risks under selected air
quality scenarios, the 2007 Staff Paper utilized 2001 base year O3 air
quality distributions that had been adjusted with a rollback method
(Horst and Duff, 1995; Rizzo, 2005, 2006) to reflect meeting the then
current and alternative secondary standard options.  This technique
combines both linear and quadratic elements to reduce higher O3
concentrations more than lower ones.  In this regard, the rollback
method attempts to account for reductions in emissions without greatly
affecting lower concentrations.  The following O3 air quality scenarios
were analyzed: (1) 4th-highest daily maximum 8-hour average: 0.084 ppm
(the effective level of the then current standard) and 0.070 ppm levels;
(2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 1997 review)
and 15 ppm-hour levels; and (3) 3-month, 12-hour W126: 21 ppm-hour and
13 ppm-hour levels.

	The two 8-hour average levels were chosen as possible alternatives of
the then current form for comparison with the cumulative, seasonal
alternative forms.  The SUM06 scenarios were very similar to the W126
scenarios.  Since the W126 was judged to be the more
biologically-relevant cumulative, seasonal form, only the results for
the W126 scenarios are summarized below.  For the W126 form, the two
levels were selected on the basis of the associated levels of tree
seedling biomass loss and crop yield loss protection identified in the
NHEERL-WED and NCLAN studies, respectively.  Specifically, the upper
level of W126 (21 ppm-hour) was associated with a level of tree and crop
protection of approximately no more than 10 percent growth or yield loss
in 50 percent of cases studied.  Alternatively, the lower level of W126
(13 ppm-hour) was associated with a level of tree seedling and crop
protection of approximately no more than 10 percent growth or yield loss
in 75 percent of studied cases.

	The following discussion highlights key observations drawn from
comparing predicted changes in interpolated air quality under each
alternative standard form and level scenario for the base year, 2001:

(1) Under the base year (2001) “as is” air quality, a large portion
of California had 12-hr W126 O3 levels above 31 ppm-hour, which has been
associated with approximately no more than 14 percent biomass loss in 50
percent of tree seedling cases studies.  Broader multi-state regions in
the east (NC, TN, KY, IN, OH, PA, NJ, NY, DE, MD, VA) and west (CA, NV,
AZ, OK, TX) are predicted to have levels of air quality above the W126
level of 21 ppm-hour, which is approximately equal to the secondary
standard proposed in 1996 and is associated with approximately no more
than 10 percent biomass loss in 50 percent of tree seedling cases
studied.  Much of the east and Arizona and California have 12-hour W126
O3 levels above 13 ppm-hour, which has been associated with
approximately no more than 10 percent biomass loss in 75 percent of tree
seedling cases studied.  The results of the exposure assessment indicate
that current air quality levels could result in significant impacts to
vegetation in some areas.

	(2) When 2001 air quality was rolled back to meet the then current
8-hour, 0.084 ppm secondary standard, the overall 3-month 12-hour W126
O3 levels were somewhat improved, but not substantially.  Under this
scenario, there were still many areas in California with 12-hour W126 O3
levels above 31 ppm-hour.  A broad multi-state region in the east (NC,
TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, OK, TX) were still
predicted to have O3 levels above the W126 level of 21 ppm-hour.

	(3) Exposures generated for just meeting a 0.070 ppm, 4th-highest
maximum 8-hour average alternative standard showed substantially
improved O3 air quality when compared to just meeting the then current
8-hour standard.  Most areas were predicted to have O3 levels below the
W126 level of 21 ppm-hour, although some areas in the east (KY, TN, MI,
AR, MO, IL) and west (CA, NV, AZ, UT, NM, CO, OK, TX) were still
predicted to have O3 levels above the W126 level of 13 ppm-hour.

	These results suggest that meeting a 0.070 ppm, 8-hour secondary
standard would provide substantially improved protection in some areas
for vegetation from seasonal O3 exposures of concern.  The 2007 Staff
Paper recognizes, however, that some areas meeting a 0.070 ppm 8-hour
standard could continue to have elevated seasonal exposures, including
forested park lands and other natural areas, and Class I areas which are
federally mandated to preserve certain air quality related values.  This
is especially important in the high elevation forests in the Western
U.S. where there are few O3 monitors.  This is because the air quality
patterns in remote areas can result in relatively low 8-hour averages
while still experiencing relatively high cumulative exposures.

	To further characterize O3 air quality in terms of various secondary
standard forms, an analysis was performed in the 2007 Staff Paper to
evaluate the extent to which county-level O3 air quality measured in
terms of various levels of the current 8-hour average form overlapped
with that measured in terms of various levels of the 12-hour W126
cumulative, seasonal form.  The 2007 Staff Paper presented this analysis
using 2002-2004 county-level O3 air quality data from AQS sites and the
subset of CASTNET sites having the highest O3 levels for the counties in
which they are located.  Since the current 8-hour average secondary form
is a 3-year average, the analysis initially compared the 3-year averages
of both the 8-hour and W126 forms.  In addition, recognizing that some
vegetation effects (e.g. crop yield loss and foliar injury) are driven
solely by annual O3 exposures and are typically evaluated with respect
to exposures within the annual growing season, the 2007 Staff Paper also
presented a comparison of the current 3-year average 8-hour form to the
annual W126 form for the individual years, 2002 and 2004.

	Results of the 3-year average comparisons showed that of the counties
with air quality meeting the 3-year average form of a 0.084 ppm, 8-hour
average standard, 7 counties showed 3-year average W126 values above the
21 ppm-hour level.  At the lower W126 level of 13 ppm-hour, 135 counties
with air quality meeting the 3-year average form of a 0.084 ppm, 8-hour
average standard, would be above this W126 level.  In addition, when the
3-year average of an 8-hour form was compared to annual W126 values,
further variability in the degree of overlap between the 8-hour form and
W126 form became apparent.  For example, the relatively high 2002 O3 air
quality year showed a greater degree of overlap between those areas that
would meet the levels analyzed for the current 8-hour and alternative
levels of the W126 form than did the relatively low O3 2004 air quality
year.  This lack of a consistent degree of overlap between the two forms
in different air quality years demonstrates that annual vegetation would
be expected to receive widely differing degrees of protection from
cumulative seasonal exposures in some areas from year to year, even when
the 3-year average of the 8-hour form was consistently met.

It is clear that this analysis is limited by the lack of monitoring in
rural areas where important vegetation and ecosystems are located,
especially at higher elevation sites.  This is because O3 air quality
distributions at high elevation sites often do not reflect the typical
urban and near-urban pattern of low morning and evening O3
concentrations with a high mid-day peak, but instead maintain relatively
flat patterns with many concentrations in the mid-range (e.g., 0.05-0.09
ppm) for extended periods.  These conditions can lead to relatively low
daily maximum 8-hour averages concurrently with high cumulative values
so that there is potentially less overlap between an 8-hour average and
a cumulative, seasonal form at these sites.  The 2007 Staff Paper
concluded that it is reasonable to anticipate that additional
unmonitored rural high elevation areas important for vegetation may not
be adequately protected even with a lower level of the 8-hour form.

The 2006 Criteria Document discusses policy relevant background (PRB)
levels for high elevation sites and makes the following observations:
(1) PRB concentrations of 0.04 to 0.05 ppm occur occasionally at
high-elevation sites (e.g., >1.5 km) in the spring due to the
free-tropospheric influence, including some limited contribution from
hemispheric pollution (O3 produced from anthropogenic emissions outside
North America); and (2) while stratospheric intrusions might
occasionally elevate O3 at high-altitude sites, these events are rare at
surface sites.  Therefore, the 2007 Staff Paper concluded that
springtime PRB levels in the range identified above and rare
stratospheric intrusions of O3 are unlikely to be a major influence on
3-month cumulative seasonal W126 values.

It further remains uncertain as to the extent to which air quality
improvements designed to reduce 8-hour O3 average concentrations would
reduce O3 exposures measured by a seasonal, cumulative W126 index.  The
2007 Staff Paper indicated this to be an important consideration
because:  (1) the biological database stresses the importance of
cumulative, seasonal exposures in determining plant response; (2) plants
have not been specifically tested for the importance of daily maximum
8-hour O3 concentrations in relation to plant response; and (3) the
effects of attainment of a 8-hour standard in upwind urban areas on
rural air quality distributions cannot be characterized with confidence
due to the lack of monitoring data in rural and remote areas.  These
factors are important considerations in determining whether the current
8-hour form can appropriately provide requisite protection for
vegetation.

2. 	Assessment of Risks to Vegetation

	The 2007 Staff Paper presents results from quantitative and qualitative
risk assessments of O3 risks to vegetation (EPA, 2007).  In the 1997
review, crop yield and seedling biomass loss OTC data provided the basis
for staff analyses, conclusions, and recommendations (EPA, 1996b).
Since then, several additional lines of evidence have progressed
sufficiently to provide staff with a more complete and coherent picture
of the scope of O3-related vegetation risks, especially those faced by
seedling, sapling and mature tree species growing in field settings, and
indirectly, forested ecosystems.  Specifically, research published after
the 1997 review reflects an increased emphasis on field-based exposure
methods (e.g., free air exposure and ambient gradient), improved field
survey biomonitoring techniques, and mechanistic tree process models.
Findings from each of these research areas are discussed separately
below.  In conducting these assessments, the Staff Paper analyses relied
on both measured and modeled air quality information.  For some effects,
like visible foliar injury and modeled mature tree growth response, only
monitored air quality information was used.  For other effects
categories (e.g., crop yield and tree seedling growth), staff relied on
interpolated O3 exposures.

a.	Visible foliar injury

	As discussed above (section IV.A.2.c), systematic injury surveys have
documented visible foliar injury symptoms diagnostic of phytotoxic O3
exposures on sensitive bioindicator plants.  These surveys have produced
more expansive evidence than that available at the time of the 1997
review that visible foliar injury is occurring in many areas of the U.S.
under current ambient conditions.  The 2007 Staff Paper presents an
assessment combining recent U.S. Forest Service Forest Inventory and
Analysis (FIA) biomonitoring site data with the county level air quality
data for those counties containing the FIA biomonitoring sites.  This
assessment showed that incidence of visible foliar injury ranged from 21
to 39 percent during the four-year period (2001-2004) across all
counties with air quality levels at or below that of a 0.084 ppm, 8-hour
standard.  Of the counties that met an 8-hour level of 0.070 ppm in
those years, 11 to 30 percent still had incidence of visible foliar
injury.  The magnitude of these percentages suggests that phytotoxic
exposures sufficient to induce visible foliar injury would still occur
in many areas after meeting the level of a 0.084 ppm secondary standard
or alternative 0.070 ppm 8-hour standard.  Additionally, the data showed
that visible foliar injury occurrence was geographically widespread and
occurring on a variety of plant species in forested and other natural
systems.  Linking visible foliar injury to other plant effects is still
problematic.  However, its presence indicates that other O3–related
vegetation effects could also be present.

b.	Seedling and mature tree biomass loss

	In the 1997 review, analyses of the effects of O3 on trees were limited
to 11 tree species for which C-R functions for the seedling growth stage
had been developed from OTC studies conducted by the NHEERL-WED.
Important tree species such as quaking aspen, ponderosa pine, black
cherry, and tulip poplar were found to be sensitive to cumulative
seasonal O3 exposures.  Work done since the 1997 review at the AspenFACE
site in Wisconsin on quaking aspen (Karnosky et al., 2005) and a
gradient study performed in the New York City area (Gregg et al. 2003)
has confirmed the detrimental effects of O3 exposure on tree growth in
field studies without chambers and beyond the seedling stage (King et al
2005).  These field studies are discussed above in section IV.A.

	To update the seedling biomass loss risk analysis, C-R functions for
biomass loss for available seedling tree species taken from the 2006
Criteria Document and information on tree growing regions derived from
the U.S. Department of Agriculture's Atlas of United States Trees were
combined with projections of O3 air quality based on 2001 interpolated
exposures, to produce estimated biomass loss for each of the seedling
tree species individually.  Maps of these biomass loss projections are
presented in the 2007 Staff Paper.  For example, quaking aspen had a
wide range of O3 exposures across its growing range and therefore,
showed significant variability in percentages of projected seedling
biomass loss across its range.  Quaking aspen seedling biomass loss was
projected to be greater than 4 percent over much of its geographic
range, though it can reach above 10 percent in areas of Ohio,
Pennsylvania, New York, New Jersey and California.  Biomass loss for
black cherry was projected to be greater than 20 percent in
approximately half its range.  Greater than 30 percent biomass loss for