(e.g., indoor) concentrations.  In EPA’s judgment, the most important
uncertainties affecting the exposure estimates are related to the
modeling of human activity patterns over an O3 season, the modeling of
variations in ambient concentrations near roadways, and the modeling of
air exchange rates that affect the amount of O3 that penetrates indoors.
 Another important uncertainty that affects the estimation of how many
exposures are associated with moderate or greater exertion is the
characterization of energy expenditure for children engaged in various
activities.  As discussed in more detail in the 2007 Staff Paper (EPA,
2007b, section <IP_ADDRESS>), the uncertainty in energy expenditure values
carries over to the uncertainty of the modeled breathing rates, which
are important since they are used to classify exposures occurring at
moderate or greater exertion which are the relevant exposures since
O3-related effects observed in controlled human exposure studies only
are observed when individuals are engaged in some form of exercise.
The uncertainties in the exposure model inputs and the estimated
exposures have been assessed using quantitative uncertainty and
sensitivity analyses.  Details are discussed in the 2007 Staff Paper
(section 4.6) and in a technical memorandum describing the exposure
modeling uncertainty analysis (Langstaff, 2007).

b.	Scope and Key Components

	Population exposures to O3 are primarily driven by ambient outdoor
concentrations, which vary by time of day, location, and peoples’
activities.  Outdoor O3 concentration estimates used in the exposure
assessment are provided by measurements and statistical adjustments to
the measured concentrations.  The current exposure analysis allows
comparisons of population exposures to O3 within each urban area,
associated with current O3 levels and with O3 levels just meeting
several potential alternative air quality standards or scenarios.  Human
exposure, regardless of the pollutant, depends on where individuals are
located and what they are doing.  Inhalation exposure models are useful
in realistically estimating personal exposures to O3 based on
activity-specific breathing rates, particularly when recognizing that
large scale population exposure measurement studies have not been
conducted that are representative of the overall population or at risk
subpopulations.

	The model EPA used to simulate O3 population exposure is the Air
Pollutants Exposure Model (APEX), the human inhalation exposure model
within the Total Risk Integrated Methodology (TRIM) framework (EPA,
2006c,d).  APEX is conceptually based on the probabilistic NAAQS
exposure model for O3 (pNEM/O3) used in the last O3 NAAQS review.  Since
that time the model has been restructured, improved, and expanded to
reflect conceptual advances in the science of exposure modeling and
newer input data available for the model.  Key improvements to
algorithms include replacement of the cohort approach with a
probabilistic sampling approach focused on individuals, accounting for
fatigue and oxygen debt after exercise in the calculation of breathing
rates, and a new approach for construction of longitudinal activity
patterns for simulated persons.  Major improvements to data input to the
model include updated air exchange rates, more recent census and
commuting data, and a greatly expanded daily time-activities database.

	APEX is a probabilistic model designed to explicitly model the numerous
sources of variability that affect people’s exposures.  APEX simulates
the movement of individuals through time and space and estimates their
exposures to O3 in indoor, outdoor, and in-vehicle microenvironments.
The exposure model takes into account the most significant factors
contributing to total human O3 exposure, including the temporal and
spatial distribution of people and O3 concentrations throughout an urban
area, the variation of O3 levels within each microenvironment, and the
effects of exertion on breathing rate in exposed individuals.  A more
detailed description of APEX and its application is presented in chapter
4 of the 2007 Staff Paper and associated technical documents (EPA,
2006b,c,d).

Several methods have been used to evaluate the APEX model and to
characterize the uncertainty of the model estimates.  These include
conducting model evaluation, sensitivity analyses, and a detailed
uncertainty analysis for one urban area.  These are discussed fully in
the 2007 Staff Paper (section 4.6) and in Langstaff (2007).  The
uncertainty of model structure was judged to be of lesser importance
than the uncertainties of the model inputs and parameters.  Model
structure refers to the algorithms in APEX designed to simulate the
processes that result in people’s exposures, for example, the way that
APEX models exposures to individuals when they are near roads.  The
uncertainties in the model input data (e.g., measurement error, ambient
concentrations, air exchange rates, and activity pattern data) have been
assessed individually, and their impact on the uncertainty in the
modeled exposure estimates was assessed in a unified quantitative
analysis with results expressed in the form of estimated confidence
ranges around the estimated measures of exposure.  This uncertainty
analysis was conducted for one urban area (Boston) using the observed
2002 O3 concentrations and 2002 concentrations adjusted to simulate just
meeting the current standard, with the expectation that the results
would be similar for other cities and years.  One significant source of
uncertainty, due to limitations in the database used to model peoples’
daily activities, was not included in the unified analysis, and was
assessed through separate sensitivity analyses.  This analysis indicates
that the uncertainty of the exposure results is relatively small.  For
example, 95 percent uncertainty intervals were calculated for the APEX
estimates of the percent of children or asthmatic children with
exposures above 0.060, 0.070, or 0.080 ppm under moderate exertion, for
two air quality scenarios (current 2002 and 2002 adjusted to simulate
just meeting the current standard) in Boston (Langstaff, 2007, Tables 26
and 27).  The 95 percent uncertainty intervals for this set of 12
exposure estimates indicate the possibility of underpredictions of the
exposure estimates ranging from 3 to 25 percent of the modeled
estimates, and overpredictions ranging from 4 to 11 percent of the
estimates.  For example, APEX estimates the percent of asthmatic
children with exposures above 0.070 ppm under moderate exertion to be 24
percent, for Boston 2002 O3 concentrations adjusted to simulate just
meeting the current standard.  The 95 percent uncertainty interval for
this estimate is 23 − 30 percent, or -4 to +25 percent of the
estimate.  These uncertainty intervals do not include the uncertainty
engendered by limitations of the activity database, which is in the
range of one to ten percent.

The exposure periods modeled here are the O3 seasons in 2002, 2003, and
2004.  The O3 season in each area includes the period of the year where
elevated O3 levels tend to be observed and for which routine hourly O3
monitoring data are available.  Typically this period spans from March
or April through September or October, or in some areas, spanning the
entire year.  Three years were modeled to reflect the substantial
year-to-year variability that occurs in O3 levels and related
meteorological conditions, and because the standard is specified in
terms of a three-year period.  The year-to-year variability observed in
O3 levels is due to a combination of different weather patterns and the
variation in emissions of O3 precursors.  Nationally, 2002 was a
relatively high year with respect to the 4th highest daily maximum
8-hour O3 levels observed in urban areas across the U.S. (EPA, 2007b,
Figure 2-16), with the mean of the distribution of O3 levels for the
urban monitors being in the upper third among the years 1990 through
2006.  In contrast, on a national basis, 2004 is the lowest year on
record through 2006 for this same air quality statistic, and 8-hour
daily maximum O3 levels observed in most, but not all of the 12 urban
areas included in the exposure and risk analyses were relatively low
compared to other recent years.  The 4th highest daily maximum 8-hour O3
levels observed in 2003 in the 12 urban areas and nationally generally
were between those observed in 2002 and 2004.

Regulatory scenarios examined in the 2008 rulemaking include the then
current 0.08 ppm, average of the 4th daily maximum 8-hour averages over
a three year period standard; standards with the same form but with
alternative levels of 0.080, 0.074, 0.070, and 0.064 ppm; standards
specified as the average of the 3rd highest daily maximum 8-hour
averages over a three year period with alternative levels of 0.084 and
0.074 ppm; and a standard specified as the average of the 5th highest
daily maximum 8-hour averages over a three year period with a level of
0.074 ppm.  The then current standard used a rounding convention that
allows areas to have an average of the 4th daily maximum 8-hour averages
as high as 0.084 ppm and still meet the standard.  All alternative
standards analyzed were intended to reflect improved precision in the
measurement of ambient concentrations (in ppm), where the precision
would extend to three instead of two decimal places.

	The then current standard and all alternative standards were modeled
using a quadratic rollback approach to adjust the hourly concentrations
observed in 2002-2004 to yield a design value corresponding to the
standard being analyzed.  The quadratic rollback technique reduces
higher concentrations more than lower concentrations near ambient
background levels.  This procedure was considered in a sensitivity
analysis in the 1997 review of the O3 standard and has been shown to be
more realistic than a linear, proportional rollback method, where all of
the ambient concentrations are reduced by the same factor.

c.	Exposure Estimates and Key Observations

	The exposure assessment, which provides estimates of the number of
people exposed to different levels of ambient O3 while at specified
exertion levels, serve two purposes.  First, the entire range of modeled
personal exposures to ambient O3 is an essential input to the portion of
the health risk assessment based on exposure-response functions from
controlled human exposure studies, discussed in the next section.
Second, estimates of personal exposures to ambient O3 concentrations at
and above specific benchmark levels provide some perspective on the
public health impacts of health effects that cannot currently be
evaluated in quantitative risk assessments that may occur at current air
quality levels, and the extent to which such impacts might be reduced by
meeting the current and alternative standards.  This is especially true
when there are exposure levels at which it is known or can reasonably be
inferred that specific O3-related health effects are occurring.  In this
notice, exposures at and above these benchmark concentrations are
referred to as “exposures of concern.”

	It is important to note that although the analysis of “exposures of
concern” was conducted using three discrete benchmark levels (i.e.,
0.080, 0.070, and 0.060 ppm), the concept 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.  The EPA recognizes that there is no sharp breakpoint within the
continuum ranging from at and above 0.080 ppm down to 0.060 ppm.  In
considering the concept of exposures of concern, 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 health 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 the current and alternative
standards.  In the selection of specific benchmark concentrations for
this analysis, staff first considered the exposure level of 0.080 ppm,
at which there is a substantial amount of controlled human exposure
evidence demonstrating a range of O3-related health effects including
lung inflammation and airway responsiveness in healthy individuals.
Thus, as in the 1997 review, this level was selected as a benchmark
level for this assessment of exposures of concern.  Evidence newly
available in this review is the basis for identifying additional, lower
benchmark levels of 0.070 and 0.060 ppm for this assessment.

	More specifically, as discussed above in section II.A.2, evidence
available from controlled human exposure and epidemiological studies
indicates that people with asthma have larger and more serious effects
than healthy individuals, including lung function, respiratory symptoms,
increased airway responsiveness, and pulmonary inflammation, which has
been shown to be a more sensitive marker than lung function responses.
Further, a substantial new body of evidence from epidemiological studies
shows associations with serious respiratory morbidity and
cardiopulmonary mortality effects at O3 levels that extend below 0.080
ppm.  Additional, but very limited new evidence from controlled human
exposure studies shows lung function decrements and respiratory symptoms
in healthy subjects at an O3 exposure level of 0.060 ppm.  The selected
benchmark level of 0.070 ppm reflects the new information that
asthmatics have larger and more serious effects than healthy people and
therefore controlled human exposure studies done with healthy subjects
may underestimate effects in this group, as well as the substantial body
of epidemiological evidence of associations with O3 levels below 0.080
ppm.  The selected benchmark level of 0.060 ppm additionally reflects
the very limited new evidence from controlled human exposure studies
that show lung function decrements and respiratory symptoms in some
healthy subjects at the 0.060 ppm exposure level, recognizing that
asthmatics are likely to have more serious responses and that lung
function is not likely to be as sensitive a marker for O3 effects as is
lung inflammation.

	The estimates of exposures of concern were reported in terms of both
“people exposed” (the number and percent of people who experience a
given level of O3 concentrations, or higher, at least one time during
the O3 season in a given year) and “occurrences of exposure” (the
number of times a given level of pollution is experienced by the
population of interest, expressed in terms of person-days of
occurrences).  Estimating exposures of concern is important because it
provides some indication of the potential public health impacts of a
range of O3-related health outcomes, such as lung inflammation,
increased airway responsiveness, and changes in host defenses.  These
particular health effects have been demonstrated in controlled human
exposure studies of healthy individuals to occur at levels as low as
0.080 ppm O3, but have not been evaluated at lower levels in controlled
human exposure studies.  The EPA did not include these effects in the
quantitative risk assessment due to a lack of adequate information on
the exposure-response relationships.

	The 1997 O3 NAAQS review estimated exposures associated with 1-hour
heavy exertion, 1-hour moderate exertion, and 8-hour moderate exertion
for children, outdoor workers, and the general population.  The EPA’s
analysis in the 1997 Staff Paper showed that exposure estimates based on
the 8-hour moderate exertion scenario for children yielded the largest
number of children experiencing exposures at or above exposures of
concern.  Consequently, EPA chose to focus on the 8-hour moderate and
greater exertion exposures in all and asthmatic school age children in
the current exposure assessment. While outdoor workers and other adults
who engage in moderate or greater exertion for prolonged durations while
outdoors during the day in areas experiencing elevated O3 concentrations
also are at risk for experiencing exposures associated with O3-related
health effects, EPA did not focus on quantitative estimates for these
populations due to the lack of information about the number of
individuals who regularly work or exercise outdoors.  Thus, the exposure
estimates presented here and in the 2007 Staff Paper are most useful for
making relative comparisons across alternative air quality scenarios and
do not represent the total exposures in all children or other groups
within the general population associated with the air quality scenarios.

	Population exposures to O3 were estimated in 12 urban areas for 2002,
2003, and 2004 air quality, and also using O3 concentrations adjusted to
just meet the then current and several alternative standards.  The
estimates of 8-hour exposures of concern at and above benchmark levels
of 0.080, 0.070, and 0.060 ppm aggregated across all 12 areas are shown
in Table 1 for air quality scenarios just meeting the current and four
alternative 8-hour average standards.  Table 1 provides estimates of the
number and percent of school age children and asthmatic school age
children exposed, with daily 8-hour maximum exposures at or above each
O3 benchmark level of exposures of concern, while at intermittent
moderate or greater exertion and based on O3 concentrations observed in
2002 and 2004.  Table 1 summarizes estimates for 2002 and 2004 because
these years reflect years that bracket relatively higher and lower O3
levels, with year 2003 generally containing O3 levels in between when
considering the 12 urban areas modeled.  This table also reports the
percent change in the number of persons exposed when a given alternative
standard is compared with the then current standard.

	Key observations important in comparing exposure estimates associated
with just meeting the current NAAQS and alternative standards under
consideration include:

	(1)  As shown in Table 6-1 of the 2007 Staff Paper, the patterns of
exposure in terms of percentages of the population exceeding a given
exposure level are very similar for the general population and for
asthmatic and all school age (5-18) children, although children are
about twice as likely to be exposed, based on the percent of the
population exposed, at any given level.

	(2)  As shown in Table 1 below, the number and percentage of asthmatic
and all school-age children aggregated across the 12 urban areas
estimated to experience one or more exposures of concern decline from
simulations of just meeting the then current 0.084 ppm standard to
simulations of alternative 8-hour standards by varying amounts depending
on the benchmark level, the population subgroup considered, and the year
chosen.  For example, the estimated percentage of school age children
experiencing one or more exposures ≥ 0.070 ppm, while engaged in
moderate or greater exertion, during an O3 season is about 18 percent of
this population when the 0.084 ppm standard is met using the 2002
simulation; this is reduced to about 12, 4, 1, and 0.2 percent of
children upon meeting alternative standards of 0.080, 0.074, 0.070, and
0.064 ppm, respectively (all specified in terms of the 4th highest daily
maximum 8-hour average), using the 2002 simulation.

Table 1.  Number and Percent of All and Asthmatic School Age Children
in 12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above
0.080, 0.070, and 0.060 ppm While at Moderate or Greater Exertion, One
or More Times Per Season, and the Number of Occurrences Associated with
Just Meeting Alternative 8-Hour Standards Based on Adjusting 2002 and
2004 Air Quality Data1,2

Benchmark Levels of Exposures

of Concern

(ppm)	8-Hour Air Quality Standards3

(ppm)	All Children, ages 5-18

Aggregate for 12 urban areas	Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all)

[% reduction from 0.084 ppm standard]	Number of Children Exposed (% of
group)

[% reduction from 0.084 ppm standard]

2002	2004	2002	2004

0.080	0.084	700,000 (4%)	30,000 (0%)	110,000 (4%)	0 (0%)

	0.080	290,000 (2%)

[70%]	10,000 (0%)

[67%]	50,000 (2%)

[54%]	0 (0%)

	0.074	60,000 (0%)

[91%]	0 (0%)

[100%]	10,000 (0%)

[91%]	0 (0%)

	0.070	10,000 (0%)

[98%]	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

	0.064	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

0.070	0.084	3,340,000 (18%)	260,000 (1%)	520,000 (20%)	40,000 (1%)

	0.080	2,160,000 (12%)

[35%]	100,000 (1%)

[62%]	330,000 (13%)

[36%]	10,000 (0%)

[75%]

	0.074	770,000 (4%)

[77%]	20,000 (0%)

[92%]	120,000 (5%)

[77% ]	0 (0%)

[100%]

	0.070	270,000 (1%)

[92%]	0 (0%)

[100%]	50,000 (2%)

[90%]	0 (0%)

[100%]

	0.064	30,000 (0.2%)

[99%]	0 (0%)

[100%]	10,000 (0.2%)

[98% ]	0 (0%)

[100%]

0.060	0.084	7,970,000 (44%)	1,800,000 (10%)	1,210,000 (47%)	270,000
(11%)

	0.080	6,730,000 (37%

[16%]	1,050,000 (6%)

[42%]	1,020,000 (40%)

[16%]	150,000 (6%)

[44%]

	0.074	4,550,000 (25%)

[43%]	350,000 (2%)

[80%]	700,000 (27%)

[42%]	50,000 (2%)

[81%]

	0.070	3,000,000 (16%)

[62%]	110,000 (1%)

[94%]	460,000 (18%)

[62%]	10,000 (1%)

[96%]

	0.064	950,000 (5%)

[88%]	10,000 (0%)

[99%]	150,000 (6%)

[88%]	0 (0%)

[100%]

1 Moderate or greater exertion is defined as having an 8-hour average
equivalent ventilation rate > 13 l-min/m2.

2 Estimates are the aggregate results based on 12 combined statistical
areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.).  Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3 All standards summarized here have the same form as the 8-hour
standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must
be at or below the concentration level specified.  As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard and selected alternative standards.  These
simulations do not represent predictions of when, whether, or how areas
might meet the specified standards.

	(3)  Substantial year-to-year variability in exposure estimates is
observed over the three-year modeling period.  For example, the
estimated number of school age children experiencing one or more
exposures ( 0.070 ppm during an O3 season when a 0.084 ppm standard is
met in the 12 urban areas included in the analysis is 3.3, 1.0, or 0.3
million for the 2002, 2003, and 2004 simulations, respectively.

	(4)  There is substantial variability observed across the 12 urban
areas in the percent of the population subgroups estimated to experience
exposures of concern.  For example, when 2002 O3 concentrations are
simulated to just meet a 0.084 ppm standard, the aggregate 12 urban area
estimate is 18 percent of all school age children are estimated to
experience O3 exposures ( 0.070 ppm (Table 1 below), while the range of
exposure estimates in the 12 urban areas considered separately for all
children range from 1 to 38 percent (EPA, 2007b, p. 4-48, Exhibit 2).
There was also variability in exposure estimates among the modeled areas
when using the 2004 air quality simulation for the same scenario;
however it was reduced and ranged from 0 to 7 percent in the 12 urban
areas (EPA, 2007b, p. 4-60, Exhibit 8).

	(5) Of particular note, as discussed above in section II.A of this
notice, high inter-individual variability in responsiveness means that
only a subset of individuals in these groups who are exposed at and
above a given benchmark level would actually be expected to experience
such adverse health effects.

 	(6)  In considering these observations, it is important to take into
account the variability, uncertainties, and limitations associated with
this assessment, including the degree of uncertainty associated with a
number of model inputs and uncertainty in the model itself, as discussed
above.

2.	Quantitative Health Risk Assessment

This section discusses the approach used to develop quantitative health
risk estimates associated with exposures to O3 building upon a more
limited risk assessment that was conducted during the last review.  As
part of the 1997 review, EPA conducted a health risk assessment that
produced risk estimates for the number and percent of children and
outdoor workers experiencing lung function and respiratory symptoms
associated with O3 exposures for 9 urban areas.  The risk assessment for
the 1997 review also included risk estimates for excess
respiratory-related hospital admissions related to O3 concentrations for
New York City.  In the last review, the risk estimates played a
significant role in both the staff recommendations and in the proposed
and final decisions to revise the O3 standards.  The health risk
assessment conducted for the current review builds upon the methodology
and lessons learned from the prior review.

Overview

The updated health risk assessment conducted as part of the 2008
rulemaking includes estimates of (1) risks of lung function decrements
in all and asthmatic school age children, respiratory symptoms in
asthmatic children, respiratory-related hospital admissions, and
non-accidental and cardiorespiratory-related mortality associated with
recent ambient O3 levels; (2) risk reductions and remaining risks
associated with just meeting the then current 0.084 ppm 8-hour O3 NAAQS;
and (3) risk reductions and remaining risks associated with just meeting
various alternative 8-hour O3 NAAQS in a number of example urban areas.
This risk assessment is more fully described and presented in chapter 5
of the 2007 Staff Paper and in a technical support document (TSD), Ozone
Health Risk Assessment for Selected Urban Areas (Abt Associates, 2007a,
hereafter referred to as “Risk Assessment TSD”).  The scope and
methodology for this risk assessment were developed over the last few
years with considerable input from the CASAC O3 Panel and the public.
The information contained in these documents included specific criteria
for the selection of health endpoints, studies, and locations to include
in the assessment.  In a peer review letter sent by CASAC to the
Administrator documenting its advice in October 2006 (Henderson, 2006c),
the CASAC O3 Panel concluded that the risk assessment was “well done,
balanced, and reasonably communicated” and that the selection of
health endpoints for inclusion in the quantitative risk assessment was
appropriate.

	The goals of the risk assessment are: (1) to provide estimates of the
potential magnitude of several morbidity effects and mortality
associated with current O3 levels, and with meeting the then current
0.084 ppm standard and alternative 8-hour O3 standards in specific urban
areas; (2) to develop a better understanding of the influence of various
inputs and assumptions on the risk estimates; and (3) to gain insights
into the distribution of risks and patterns of risk reductions
associated with meeting alternative O3 standards.  The health risk
assessment is intended to be dependent on and reflect the overall weight
and nature of the health effects evidence discussed above in section
II.A and in more detail in the 2006 Criteria Document and 2007 Staff
Paper.  While not independent of the overall evaluation of the health
effects evidence, the quantitative health risk assessment provides
additional insights regarding the relative public health implications
associated with just meeting a 0.084 ppm standard and several
alternative 8-hour standards.

	The risk assessment covers a variety of health effects for which there
is adequate information to develop quantitative risk estimates.
However, as noted by CASAC (Henderson, 2007) and in the 2007 Staff
Paper, there are a number of health endpoints (e.g., increased lung
inflammation, increased airway responsiveness, impaired host defenses,
increased medication usage for asthmatics, increased emergency
department visits for respiratory causes, and increased school absences)
for which there currently is insufficient information to develop
quantitative risk estimates, but which are important to consider in
assessing the overall public health impacts associated with exposures to
O3.  These additional health endpoints are discussed above in section
II.A.2 and are also taken into account in considering the level of
exposures of concern in populations particularly at risk, discussed
above in this notice.

	There are two parts to the health risk assessment:  one based on
combining information from controlled human exposure studies with
modeled population exposure and the other based on combining information
from community epidemiological studies with either monitored or adjusted
ambient concentrations levels.  Both parts of the risk assessment were
implemented within a new probabilistic version of TRIM.Risk, the
component of EPA’s Total Risk Integrated Methodology (TRIM) model
framework that estimates human health risks.

	The EPA recognizes that there are many sources of uncertainty and
variability in the inputs to this assessment and that there is
significant variability and uncertainty in the resulting O3 risk
estimates.  As discussed in chapters 2, 5, and 6 of the 2007 Staff
Paper, there is significant year-to-year and city-to-city variability
related to the air quality data that affects both the controlled human
exposure studies-based and epidemiological studies-based parts of the
risk assessment.  There are also uncertainties associated with the air
quality adjustment procedure used to simulate just meeting various
alternative standards.  In the prior review, different statistical
approaches using alternative functional forms (i.e., quadratic,
proportional, Weibull) were used to reflect how O3 air quality
concentrations have historically changed.  Based on sensitivity analyses
conducted in the prior review, the choice of alternative air quality
adjustment procedures had only a modest impact on the risk estimates
(EPA, 2007b, p. 6-20).  With respect to uncertainties about estimated
background concentrations, as discussed below and in the 2007 Staff
Paper (section 5.4.3), alternative assumptions about background levels
have a variable impact depending on the location, standard, and health
endpoint analyzed.

	With respect to the lung function part of the health risk assessment,
key uncertainties include uncertainties in the exposure estimates,
discussed above, and uncertainties associated with the shape of the
exposure-response relationship, especially at levels below 0.08 ppm,
8-hour average, where only very limited data are available down to 0.04
ppm and there is an absence of data below 0.04 ppm (EPA, 2007b, pp.6-20
to 6-21).  Concerning the part of the risk assessment based on effects
reported in epidemiological studies, important uncertainties include
uncertainties (1) surrounding estimates of the O3 coefficients for
concentration-response relationships used in the assessment, (2)
involving the shape of the concentration-response relationship and
whether or not a population threshold or non-linear relationship exists
within the range of concentrations examined in the studies, (3) related
to the extent to which concentration-response relationships derived from
studies in a given location and time when O3 levels were higher or
behavior and /or housing conditions were different provide accurate
representations of the relationships for the same locations with lower
air quality distributions and/or different behavior and/or housing
conditions, and (4) concerning the possible role of co-pollutants which
also may have varied between the time of the studies and the current
assessment period.  An important additional uncertainty for the
mortality risk estimates is the extent to which the associations
reported between O3 and non-accidental and cardiorespiratory mortality
actually reflect causal relationships.

	As discussed below, some of these uncertainties have been addressed
quantitatively in the form of estimated confidence ranges around central
risk estimates; others are addressed through separate sensitivity
analyses (e.g., the influence of alternative estimates for
policy-relevant background levels) or are characterized qualitatively.
For both parts of the health risk assessment, statistical uncertainty
due to sampling error has been characterized and is expressed in terms
of 95 percent credible intervals.  The EPA recognizes that these
credible intervals do not reflect all of the uncertainties noted above.

b.	Scope and Key Components

	The health risk assessment is based on the information evaluated in the
2006 Criteria Document.  The risk assessment includes several categories
of health effects and estimates risks associated with just meeting a
0.084 ppm standard and alternative 8-hour O3 NAAQS and with several
individual recent years of air quality (i.e., 2002, 2003, and 2004).
The risk assessment considers the same alternative air quality scenarios
that were examined in the human exposure analyses described above.  Risk
estimates were developed for up to 12 urban areas selected to illustrate
the public health impacts associated with these air quality scenarios.
As discussed above in section II.B.1, the selection of urban areas was
largely determined by identifying areas in the U.S. which represented a
range of geographic areas, population demographics, and climatology;
with an emphasis on areas that did not meet the then current 0.084 ppm
8-hour O3 NAAQS and which included the largest areas with O3
nonattainment problems.  The selection criteria also included whether or
not there were acceptable epidemiological studies available that
reported concentration-response relationships for the health endpoints
selected for inclusion in the assessment.

	The short-term exposure related health endpoints selected for inclusion
in the quantitative risk assessment include those for which the 2006
Criteria Document or the 2007 Staff Paper concluded that the evidence as
a whole supports the general conclusion that O3, acting alone and/or in
combination with other components in the ambient air pollution mix, is
either clearly causal or is judged to be likely causal.  Some health
effects met this criterion of likely causality, but were not included in
the risk assessment for other reasons, such as insufficient
exposure-response data or lack of baseline incidence data.

	As discussed in the section above describing the exposure analysis, in
order to estimate the health risks associated with just meeting various
alternative 8-hour O3 NAAQS, it is necessary to estimate the
distribution of hourly O3 concentrations that would occur under any
given standard.  Since compliance is based on a 3-year average, the
amount of control has been applied to each year of data (i.e., 2002 to
2004) to estimate risks for a single O3 season or single warm O3 season,
depending on the health effect, based on a simulation that adjusted each
of these individual years so that the three year period would just meet
the specified standard.

	Consistent with the risk assessment approach used in the last review,
the risk estimates developed for both recent air quality levels and just
meeting the then current 0.084 ppm standard and selected alternative
8-hour standards represent risks associated with O3 levels attributable
to anthropogenic sources and activities (i.e., risk associated with
concentrations above “policy-relevant background”).  Policy-relevant
background O3 concentrations used in the O3 risk assessment were defined
in chapter 2 of the 2007 Staff Paper (pp. 2-48 – 2-55) as the O3
concentrations that would be observed in the U.S. in the absence of
anthropogenic emissions of precursors (e.g., VOC, NOx, and CO) in the
U.S., Canada, and Mexico.  The results of a global tropospheric O3 model
(GEOS-CHEM) have been used to estimate monthly background daily diurnal
profiles for each of the 12 urban areas for each month of the O3 season
using meteorology for the year 2001.  Based on the results of the
GEOS-CHEM model, the Criteria Document indicates that background O3
concentrations are generally predicted to be in the range of 0.015 to
0.035 ppm in the afternoon, and they are generally lower under
conditions conducive to man-made O3 episodes.

	This approach of estimating risks in excess of background is judged to
be more relevant to policy decisions regarding ambient air quality
standards than risk estimates that include effects potentially
attributable to uncontrollable background O3 concentrations.
Sensitivity analyses examining the impact of alternative estimates for
background on lung function and mortality risk estimates have been
developed and are included in the 2007 Staff Paper and Risk Assessment
TSD and key observations are discussed below.  Further, CASAC noted the
difficulties and complexities associated with available approaches to
estimating policy-relevant background concentrations (Henderson, 2007).

In the first part of the risk assessment, lung function decrement, as
measured by FEV1, is the only health response that is based on data from
controlled human exposure studies.  As discussed above, there is clear
evidence of a causal relationship between lung function decrements and
O3 exposures for school age children engaged in moderate exertion based
on numerous controlled human exposure and summer camp field studies
conducted by various investigators.  Risk estimates have been developed
for O3-related lung function decrements (measured as changes in FEV1)
for all school age children (ages 5 to 18) and a subset of this group,
asthmatic school age children (ages 5 to 18), whose average exertion
over an 8-hour period was moderate or greater.  The exposure period and
exertion level were chosen to generally match the exposure period and
exertion level used in the controlled human exposure studies that were
the basis for the exposure-response relationships.  A combined data set
including individual level data from the Folinsbee et al. (1988),
Horstman et al. (1990), and McDonnell et al. (1991) studies, used in the
previous risk assessment, and more recent data from Adams (2002, 2003a,
2006) have been used to estimate probabilistic exposure-response
relationships for 8-hour exposures under different definitions of lung
function response (i.e., ≥10, 15, and 20 percent decrements in FEV1).
As discussed in the 2007 Staff Paper (p.5-27), while these specific
controlled human exposure studies only included healthy adults aged
18-35, findings from other controlled human exposure studies and summer
camp field studies involving school age children in at least six
different locations in the northeastern United States, Canada, and
Southern California indicated changes in lung function in healthy
children similar to those observed in healthy adults exposed to O3 under
controlled chamber conditions.

	Consistent with advice from CASAC (Henderson, 2006c), EPA has
considered both linear and logistic functional forms in estimating the
probabilistic exposure-response relationships for lung function
responses.  A Bayesian Markov Chain Monte Carlo approach, described in
more detail in the Risk Assessment TSD, has been used that incorporates
both model uncertainty and uncertainty due to sample size in the
combined data set that served as the basis for the assessment.  The EPA
has chosen a model reflecting a 90 percent weighting on a logistic form
and a 10 percent weighting on a linear form as the base case for the
risk assessment.  The basis for this choice is that the logistic form
provides a very good fit to the combined data set, but a linear model
cannot be entirely ruled out since there are only very limited data
(i.e., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and
0.060 ppm).  The EPA has conducted a sensitivity analysis which examines
the impact on the lung function risk estimates of two alternative
choices, an 80 percent logistic/20 percent linear split and a 50 percent
logistic/50 percent linear split.

	As noted above, risk estimates have been developed for three measures
of lung function response (i.e., ≥10, 15, and 20 percent decrements in
FEV1).  However, the 2007 Staff Paper and risk estimates summarized
below focus on FEV1 decrements ≥15 percent for all school age children
and ≥10 percent for asthmatic school age children, consistent with the
advice from CASAC (Henderson, 2006c) that these levels of response
represent indicators of adverse health effects in these populations.
The Risk Assessment TSD and 2007 Staff Paper present the broader range
of risk estimates including all three measures of lung function
response.

	Developing risk estimates for lung function decrements involved
combining probabilistic exposure-response relationships based on the
combined data set from several controlled human exposure studies with
population exposure distributions for all and asthmatic school age
children associated with recent air quality and air quality simulated to
just meet the then current 0.084 ppm standard and alternative 8-hour O3
NAAQS based on the results from the exposure analysis described in the
previous section.  The risk estimates have been developed for 12 large
urban areas for the O3 season.  These 12 urban areas include
approximately 18.3 million school age children, of which 2.6 million are
asthmatic school age children.

	In addition to uncertainties arising from sample size considerations,
which are quantitatively characterized and presented as 95 percentile
credible intervals, there are additional uncertainties and caveats
associated with the lung function risk estimates.  These include
uncertainties about the shape of the exposure-response relationship,
particularly at levels below 0.080 ppm, and about policy-relevant
background levels, for which sensitivity analyses have been conducted.
Additional important caveats and uncertainties concerning the lung
function portion of the health risk assessment include:  (1) the
uncertainties and limitations associated with the exposure estimates
discussed above and (2) the inability to account for some factors which
are known to affect the exposure-response relationships (e.g., assigning
healthy and asthmatic children the same responses as observed in
healthy adult subjects and not adjusting response rates to reflect the
increase and attenuation of responses that have been observed in studies
of lung function responses upon repeated exposures).  A more complete
discussion of assumptions and uncertainties is contained in chapter 5 of
the 2007 Staff Paper and in the Risk Assessment TSD.

	The second part of the risk assessment is based on health effects
observed in epidemiological studies.  Based on a review of the evidence
evaluated in the 2006 Criteria Document and 2007 Staff Paper, as well as
the criteria discussed in chapter 5 of the 2007 Staff Paper, the
following categories of health endpoints associated with short-term
exposures to ambient O3 concentrations were included in the risk
assessment:  respiratory symptoms in moderate to severe asthmatic
children, hospital admissions for respiratory causes, and non-accidental
and cardiorespiratory mortality.  As discussed above, there is strong
evidence of a causal relationship for the respiratory morbidity
endpoints included in the risk assessment.  With respect to
nonaccidental and cardiorespiratory mortality, the 2006 Criteria
Document concludes that there is strong evidence which is highly
suggestive of a causal relationship between nonaccidental and
cardiorespiratory-related mortality and O3 exposures during the warm O3
season.  As discussed in the 2007 Staff Paper (chapter 5), EPA also
recognizes that for some of the effects observed in epidemiological
studies, such as increased respiratory-related hospital admissions and
nonaccidental and cardiorespiratory mortality, O3 may be serving as an
indicator for reactive oxidant species in the overall photochemical
oxidant mix and that these other constituents may be responsible in
whole or part for the observed effects.

	Risk estimates for each health endpoint category were only developed
for areas that were the same or close to the location where at least one
concentration-response function for the health endpoint had been
estimated.  Thus, for respiratory symptoms in moderate to severe
asthmatic children only the Boston urban area was included and four
urban areas were included for respiratory-related hospital admissions.
Nonaccidental mortality risk estimates were developed for 12 urban areas
and 8 urban areas were included for cardiorespiratory mortality.

	The concentration-response relationships used in the assessment are
based on findings from human epidemiological studies that have relied on
fixed-site ambient monitors as a surrogate for actual ambient O3
exposures.  In order to estimate the incidence of a particular health
effect associated with recent air quality in a specific county or set of
counties attributable to ambient O3 exposures in excess of background,
as well as the change in incidence corresponding to a given change in O3
levels resulting from just meeting various 8-hour O3 standards, three
elements are required for this part of the risk assessment.  These
elements are:  (1) air quality information (including recent air quality
data for O3 from ambient monitors for the selected location, estimates
of background O3 concentrations appropriate for that location, and a
method for adjusting the recent data to reflect patterns of air quality
estimated to occur when the area just meets a given O3 standard); (2)
relative risk-based concentration-response functions that provide an
estimate of the relationship between the health endpoints of interest
and ambient O3 concentration; and (3) annual or seasonal baseline health
effects incidence rates and population data, which are needed to provide
an estimate of the seasonal baseline incidence of health effects in an
area before any changes in O3 air quality.

	A key component in the portion of the risk assessment based on
epidemiological studies is the set of concentration-response functions
which provide estimates of the relationships between each health
endpoint of interest and changes in ambient O3 concentrations.  Studies
often report more than one estimated concentration-response function for
the same location and health endpoint.  Sometimes models include
different sets of co-pollutants and/or different lag periods between the
ambient concentrations and reported health responses.  For some health
endpoints, there are studies that estimated multicity and single-city O3
concentration-response functions.  While the Risk Assessment TSD and
chapter 5 of the 2007 Staff Paper present a more comprehensive set of
risk estimates, EPA has focused on estimates based on multicity studies
where available.  As discussed in chapter 5 of the 2007 Staff Paper, the
advantages of relying more heavily on concentration-response functions
based on multicity studies include: (1) more precise effect estimates
due to larger data sets, reducing the uncertainty around the estimated
coefficient; (2) greater consistency in data handling and model
specification that can eliminate city-to-city variation due to study
design; and (3) less likelihood of publication bias or exclusion of
reporting of negative or nonsignificant findings.  Where studies
reported different effect estimates for varying lag periods, consistent
with the 2006 Criteria Document, single day lag periods of 0 to 1 days
were used for associations with respiratory hospital admissions and
mortality.  For mortality associated with exposure to O3 which may
result over a several day period after exposure, distributed lag models,
which take into account the contribution to mortality effects over
several days, were used where available

	One of the most important elements affecting uncertainties in the
epidemiological-based portion of the risk assessment is the
concentration-response relationships used in the assessment.  The
uncertainty resulting from the statistical uncertainty associated with
the estimate of the O3 coefficient in the concentration-response
function was characterized either by confidence intervals or by Bayesian
credible intervals around the corresponding point estimates of risk.
Confidence and credible intervals express the range within which the
true risk is likely to fall if the only uncertainty surrounding the O3
coefficient involved sampling error.  Other uncertainties, such as
differences in study location, time period (i.e., the years in which the
study was conducted), and model uncertainties are not represented by the
confidence or credible intervals presented, but were addressed by
presenting estimates for different urban areas, by including risk
estimates based on studies using different time periods and models,
where available, and/or are discussed throughout section 5.3 of the 2007
Staff Paper.  Because O3 effects observed in the epidemiological studies
have been more clearly and consistently shown for warm season analyses,
all analyses for this portion of the risk assessment were carried out
for the same time period, April through September.

	The 2006 Criteria Document (p. 8-44) finds that no definitive
conclusion can be reached with regard to the existence of population
thresholds in epidemiological studies.  The EPA recognizes, however, the
possibility that thresholds for individuals may exist for 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.  Based on the 2006 Criteria Document’s
conclusions, EPA judged and CASAC concurred, that there is insufficient
evidence to support use of potential population threshold levels in the
quantitative risk assessment.  However, EPA recognizes that there is
increasing uncertainty about the concentration-response relationship at
lower concentrations which is not captured by the characterization of
the statistical uncertainty due to sampling error.  Therefore, the risk
estimates for respiratory symptoms in moderate to severe asthmatic
children, respiratory-related hospital admissions, and premature
mortality associated with exposure to O3 must be considered in light of
uncertainties about whether or not these O3-related effects occur in
these populations at very low O3 concentrations.

	With respect to variability within this portion of the risk assessment,
there is variability among concentration-response functions describing
the relation between O3 and both respiratory-related hospital admissions
and nonaccidental and cardiorespiratory mortality across urban areas.
This variability is likely due to differences in population (e.g., age
distribution), population activities that affect exposure to O3 (e.g.,
use of air conditioning), levels and composition of co-pollutants,
baseline incidence rates, and/or other factors that vary across urban
areas.  The risk assessment incorporates some of the variability in key
inputs to the analysis by using location-specific inputs (e.g.,
location-specific concentration-response functions, baseline incidence
rates, and air quality data).  Although spatial variability in these key
inputs across all U.S. locations has not been fully characterized,
variability across the selected locations is imbedded in the analysis by
using, to the extent possible, inputs specific to each urban area.

c.	Risk Estimates and Key Observations

	The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present risk
estimates associated with just meeting the then current 0.084 ppm
standard and several alternative 8-hour standards, as well as three
recent years of air quality as represented by 2002, 2003, and 2004
monitoring data.  As discussed in the exposure analysis section above,
there is considerable city-to-city and year-to-year variability in the
O3 levels during this period, which results in significant variability
in both portions of the health risk assessment.

	In the 1997 risk assessment, risks for lung function decrements
associated with 1-hour heavy exertion, 1-hour moderate exertion, and
8-hour moderate exertion exposures were estimated.  Since the 8-hour
moderate exertion exposure scenario for children clearly resulted in the
greatest health risks in terms of lung function decrements, EPA chose to
include only the 8-hour moderate exertion exposures in the risk
assessment for this health endpoint.  Thus, the risk estimates presented
here and in the 2007 Staff Paper are most useful for making relative
comparisons across alternative air quality scenarios and do not
represent the total risks for lung function decrements in children or
other groups within the general population associated with any of the
air quality scenarios.  Thus, some outdoor workers and adults engaged in
moderate exertion over multi-hour periods (e.g., 6-8 hour exposures)
also would be expected to experience similar lung function decrements.
However, the percentage of each of these other subpopulations expected
to experience these effects is expected to be smaller than all school
age children who tend to spend more hours outdoors while active based on
the exposure analyses conducted during the prior review.

	Table 2 presents a summary of the risk estimates for lung function
decrements for the 0.084 ppm standard set in 1997 and several
alternative 8-hour standard levels with the same form.  The estimates
are for the aggregate number

Table 2.  Number and Percent of All and Asthmatic School Age Children
in Several Urban Areas Estimated to Experience Moderate or Greater Lung
Function Responses One or More Times Per Season Associated with 8-Hour
Ozone Exposures  Associated with Just Meeting Alternative 8-Hour
Standards Based on Adjusting 2002 and 2004 Air Quality Data1,2

8-Hour Air Quality Standards3	All Children, ages 5-18

FEV1  > 15 percent

Aggregate for 12 urban areas

Number of Children Affected (% of all)

[% reduction from 0.084 ppm standard]	Asthmatic Children, ages 5-18

FEV1  > 10 percent

Aggregate for 5 urban areas

Number of Children Affected (% of group)

[% reduction from 0.084 ppm standard]

	2002	2004	2002	2004]

0.084 ppm

(Standard set in 1997)	610,000 (3.3%)

	230,000 (1.2%)	130,000 (7.8%)

	70,000 (4.2%)

0.080 ppm	490,000 (2.7%)

[20% reduction]	180,000 (1.0%)

[22% reduction]	NA4	NA

0.074 ppm	340,000 (1.9%)

[44% reduction]	130,000 (0.7%)

[43% reduction]	90,000 (5.0%)

[31 % reduction]	40,000 (2.7%)

[43% reduction]

0.070 ppm	260,000 (1.5%)

[57% reduction]	100,000 (0.5%)

[57% reduction]	NA	NA

0.064 ppm	180,000 (1.0%)

[70% reduction]	70,000 (0.4%)

[70% reduction]	50,000 (3.0%)

[62% reduction]	20,000 (1.5%)

[71% reduction]

1Associated with exposures while engaged in moderate or greater
exertion, which is defined as having an 8-hour average equivalent
ventilation rate > 13 l-min/m2.

2Estimates are the aggregate central tendency results based on either 12
urban areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New
York).  Estimates are for the O3 season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3All standards summarized here have the same form as the 8-hour standard
set in 1997, which is specified as the 3-year average of the annual 4th
highest daily maximum 8-hour average concentrations.  As described in
the 2007 Staff Paper (section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard set in 1997 and selected alternative standards.
These simulations do not represent predictions of when, whether, or how
areas might meet the specified standards

4NA (not available) indicates that EPA did not develop risk estimates
for these scenarios for the asthmatic school age children population.

and percent of all school age children across 12 urban areas and the
aggregate number and percent of asthmatic school age children across 5
urban areas who are estimated to have at least 1 moderate or greater
lung function response (defined as FEV1 > 15 percent in all children and
> 10 percent in asthmatic children) associated with 8-hour exposures to
O3 while engaged in moderate or greater exertion on average over the
8-hour period.  The lung function risk estimates summarized in Table 2
illustrate the year-to-year variability in both remaining risk
associated with a relatively high year (i.e., based on adjusting 2002 O3
air quality data) and relatively low year (based on adjusting 2004 O3
air quality data) as well as the year-to-year variability in the risk
reduction estimated to occur associated with various alternative
standards relative to just meeting the then current 0.084 ppm standard.
For example, it is estimated that about 610,000 school age children (3.2
percent of school age children) would experience 1 or more moderate lung
function decrements for the 12 urban areas associated with O3 levels
just meeting a 0.084 ppm standard based on 2002 air quality data
compared to 230,000 (1.2 percent of children) associated with just
meeting a 0.084 ppm standard based on 2004 air quality data.

	As discussed in the 2007 Staff Paper, a child may experience multiple
occurrences of a lung function response during the O3 season.  For
example, upon meeting a 0.084 ppm 8-hour standard, the median estimates
are that about 610,000 children would experience a moderate or greater
lung function response 1 or more times for the aggregate of the 12 urban
areas over a single O3 season (based on the 2002 simulation), and that
there would be almost 3.2 million total occurrences.  Thus, on average
it is estimated that there would be about 5 occurrences per O3 season
per responding child for air quality just meeting a 0.084 ppm 8-hour
standard across the 12 urban areas.  While the estimated number of
occurrences per O3 season is lower when based on the 2004 simulation
than for the 2002 simulation, the estimated number of occurrences per
responding child is similar. The EPA recognizes that some children in
the population might have only 1 or 2 occurrences while others may have
6 or more occurrences per O3 season.  Risk estimates based on adjusting
2003 air quality to simulate just meeting the a 0.084 ppm standard and
alternative 8-hour standards are intermediate to the estimates presented
in Table 2 above in this notice and are presented in the 2007 Staff
Paper (chapter 5) and Risk Assessment TSD.

	For just meeting a 0.084 ppm 8-hour standard, Table 5-8 in the 2007
Staff Paper shows that median estimates across the 12 urban areas for
all school age children experiencing 1 or more moderate lung function
decrements ranges from 0.9 to 5.4 percent based on the 2002 simulation
and from 0.8 to 2.2 percent based on the 2004 simulation.  Risk
estimates for each urban area included in the assessment, for each of
the three years analyzed, and for additional alternative standards are
presented in chapter 5 of the 2007 Staff Paper and in the Risk
Assessment TSD.

	For just meeting a 0.084 ppm 8-hour standard, the median estimates
across the 5 urban areas for asthmatic school age children range from
3.4 to 10.9 percent based on the 2002 simulation and from 3.2 to 6.9
percent based on the 2004 simulation.

	Key observations important in comparing estimated lung function risks
associated with just meeting the 0.084 ppm NAAQS and alternative
standards under consideration include:

	(1)  As discussed above, there is significant year to year variability
in the range of median estimates of the number of school age children
(ages 5-18) estimated to experience at least one FEV1 decrement ( 15
percent due to 8-hour O3 exposures across the 12 urban areas analyzed,
and similarly across the 5 urban areas analyzed for asthmatic school age
children (ages 5-18) estimated to experience at least one FEV1 decrement
> 10 percent, when various 8-hour standards are just met.

	(2)  For asthmatic school age children, the median estimates of
occurrences of FEV1 decrements >10% range from 52,000 to nearly 510,000
responses associated with just meeting a 0.084 ppm standard (based on
the 2002 simulation) and range from 61,000 to about 240,000 occurrences
(based on the 2004 simulation).  These risk estimates would be reduced
to a range of 14,000 to about 275,000 occurrences (2002 simulation) and
to about 18,000 to nearly 125,000 occurrences (2004 simulation) upon
just meeting the most stringent alternative 8-hour standard (0.064 ppm,
4th highest).  The average number of occurrences per asthmatic child in
an O3 season ranged from about 6 to 11 associated with just meeting a
0.084 ppm standard (2002 simulation).  The average number of occurrences
per asthmatic child ranged from 4 to 12 upon meeting the most stringent
alternative examined (0.064 ppm, 4th-highest) based on the 2002
simulation.  The number of occurrences per asthmatic child is similar
for the scenarios based on the 2004 simulation.

	As discussed above, several epidemiological studies have reported
increased respiratory morbidity outcomes (e.g., respiratory symptoms in
moderate to severe asthmatic children, respiratory-related hospital
admissions) and increased nonaccidental and cardiorespiratory mortality
associated with exposure to ambient O3 concentrations.  The results and
key observations from this portion of the risk assessment are presented
below:

	(1)  Estimates for increased respiratory symptoms (i.e., chest
tightness, shortness of breath, and wheeze) in moderate/severe asthmatic
children (ages 0-12) were developed for the Boston urban area only.  The
median estimated number of days involving chest tightness (using the
concentration-response relationship with only O3 in the model) is about
6,100 (based on the 2002 simulation) and about 4,500 (based on the 2004
simulation) upon meeting a 0.084 ppm 8-hour standard and this is reduced
to about 4,600 days (2002 simulation) and 3,100 days (2004 simulation)
upon meeting the most stringent alternative examined (0.064 ppm,
4th-highest daily maximum 8-hour average).  This corresponds to 11
percent (2002 simulation) and 8 percent (2004 simulation) of total
incidence of chest tightness upon meeting a 0.084 ppm 8-hour standard
and to about 8 percent (2002 simulation) and 5.5 percent (2004
simulation) of total incidence of chest tightness upon meeting a 0.064
ppm, 4th-highest daily maximum 8-hour average standard.  Similar
patterns of effects and reductions in effects are observed for each of
the respiratory symptoms examined.

	(2)  The 2007 Staff Paper and Risk Assessment TSD present unscheduled
hospital admission risk estimates for respiratory illness and asthma in
New York City associated with short-term exposures to O3 concentrations
in excess of background levels from April through September for several
recent years (2002, 2003, and 2004) and upon just meeting a 0.084 ppm
standard and alternative 8-hour standards based on simulating O3 levels
using 2002-2004 O3 air quality data.  For total respiratory illness, EPA
estimates about 6.4 cases per 100,000 relevant population (2002
simulation) and about 4.6 cases per 100,000 relevant population (2004
simulation), which represents 1.5 percent (2002 simulation) and 1.0
percent (2004 simulation) of total incidence or about 510 cases (2002
simulation) and about 370 cases (2004 simulation) upon just meeting a
0.084 ppm 8-hour standard.  For asthma-related hospital admissions,
which are a subset of total respiratory illness admissions, the
estimates are about 5.5 cases per 100,000 relevant population (2002
simulation) and about 3.9 cases per 100,000 relevant population (2004
simulation), which represents about 3.3 percent (2002 simulation) and
2.4 percent (2004 simulation) of total incidence or about 440 cases
(2002) and about 310 cases (2004) for this same air quality scenario.

	For increasingly more stringent alternative 8-hour standards, there is
a gradual reduction in respiratory illness cases per 100,000 relevant
population from 6.4 cases per 100,000 upon just meeting a 0.084 ppm
8-hour standard to 4.6 cases per 100,000 under the most stringent 8-hour
standard (i.e., 0.064 ppm, average 4th-highest daily maximum) analyzed
based on the 2002 simulation.  Similarly, based on the 2004 simulation
there is a gradual reduction from 4.6 cases per 100,000 relevant
population upon just meeting a 0.084 ppm 8-hour standard to 3.0 cases
per 100,000 under a 0.064 ppm, average 4th –highest daily maximum
standard.

	Additional respiratory-related hospital admission estimates for three
other locations are provided in the Risk Assessment TSD.  The EPA notes
that the concentration-response functions for each of these locations
examined different outcomes in different age groups (e.g., > age 30 in
Los Angeles, >age 64 in Cleveland and Detroit, vs. all ages in New York
City), making comparison of the risk estimates across the areas very
difficult.

	(3)  Based on the median estimates for incidence for nonaccidental
mortality (based on the Bell et al. (2004) 95 cities
concentration-response function), meeting the most stringent standard
(0.064 ppm) is estimated to reduce mortality by 40 percent of what it
would be associated with just meeting a 0.084 ppm standard (based on the
2002 simulation).  The patterns for cardiorespiratory mortality are
similar.  The aggregate O3-related cardiorespiratory mortality upon just
meeting the most stringent standard shown is estimated to be about 42
percent of what it would be upon just meeting a 0.084 ppm standard,
using simulated O3 concentrations that just meet a 0.084 ppm standard
and alternative 8-hour standards based on the 2002 simulation.  Using
the 2004 simulation, the corresponding reductions show a similar pattern
but are somewhat greater.

	(4)  Much of the contribution to the risk estimates for non-accidental
and cardiorespiratory mortality upon just meeting a 0.084 ppm 8-hour
standard is associated with 24-hour O3 concentrations between background
and 0.040 ppm.  Based on examining relationships between 24-hour
concentrations averaged across the monitors within an urban area and
8-hour daily maximum concentrations, 8-hour daily maximum levels at the
highest monitor in an urban area associated with these averaged 24-hour
levels are generally about twice as high as the 24-hour levels.  Thus,
most O3-related nonaccidental mortality is estimated to occur when O3
concentrations are between background and when the highest monitor in
the urban area is at or below 0.080 ppm, 8-hour average concentration.

	The discussion below highlights additional observations and insights
from the O3 risk assessment, together with important uncertainties and
limitations.

	(1)  As discussed in the 2007 Staff Paper (section 5.4.5), EPA has
greater confidence in relative comparisons in risk estimates between
alternative standards than in the absolute magnitude of risk estimates
associated with any particular standard.

	(2)  Significant year-to-year variability in O3 concentrations combined
with the use of a 3-year design value to determine the amount of air
quality adjustment to be applied to each year analyzed, results in
significant year-to-year variability in the annual health risk estimates
upon just meeting various 8-hour standards.

	(3)  There is noticeable city-to-city variability in estimated
O3-related incidence of morbidity and mortality across the 12 urban
areas analyzed for both recent years of air quality and for air quality
adjusted to simulate just meeting a 0.084 ppm standard and selected
potential alternative standards.  This variability is likely due to
differences in air quality distributions, differences in exposure
related to many factors including varying activity patterns and air
exchange rates, differences in baseline incidence rates, and differences
in susceptible populations and age distributions across the 12 urban
areas.

	(4)  With respect to the uncertainties about estimated policy-relevant
background concentrations, as discussed in the 2007 Staff Paper (section
5.4.3), alternative assumptions about background levels had a variable
impact depending on the health effect considered and the location and
standard analyzed in terms of the absolute magnitude and relative
changes in the risk estimates.  There was relatively little impact on
either absolute magnitude or relative changes in lung function risk
estimates due to alternative assumptions about background levels.  With
respect to O3-related non-accidental mortality, while notable
differences (i.e., greater than 50 percent) were observed for
nonaccidental mortality in some areas, particularly for more stringent
standards, the overall pattern of estimated reductions, expressed in
terms of percentage reduction relative to the 0.084 ppm standard, was
significantly less impacted.

C.	Reconsideration of the Level of the Primary Standard

1.	Evidence and Exposure/Risk-Based Considerations

The approach used in the 2007 Staff Paper as a basis for staff
recommendations on standard levels builds upon and broadens the general
approach used by EPA in the 1997 review.  This approach reflects the
more extensive and stronger body of evidence available for the 2008
rulemaking on a broader range of health effects associated with exposure
to O3, including:  (1) additional respiratory-related endpoints; (2) new
information about the mechanisms underlying respiratory morbidity
effects supporting a judgment that the link between O3 exposure and
these effects is causal; (3) newly identified cardiovascular-related
health endpoints from animal toxicology and controlled human exposures
studies that are highly suggestive that O3 can directly or indirectly
contribute to cardiovascular morbidity, and (4) new U.S. multicity time
series studies, single city studies, and several meta-analyses of these
studies that provide relatively strong evidence for associations between
short-term O3 exposures and all-cause (nonaccidental) mortality, at
levels below the current primary standard: as well as (5) a substantial
body of new evidence of increased susceptibility in people with asthma
and other lung diseases.  In evaluating evidence-based and
exposure/risk-based considerations, the 2007 Staff Paper considered:
(1) the ranges of levels of alternative standards that are supported by
the evidence, and the uncertainties and limitations in that evidence and
(2) the extent to which specific levels of alternative standards reduce
the estimated exposures of concern and risks attributable to O3 and
other photochemical oxidants, and the uncertainties associated with the
estimated exposure and risk reductions.

a.	Evidence-based Considerations

In taking into account evidence-based considerations, the 2007 Staff
Paper evaluated available evidence from controlled human exposure
studies and epidemiological studies, as well as the uncertainties and
limitations in that evidence.  In particular, it focused on the extent
to which controlled human exposure studies provide evidence of
lowest-observed-effects levels and the extent to which epidemiological
studies provide evidence of associations that extend down to the lower
levels of O3 concentrations observed in the studies or some indication
of potential effect thresholds in terms of 8-hour average O3
concentrations.

The most certain evidence of adverse health effects from exposure to O3
comes from the controlled human exposure studies, as discussed above in
section II.A.2, and 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.

	Two studies by Adams (2002, 2006), newly available for consideration in
the 2008 rulemaking, are the only available controlled human exposure
studies that examine respiratory effects associated with prolonged O3
exposures at levels below 0.080 ppm, which was the lowest exposure level
that had been examined in the 1997 review.  As discussed above in
section II.A.2.a.i.(a)(i), the Adams (2006) study investigated a range
of exposure levels, including 0.060 and 0.080 ppm O3, and analyzed
hour-by-hour changes in responses, including lung function (measured in
term of decrements in FEV1) and respiratory symptoms, to investigate the
effects of different patterns of exposure.  At the 0.060 ppm exposure
level, the author reported no statistically significant differences for
lung function decrements; statistically significant responses were
reported for total subjective respiratory symptoms toward the end of the
exposure period for one exposure pattern.  The EPA’s reanalysis
(Brown, 2007) of the data from the Adams (2006) study addressed the more
fundamental question of whether there were statistically significant
changes in lung function from a 6.6-hour exposure to 0.060 ppm O3 versus
filtered air and used a standard statistical method appropriate for a
simple paired comparison.  This reanalysis found small group mean lung
function decrements in healthy adults at the 0.060 ppm exposure level to
be statistically significantly different from responses associated with
filtered air exposure.

Moreover, the Adams’ studies also report a small percentage of
subjects (7 to 20 percent) experienced lung function decrements (> 10
percent) at the 0.060 ppm exposure level.  This is a concern because,
for active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of > 10% but < 20%) and/or moderate respiratory
symptom responses would likely interfere with normal activity for
relatively few responsive individuals.  However, for people with lung
disease, even 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 the context of standard
setting, the CASAC indicated (Henderson, 2006c) that a focus on the
lower end of the range of moderate levels of functional responses (e.g.,
FEV1 decrements ( 10%) is most appropriate for estimating potentially
adverse lung function decrements in people with lung disease.
Therefore, the results of the Adams studies which indicate that a small
percentage of healthy, non-asthmatic subjects are likely to experience
FEV1 decrements ( 10% when exposed to 0.060 ppm O3 have implications for
setting a standard that protects public health, including the health of
sensitive populations such as asthmatics, with an adequate margin of
safety.

In considering these most recent controlled human exposure studies, the
2007 Staff Paper concluded that these studies provide evidence of a
lowest-observed-effects level of 0.060 ppm for potentially adverse lung
function decrements and respiratory symptoms in some healthy adults
while at prolonged moderate exertion.  It further concluded that since
people with asthma, particularly children, have been found to be more
sensitive and to experience larger decrements in lung function in
response to O3 exposures than would healthy adults, the 0.060 ppm
exposure level also can be interpreted as representing a level likely to
cause adverse lung function decrements and respiratory symptoms in
children with asthma and more generally in people with respiratory
disease.

In considering controlled human exposure studies of pulmonary
inflammation, airway responsiveness, and impaired host defense
capabilities, discussed above in section II.A.2.a.i, the 2007 Staff
Paper noted that these studies provide evidence of a
lowest-observed-effects level for such effects in healthy adults at
prolonged moderate exertion of 0.080 ppm, the lowest level tested.
Moreover there is no evidence that the 0.080 ppm level is a threshold
for these effects.  Studies reporting inflammatory responses and markers
of lung injury have clearly demonstrated that there is significant
variation in response of subjects exposed, even to O3 exposures at 0.080
ppm.  One study showed notable interindividual variability in young
healthy adult subjects in most of the inflammatory and cellular injury
indicators analyzed at 0.080 ppm.  This inter-individual variability
suggests that some portion of the population would likely experience
such effects at exposure levels extending well below 0.080 ppm.

As discussed above, these physiological effects have been linked to
aggravation of asthma and increased susceptibility to respiratory
infection, potentially leading to increased medication use, increased
school and work absences, increased visits to doctors’ offices and
emergency departments, and increased hospital admissions.  Further,
pulmonary inflammation is related to increased cellular permeability in
the lung, which may be a mechanism by which O3 exposure can lead to
cardiovascular system effects, and to potential chronic effects such as
chronic bronchitis or long-term damage to the lungs that can lead to
reduced quality of life.  These are all indicators of adverse O3-related
morbidity effects, which are consistent with and lend plausibility to
the adverse morbidity effects and mortality effects observed in
epidemiological studies.

Significant associations between ambient O3 exposures and a wide variety
of respiratory symptoms and other morbidity outcomes (e.g., asthma
medication use, school absences, emergency department visits, and
hospital admissions) have been reported in epidemiological studies, as
discussed above in section II.A.2.a.i.  Overall, the 2006 Criteria
Document concludes that positive and robust associations were found
between ambient O3 concentrations and various respiratory disease
hospitalization outcomes, when focusing particularly on results of
warm-season analyses.  Recent studies also generally indicate a positive
association between O3 concentrations and emergency department visits
for asthma during the warm season.  These positive and robust
associations are supported by the controlled human exposure, animal
toxicological, and epidemiological evidence for lung function
decrements, increased respiratory symptoms, airway inflammation, and
increased airway responsiveness.  Taken together, the overall evidence
supports 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
(EPA, 2006a, p. 8-77).

Moreover, many single- and multicity epidemiological studies observed
positive associations of ambient O3 concentrations with total
nonaccidental and cardiopulmonary mortality.  As discussed above in
section II.A.2.b.i, the 2006 Criteria Document finds that the results
from U.S. multicity time-series studies provide the strongest evidence
to date for O3 effects on acute mortality.  Recent meta-analyses also
indicate positive risk estimates that are unlikely to be confounded by
PM; however, future work is needed to better understand the influence of
model specifications on the magnitude of risk. The 2006 Criteria
Document concludes that the “positive O3 effects estimates, along with
the sensitivity analyses in these three meta-analyses, provide evidence
of a robust association between ambient O3 and mortality” (EPA, 2006a,
p. 7-97).   In summary, the 2006 Criteria Document (p. 8-78) concludes
that these findings are highly suggestive that short-term O3 exposure
directly or indirectly contribute to non-accidental and
cardiopulmonary-related mortality, but additional research is needed to
more fully establish underlying mechanisms by which such effects occur.

The 2007 Staff Paper considered the epidemiological studies to evaluate
evidence related to potential effects thresholds at the population level
for morbidity and mortality effects.  As discussed above in section
II.A.3.a (and more fully in the 2007 Staff Paper in chapter 3 and the
2006 Criteria Document in chapter 7), a number of time-series studies
have used statistical modeling approaches to evaluate potential
thresholds at the population level.  A few such studies reported some
suggestive evidence of possible thresholds for morbidity and mortality
outcomes in terms of 24-hour, 8-hour, and 1-hour averaging times.  These
results, taken together, 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, however, observe linear concentration-response functions
suggesting no effect threshold.  The 2007 Staff Paper (p.6-60) concluded
that the statistically significant associations between ambient O3
concentrations and lung function decrements, respiratory symptoms,
indicators of respiratory morbidity including increase emergency
department visits and hospital admissions, and possibly mortality
reported in a large number of studies likely extend down to ambient O3
concentrations that are well below the level of the then current
standard (0.084 ppm).  These associations also extend 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.  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), however, the 2007 Staff Paper stated that 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.

The 2007 Staff Paper also considered studies that did subset analyses,
which included only days with ambient O3 concentrations below the level
of the then current standard, or below even lower O3 concentrations, and
continue to report statistically significant associations.  Notably, as
discussed above, Bell et al. (2006) conducted a subset analysis that
continued to show statistically significant mortality associations even
when only days with a maximum 8-hour average O3 concentration below a
value of approximately 0.061 ppm were included.  Also of note is the
large multicity NCICAS (Mortimer et al., 2002) that reported
statistically significant associations between ambient O3 concentrations
and lung function decrements even when days with 8-hour average O3
levels greater than 0.080 ppm were excluded (which consisted of less
than 5 percent of the days in the eight urban areas in the study).

Further, as discussed above in section II.A.3.a, there are limitations
in epidemiological studies that make discerning thresholds in
populations difficult, including low data density in the lower
concentration ranges, the possible influence of exposure measurement
error, and interindividual differences in susceptibility to O3-related
effects in populations.  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.

Based on the above considerations, the 2007 Staff Paper recognized that
the available evidence neither supports nor refutes the existence of
effect thresholds at the population level for morbidity and mortality
effects, and that if a population threshold level does exist, it would
likely be well below the level of the then current standard and possibly
within the range of background levels.  Taken together, these
considerations also support the conclusion that if a population
threshold level does exist, it would likely be well below the level of
the 0.075 ppm, 8-hour average, standard set in 2008.

In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the 2006
Criteria Document found substantial evidence, newly available in the
2008 rulemaking, that people with asthma and other preexisting pulmonary
diseases are among those at increased risk from O3 exposure.  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 (EPA, 2006a, section 8.7).  Children and adults with asthma are
the groups that have been studied most extensively.  Evidence from
controlled human exposure studies indicates that asthmatics may exhibit
larger lung function decrements in response to O3 exposure than healthy
controls.  As discussed more fully in section II.A.4 above, asthmatics
present a different response profile for cellular, molecular, and
biochemical parameters (EPA, 2006a, Figure 8-1) that are altered in
response to acute O3 exposure.  They can have larger inflammatory
responses, as manifested by larger increases in markers of inflammation
such as white bloods cells (e.g., PMNs) or inflammatory cytokines.
Asthmatics, and people with allergic rhinitis, are more likely to have
an allergic-type response upon exposure to O3, as manifested by
increases in white blood cells associated with allergy (i.e.,
eosinophils) and related molecules, which increase inflammation in the
airways.  The increased inflammatory and allergic responses also may be
associated with the larger late-phase responses that asthmatics can
experience, which can include increased bronchoconstrictor responses to
irritant substances or allergens and additional inflammation.

In addition to the experimental evidence of lung function decrements,
respiratory symptoms, and other respiratory effects in asthmatic
populations, 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 respiratory symptoms (e.g., chest tightness, wheeze,
shortness of breath) in children with moderate to severe asthma and
between O3 and increased asthma medication use (EPA, 2007a, chapter 6).
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 emergency department visits
and hospital admissions.

The body of evidence from controlled human exposure and epidemiological
studies, which includes asthmatic as well as non-asthmatic subjects,
indicates 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.  Therefore, relative to
the healthy, non-asthmatic subjects used in most controlled human
exposure studies, including the Adams (2002, 2006) 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 at ambient exposures to 0.060 ppm O3.  This indicates that the
lowest-observed-effects levels demonstrated in controlled human exposure
studies that use only healthy subjects may not reflect the lowest levels
at which people with asthma or other lung diseases may respond.

Being mindful of the uncertainties and limitations inherent in
interpreting the available evidence, the 2007 Staff Paper stated the
view that the range of alternative O3 standards for consideration should
take into account information on lowest-observed-effects levels in
controlled human exposure studies as well as indications of possible
effects thresholds reported in some epidemiological studies and
questions of biological plausibility in attributing associations
observed down to background levels to O3 exposures alone.  Based on the
evidence and these considerations, it concluded that the upper end of
the range of consideration should be somewhat below 0.080 ppm, the
lowest-observed-effects level for effects such as pulmonary
inflammation, increased airway responsiveness and impaired host-defense
capabilities in healthy adults while at prolonged moderate exertion.
The 2007 Staff Paper also concluded that the lower end of the range of
alternative O3 standards appropriate for consideration should be the
lowest-observed-effects level for potentially adverse lung function
decrements and respiratory symptoms in some healthy adults, 0.060 ppm.

b. 	Exposure and Risk-based Considerations

	In addition to the evidence-based considerations informing staff
recommendations on alternative levels, as discussed above in section
II.B, the 2007 Staff Paper also evaluated quantitative exposures and
health risks estimated to occur upon meeting the then current 0.084 ppm
standard and alternative standards.  In so doing, it presented the
important uncertainties and limitations associated with these exposure
and risk assessments (discussed above in section II.B and more fully in
chapters 4 and 5 of the 2007 Staff Paper).

	The 2007 Staff Paper (and the CASAC) also recognized that the exposure
and risk analyses could not provide a full picture of the O3 exposures
and O3-related health risks posed nationally.  The 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, and emergency department visits that
are part of the broader pyramid of effects discussed above in section
II.A.4.d), and the scope of the 2007 Staff Paper 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 included
in the  risk assessment.  Thus, national-scale public health impacts of
ambient O3 exposures are clearly 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 0.084 ppm standard or alternative standards.  On the
other hand, inter-individual variability in responsiveness means that
only a subset of individuals in each group estimated to experience
exposures exceeding a given benchmark exposure of concern level would
actually be expected to experience such adverse health effects.

	The 2007 Staff Paper focused on alternative standards with the same
form as the then current 0.084 ppm O3 standard (i.e. the 0.074/4,
0.070/4 and 0.064/4 scenarios).  Having concluded in the 2007 Staff
Paper that it was appropriate to consider a range of standard levels
from somewhat below 0.080 ppm down to as low as 0.060 ppm, the 2007
Staff Paper looked to results of the analyses of exposure and risk for
the 0.074/4 scenario to represent the public health impacts of selecting
a standard in the upper part of the range, the results of analyses of
the 0.070/4 scenario to represent the impacts in the middle part of the
range, and the results of the analyses of the 0.064/4 scenario to
represent the lower part of the range.

	As discussed in section II.B.1 of this notice, the exposure estimates
presented in the 2007 Staff Paper are for the number and percent of all
children and asthmatic children exposed, and the number of person-days
(occurrences) of exposures, with daily 8-hour maximum exposures at or
above several benchmark levels while at intermittent moderate or greater
exertion.  Exposures above selected benchmark levels provide some
perspective on the public health impacts of health effects that cannot
currently be evaluated in quantitative risk assessments but that may
occur at existing air quality levels, and the extent to which such
impacts might be reduced by meeting alternative standard levels.  As
described in section II.B.1.c above, the 2007 Staff Paper refers to
exposures at and above these benchmark levels as “exposures of
concern.”  The 2007 Staff Paper notes that exposures of concern, and
the health outcomes they represent, likely occur across a range of O3
exposure levels, such that there is no one exposure level that addresses
all public health concerns.  As noted above in section II.B., EPA also
has acknowledged that the concept 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.

 Consistent with advice from CASAC, the 2007 Staff Paper estimates
exposures of concern not only at 0.080 ppm O3, a level at which there
are clearly demonstrated effects, but also at 0.070 and 0.060 ppm O3
levels where there is some evidence that health effects are likely to
occur in some individuals.  The 2007 Staff Paper recognizes that there
will be varying degrees of concern about exposures at each of these
levels, based in part on the population groups experiencing them.  Given
that there is clear evidence of inflammation, increased airway
responsiveness, and changes in host defenses in healthy people exposed
to 0.080 ppm and reason to infer that such effects will continue at
lower exposure levels, but with increasing uncertainty about the extent
to which such effects occur at lower O3 concentrations, the 2007 Staff
Paper and discussion below, focus on exposures of concern at or above
benchmark levels of 0.070 and 0.060 ppm O3 for purposes of evaluating
alternative standards.  The focus on these two benchmark levels reflects
the following evidence-based considerations, discussed above in section
II.C.1, 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 with O3 levels that extend well below 0.080 ppm.

 Table 3 below summarizes the exposure estimates for all children and
asthmatic children for the 0.060 and 0.070 ppm health effect benchmark
levels associated with O3 levels adjusted to just meet 0.074/4, 0.070/4,
and 0.064/4 alternative 8-hour standards based on a generally poorer
year of air quality (2002) and based on a generally better year of air
quality (2004).  This table includes exposure estimates reflecting the
aggregate estimate for the 12 urban areas as well as the range across
these same 12 areas.  As shown in Table 3 below, the percent of
population exposed over the selected benchmark levels is very similar
for all and asthmatic school age children.  Thus, the following
discussion focuses primarily on the exposure estimates for asthmatic
children, recognizing that the pattern of exposure estimates is similar
for all children when expressed in terms of percentage of the
population.

As noted in section II.B.2 and shown in Tables 1 and 3 of this notice,
substantial year-to-year variability is observed, ranging to over an
order of magnitude at the higher alternative standard levels, in
estimates of the number of children and the number of occurrences of
exposures of concern at both  the 0.060 and 0.070 ppm benchmark levels.
As shown in Table 3, and discussed more fully below, aggregate estimates
of exposures of concern for the 12 urban areas included in the
assessment are considerably larger for the benchmark level of ≥ 0.060
ppm O3, compared to the 0.070 ppm benchmark, while the pattern of
year-to-year variability is fairly similar.

   As shown in Table 3, aggregate estimates of exposures of concern for
a 0.060 ppm benchmark level vary considerably among the three
alternative standards included in this table, particularly for the 2002
simulations (a year with generally poorer air quality in most, but not
all areas).  For air quality just meeting a 0.074/4 standard
approximately 27% of asthmatic children, based on the 2002 simulation,
and approximately 2% of asthmatic children based on the 2004 simulation
(a year with better air quality in most but not all areas), are
estimated to experience one or more exposures of concern at the
benchmark level of ≥ 0.060 ppm O3.  Considering a 0.070/4 standard
using the same benchmark level (0.060 ppm), about 18% of asthmatic
children are estimated to experience one or more exposures of concern,
in a year with poorer air quality (2002), and only about 1% in a year
with better air quality (2004).  For the most stringent standard
examined (a 0.064/4 standard), about 6% of asthmatic children are
estimated to experience one or more exposures of concern in the
simulation based on the year with poorer air quality (2002), and
exposures of concern at the 0.060 ppm benchmark level are essentially
eliminated based on a year with better air quality (2004).

Table 3 also provides aggregate exposure estimates for the 12 urban
areas where a benchmark level of ≥ 0.070 ppm is used.  Based on the
year with poorer air quality (2002), the estimate of the percent of
asthmatic children exposed one or more times is about 5% when a 0.074/4
standard is just met; based on a year with better air quality (2004),
exposures of concern are essentially eliminated.  For this same
benchmark (0.070 ppm), when a 0.070/4 standard is just met, estimates
range from about 2% of asthmatic children exposed one or more times over
this benchmark based on a year with poorer air quality (2002), and
exposures of concern are essentially eliminated based on a year with
better air quality (2004).  At the 0.070 ppm benchmark, just meeting a
0.064/4 standard essentially eliminates exposures of concern regardless
of the year that is used as the basis for the analysis.

	The 2007 Staff Paper also notes that there is substantial city-to-city
variability in these estimates, and notes 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 the alternative standards.  As shown in Table 3, in
considering the benchmark level of > 0.060 ppm, while the aggregate
percentage of asthmatic children estimated to experience one or more
exposures of concern across all 12 cities for a 0.074/4 standard is
about 27% based on the year with poorer air quality (2002), it ranges up
to approximately 51% for asthmatic children in the city with the least
degree of protection from that alternative standard.  Similarly, for air
quality just meeting a 0.070/4 standard, the aggregate percentage of
asthmatic children estimated to experience one or more exposures of
concern across all 12 cities is 18% based on the year with poorer air
quality, but it ranges up to about 41% in the city with the least degree
of protection associated with just meeting that alternative standard.
For just meeting a 0.064/4 standard, the aggregate estimate of asthmatic
children experiencing exposures of concern for the 0.060 ppm benchmark
is about 6% based on the year with poorer air quality and ranges up to
16% in the city with the least degree of protection.

This pattern of city-to-city variability also occurs at the benchmark
level of ≥ 0.070 ppm associated with air quality just meeting these
same three alternative standards (i.e., 0.074/4, 0.070/4, and 0.064/4).
While the aggregate percentage of asthmatic children estimated to
experience such exposures of concern across all 12 cities is about 5%
based on the year with poorer air quality for just meeting the 0.074/4
standard, it ranges up to 14% in the city with the least degree of
protection associated with that alternative standard.  For just meeting
a 0.070/4 standard the aggregate estimate is 2% of asthmatic children
experiencing exposures of concern for the 0.070 ppm benchmark based on
the year with poorer air quality and ranges up to 6% in the city with
the least degree of protection.  The aggregate estimate for exposures of
concern is further reduced to 0.2% of asthmatic children for this same
benchmark level for air quality just meeting a 0.064/4 standard based on
the year with poorer air quality and ranges up to 1% in the city with
the least degree of protection.

In addition to observing the fraction of the population estimated to
experience exposures of concern associated with just meeting alternative
standards, EPA also took into consideration in the 2007 Staff Paper the
percent reduction in exposures of concern and health risks associated
with alternative standards relative to just meeting the then current
0.084/4 standards.  For the current decision it is also informative to
consider the incremental reductions in exposures of concern associated
with more stringent alternative standards relative to the 0.075 ppm
standard.  As shown in Table 1 above, at the > 0.060 ppm benchmark level
based on a year with poorer air quality, the reduction in exposures of
concern for asthmatic children in going from the 0.074/4 standard (which
approximates the 0.075 ppm standard adopted in 2008) down to a 0.064/4
standard is observed to be very similar to the reduction estimated to
occur in going from then current 0.084/4 standard down to a 0.074/4
standard.  More specifically, the estimates for asthmatic children are
reduced from 47% (about 1.2 million children) associated with meeting a
0.084/4 standard down to 27% (about 700,000 children) for just meeting a
0.074/4 standard and the estimates are reduced further to about 6%
(about 150,000 children) associated with just meeting a 0.064/4 standard
in the 12 urban areas included in the assessment.  In a year with better
air quality (2004), exposures estimated to exceed the 0.060 ppm
benchmark in asthmatic children one or more times in a year are reduced
from 11% associated with just meeting a 0.084/4 standard down to about
2% for a 0.074/4 standard and are essentially eliminated when a 0.064/4
standard is just met.

Turning to consideration of the risk assessment estimates, Table 2 above
summarizes the risk estimates for moderate lung function decrements in
both all school age children and asthmatic school age children
associated with just meeting several alternative standards based on
simulations involving a year with relatively poorer air quality (2002)
and a year with relatively better air quality (2004).  As shown in Table
2, for the 2002 simulation the reduction in the number of asthmatic
children estimated to experience one or more moderate lung function
decrements going from a 0.074/4 standard down to a 0.064/4 standard is
roughly equivalent to the additional health protection afforded
associated with just meeting a 0.074/4 standard relative to then current
0.084/4 standard.  More specifically, for just 5 urban areas, it is
estimated that nearly 8% of asthmatic children (130,000 children) would
experience one or more occurrences of moderate lung function decrements
per year at a 0.084/4 standard and this would be reduced to about 5%
(90,000 children) at a 0.074/4 standard and further reduced down to
about 3% (50,000 children) at a 0.064/4 standard.  Based on the 2002
simulations, the percent reduction associated with just meeting a
0.064/4 standard relative to then current 0.084/4 standard is about 62%
which is about twice the reduction in risk compared to the estimated 31%
reduction associated with just meeting a 0.074/4 standard.  As shown in
Table 2 above, similar patterns were observed in reductions in lung
function risk for all school age children in 12 urban areas associated
with these alternative standards.

Figures 6-5 and 6-6 in the 2007 Staff Paper (EPA, 2007b) show the
percent reduction in non-accidental mortality risk estimates associated
with just meeting the same alternative standards discussed above
relative to just meeting the then current 0.084/4 standard for 12 urban
areas, based on adjusting 2002 and 2004 air quality data.  These figures
also provide perspective on the extent to which the risks in these years
(i.e., 2002 and 2004) are greater than those estimated to occur upon
meeting the then current 0.084/4 standard (in terms of a negative
percent reduction relative to a 0.084/4 standard).  Based on the 2002
simulations (EPA, 2007b, Figure 6-5), the estimated reduction in
non-accidental mortality is about 30 to 70% across the 12 urban areas
for just meeting a 0.064/4 standard relative to the then current 0.084/4
standard.  This reduction is roughly twice the 15 to 30% estimated
reduction across the 12 urban areas associated with just meeting a
0.074/4 standard relative to a 0.084/4 standard.  While the estimated
incidence is lower based on the 2004 simulations (EPA, 2007b, Figure
6-6), the pattern of risk reductions among alternative standards is
roughly similar to that observed for the 2002 simulations.

In addition to the risk estimates for lung function decrements in all
school age children and non-accidental mortality that were estimated for
12 urban areas and lung function decrements in asthmatic children for 5
urban areas, a similar pattern of incremental reductions in health risks
was shown for two health outcomes where risks were estimated in one city
only for each of these outcomes.  These included reductions in
respiratory symptoms in asthmatic children (EPA, 2007b; Boston, Table
6-9) and respiratory-related hospital admissions (EPA, 2007a; New York
City, Table 6-10) associated with just meeting alternative 8-hour
standards set at 0.074 ppm, 0.070 ppm, and 0.064 ppm relative to just
meeting the then current 0.084 ppm standard.  Using the 2002 simulation,
a standard set at 0.074/4 is estimated to reduce the incidence of
symptom days in children with moderate to severe asthma in the Boston
area by about 15 percent relative to a 0.084/4 standard.  With this
reduction, it is estimated that about 1 respiratory symptom day in 8
during the O3 season would be attributable to O3 exposure.  A standard
set at 0.064/4 is estimated, based on the 2002 simulation, to reduce the
incidence of symptom days in children with moderate to severe asthma in
the Boston area by about a 25 to 30 percent reduction relative to a
0.084 ppm standard, which is roughly twice the reduction compared to
that provided by a 0.074/4 standard.  But even with this reduction, it
is estimated that 1 respiratory symptom day in 10 during the O3 season
is attributable to O3 exposure

As shown in Table 6-10 (EPA, 2007b) estimated incidence of
respiratory-related hospital admissions in one urban area (New York
City) was reduced by 14 to 17 percent by a standard set at 0.074/4
relative to then current 0.084/4 standard, in the year with relatively
high and relatively low O3 air quality levels, respectively.  Similar to
the pattern observed for the other health outcomes discussed above, the
reduction in incidence of respiratory-related hospital admissions for a
0.064/4 standard relative to a 0.084/4 standard is about twice that
associated with a 0.074/4 standard relative to a 0.084/4 standard.

Table 3.  Number and Percent of All and Asthmatic School Age Children in
12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above
0.060 and 0.070 ppm While at Moderate or Greater Exertion, One or More
Times Per Season  Associated with Just Meeting Alternative 8-Hour
Standards Based on Adjusting 2002 and 2004 Air Quality Data1,2

Benchmark Levels of Exposures

of Concern

(ppm)	8-Hour Air Quality Standards3

(ppm)	All Children, ages 5-18

Aggregate for 12 urban areas	Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all children)

[Range across 12 cities, % of all children]	Number of Children Exposed
(% of group)

[Range across 12 cities, % of group ]

2002	2004	2002	2004

0.070	0.074	770,000 (4%)

[0 – 13%]	20,000 (0%)

[0 - 1%]	120,000 (5%)

[0 - 14% ]	0 (0%)

[0 - 1%]

	0.070	270,000 (1%)

[0 - 5%]	0 (0%)

[0%]	50,000 (2%)

[0 - 6%]	0 (0%)

[0%]

	0.064	30,000 (0.2%)

[0 - 1%]	0 (0%)

[0%]	10,000 (0.2%)

[0 - 1% ]	0 (0%)

[0%]

0.060	0.074	4,550,000 (25%)

[1 - 48%]	350,000 (2%)

[0 - 9%]	700,000 (27%)

[1 -51%]	50,000 (2%)

[0 - 9%]

	0.070	3,000,000 (16%)

[1 - 36%]	110,000 (1%)

[0 - 4%]	460,000 (18%)

[0 - 41%]	10,000 (1%)

[0 - 3%]

	0.064	950,000 (5%)

[0 - 17%]	10,000 (0%)

[0 - 1%]	150,000 (6%)

[0 - 16%]	0 (0%)

[0 - 1%]

1 Moderate or greater exertion is defined as having an 8-hour average
equivalent ventilation rate > 13 l-min/m2.

2 Estimates are the aggregate results based on 12 combined statistical
areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.).  Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3 All standards summarized here have the same form as the 8-hour
standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must
be at or below the concentration level specified.  As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard and selected alternative standards.  These
simulations do not represent predictions of when, whether, or how areas
might meet the specified standards

2.	CASAC Views Prior to 2008 Decision

	In comments on the second draft Staff Paper, CASAC stated in its letter
to the Administrator, “the CASAC unanimously recommends that the
current primary ozone NAAQS be revised and that the level that should be
considered for the revised standard be from 0.060 to 0.070 ppm”
(Henderson, 2006c, p. 5).  This recommendation followed from its more
general recommendation that the 0.084 ppm standard needed to be
substantially reduced to be protective of human health, particularly in
at-risk subpopulations.

	The CASAC Panel noted that beneficial reductions in some adverse health
effects were estimated to occur upon meeting the lowest standard level
(0.064 ppm) considered in the risk assessment (Henderson, 2006c, p. 4).
The lower end of this range reflects CASAC’s views that “[w]hile
data exist that adverse health effects may occur at levels lower than
0.060 ppm, these data are less certain and achievable gains in
protecting human health can be accomplished through lowering the ozone
NAAQS to a level between 0.060 and 0.070 ppm.”  (id.).

	In a subsequent letter sent specifically to offer advice to aid the
Administrator and Agency staff in developing the O3 proposal, the CASAC
reiterated that the Panel members “were unanimous in recommending that
the level of the current primary ozone standard should be lowered from
0.08 ppm to no greater than 0.070 ppm” (Henderson, 2007, p. 2).
Further, the CASAC Panel expressed the view that the 2006 Criteria
Document and 2007 Staff Paper, together with the information in its
earlier letter, provide “overwhelming scientific evidence for this
recommendation,” and emphasized the Clean Air Act requirement that the
primary standard must be set to protect the public health with an
adequate margin of safety (id.).

3.	Basis for 2008 Decision on the Primary Standard

	This section presents the rationale for the 2008 final decision on the
primary O3 standard as presented in the 2008 final rule (73 FR 16475).
The EPA’s conclusions on the level of the standard began by noting
that, having carefully considered the public comments on the appropriate
level of the O3 standard, EPA concluded that the fundamental scientific
conclusions on the effects of O3 reached in the 2006 Criteria Document
and 2007 Staff Paper remained valid.  In considering the level at which
the primary O3 standard should be set, EPA placed primary consideration
on the body of scientific evidence available in the 2008 final
rulemaking on the health effects associated with O3 exposure, while
viewing the results of exposure and risk assessments as providing
information in support of the decision.  In considering the available
scientific evidence, EPA concluded that a focus on the proposed range of
0.070 to 0.075 ppm was appropriate in light of the large body of
controlled human exposure and epidemiological and other scientific
evidence.  The notice stated that this body of evidence did not support
retaining the then current 0.084 ppm 8-hour O3 standard, as suggested by
some commenters, nor did it support setting a level just below 0.080
ppm, because, based on the entire body of evidence, such a level would
not provide a significant increase in protection compared to the 0.084
ppm standard.  Further, such a level would not be appreciably below the
level in controlled human exposure studies at which adverse effects have
been demonstrated (i.e., 0.080 ppm).  The notice also stated that the
body of evidence did not support setting a level of 0.060 ppm or below,
as suggested by other commenters.  In evaluating the information from
the exposure assessment and the risk assessment, EPA judged that this
information did not provide a clear enough basis for choosing a specific
level within the range of 0.075 to 0.070 ppm.

In making a final judgment about the level of the primary O3 standard,
EPA noted that the level of 0.075 ppm is above the range recommended by
the CASAC (i.e., 0.070 to 0.060 ppm).  The notice stated that in placing
great weight on the views of CASAC, careful consideration had been given
to CASAC’s stated views and the scientific basis and policy views for
the range it recommended.  In so doing, EPA fully agreed that the
scientific evidence supports the conclusion that the current standard
was not adequate and must be revised.

	With respect to CASAC’s recommended range of standard levels, EPA
observed that the basis for CASAC’s recommendation appeared to be a
mixture of scientific and policy considerations.  While in general
agreement with CASAC’s views concerning the interpretation of the
scientific evidence, EPA noted that there was no bright line clearly
directing the choice of level, and the choice of what was appropriate
was clearly a public health policy judgment entrusted to the EPA
Administrator.  This judgment must include consideration of the
strengths and limitations of the evidence and the appropriate inferences
to be drawn from the evidence and the exposure and risk assessments.  In
reviewing the basis for the CASAC Panel’s recommendation for the range
of the O3 standard, EPA observed that it reached a different policy
judgment than the CASAC Panel based on apparently placing different
weight in two areas: the role of the evidence from the Adams studies and
the relative weight placed on the results from the exposure and risk
assessments. 	While EPA found the evidence reporting effects at the
0.060 ppm level from the Adams studies to be too limited to support a
primary focus at this level, EPA observed that the CASAC Panel appeared
to place greater weight on this evidence, as indicated by its
recommendation of a range down to 0.060 ppm.  It was noted that while
the CASAC Panel supported a level of 0.060 ppm, they also supported a
level above 0.060, which indicated that they did not believe that the
results of Adams studies meant that the level of the standard had to be
set at 0.060 ppm.  The EPA also observed that the CASAC Panel appeared
to place greater weight on the results of the risk assessment as a basis
for its recommended range.  In referring to the risk assessment results
for lung function, respiratory symptoms, hospital admissions and
mortality, the CASAC Panel concluded that:  “beneficial effects in
terms of reduction of adverse health effects were calculated to occur at
the lowest concentration considered (i.e., 0.064 ppm)” (Henderson,
2006c, p.4).  However, EPA more heavily weighed the implications of the
uncertainties associated with the Agency’s quantitative human exposure
and health risk assessments.  Given these uncertainties, EPA did not
agree that these assessment results appropriately served as a primary
basis for concluding that levels at or below 0.070 ppm were required for
the 8-hour O3 standard.

	The notice stated that after carefully taking the above comments and
considerations into account, and fully considering the scientific and
policy views of the CASAC, EPA decided to revise the level of the
primary 8-hour O3 standard to 0.075 ppm.  The EPA judged, based on the
available evidence, that a standard set at this level would be requisite
to protect public health with an adequate margin of safety, including
the health of sensitive subpopulations, from serious health effects
including respiratory morbidity, that were judged to be causally
associated with short-term and prolonged exposures to O3, and premature
mortality.  The EPA also judged that a standard set at this level
provides a significant increase in protection compared to the 0.084 ppm
standard, and is appreciably below 0.080 ppm, the level in controlled
human exposure studies at which adverse effects have been demonstrated.
At a level of 0.075 ppm, exposures at and above the benchmark of 0.080
ppm are essentially eliminated, and exposures at and above the benchmark
of 0.070 are substantially reduced or eliminated for the vast majority
of people in at-risk groups.  A standard set at a level lower than 0.075
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 was not
prepared to make these assumptions.  Taking into account the
uncertainties that remained in interpreting the evidence from available
controlled human exposure and epidemiological studies at very low
levels, EPA noted that the likelihood of obtaining benefits to public
health decreased with a standard set below 0.075 ppm O3, while the
likelihood of requiring reductions in ambient concentrations that go
beyond those that are needed to protect public health increased.  The
EPA judged that the appropriate balance to be drawn, based on the entire
body of evidence and information available in the 2008 final rulemaking,
was to set the 8-hour primary standard at 0.075 ppm.  The EPA expressed
the belief that a standard set at 0.075 ppm would be sufficient to
protect public health with an adequate margin of safety, and did not
believe that a lower standard was needed to provide this degree of
protection.  The EPA further asserted that this judgment appropriately
considered the requirement for a standard that was neither more nor less
stringent than necessary for this purpose and recognized that the CAA
does not require that primary standards be set at a zero-risk level, but
rather at a level that reduces risk sufficiently so as to protect public
health with an adequate margin of safety.

4. 	CASAC Advice Following 2008 Decision

	Following the 2008 decision on the O3 standard, serious questions were
raised as to whether the standard met the requirements of the CAA.  In
April 2008, the members of the CASAC Ozone Review Panel sent a letter to
EPA stating “In our most-recent letters to you on this subject - dated
October 2006 and March 2007 - the CASAC unanimously recommended
selection of an 8-hour average Ozone NAAQS within the range of 0.060 to
0.070 parts per million for the primary (human health-based) Ozone
NAAQS” (Henderson, 2008).  The letter continued: “The CASAC now
wishes to convey, by means of this letter, its additional, unsolicited
advice with regard to the primary and secondary Ozone NAAQS.  In doing
so, the participating members of the CASAC Ozone Review Panel are
unanimous in strongly urging you or your successor as EPA Administrator
to ensure that these recommendations be considered during the next
review cycle for the Ozone NAAQS that will begin next year” (id.).
Moreover, the CASAC Panel noted that “numerous medical organizations
and public health groups have also expressed their support of these
CASAC recommendations.” (id.)  The letter further stated the following
strong, unanimous view:

[the CASAC did] “not endorse the new primary ozone standard as being
sufficient protective of public health.  The CASAC — as the Agency’s
statutorily-established science advisory committee for advising you on
the national ambient air quality standards — unanimously recommended
decreasing the primary standard to within the range of 0.060–0.070
ppm. It is the Committee’s consensus scientific opinion that your
decision to set the primary ozone standard above this range fails to
satisfy the explicit stipulations of the Clean Air Act that you ensure
an adequate margin of safety for all individuals, including sensitive
populations” (Henderson, 2008).

 5.	Administrator’s Proposed Conclusions

For the reasons discussed below, the Administrator proposes to set a new
level for the 8-hour primary O3 within the range from 0.060 to 0.070
ppm.  In reaching this proposed decision, the Administrator has
considered:  the evidence-based considerations from the 2006 Criteria
Document and the 2007 Staff Paper; the results of the exposure and risk
assessments discussed above and in the 2007 Staff Paper; CASAC advice
and recommendations provided in CASAC’s letters to the Administrator
both during and following the 2008 rulemaking; EPA staff
recommendations; and public comments received in conjunction with review
of drafts of these documents and on the 2007 proposed rule.  In
considering what level of an 8-hour O3 standard is requisite to protect
public health with an adequate margin of safety, the Administrator is
mindful that this choice requires judgments based on an interpretation
of the evidence and other information that neither overstates nor
understates the strength and limitations of the evidence and
information.

The Administrator 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 O3-induced
pulmonary inflammation, airway responsiveness, impaired host defense
capabilities, and other medically significant airway responses.
Moreover, there is no evidence that the 0.080 ppm exposure level is a
threshold for any of these types of respiratory effects.  Rather, there
is now controlled human exposure evidence, including studies of lung
function decrements and respiratory symptoms at the 0.060 ppm exposure
level, that strengthens our previous understanding that this array of
respiratory responses are likely to occur in some healthy adults at such
lower levels.

In particular, the Administrator notes two studies by Adams (2002,
2006), newly available in the 2008 rulemaking, that examined lung
function and respiratory symptom effects associated with prolonged O3
exposures at levels below 0.080 ppm, as well as EPA’s reanalysis of
the data from the Adams (2006) study at a 0.060 ppm exposure level.  As
discussed above, while the author’s analysis focused on hour-by-hour
comparisons of effects, for the purpose of exploring responses
associated with different patterns of exposure, EPA’s reanalysis
focused on addressing the more fundamental question of whether the pre-
to post-exposure change in lung function differed between a 6.6-hour
exposure to 0.060 ppm O3 versus a 6.6 hour exposure to clean filtered
air.  The Administrator notes that this reanalysis found small, but
statistically significant group mean differences in lung function
decrements in healthy adults at the 0.060 ppm exposure level, which is
now the lowest-observed-effects level for these effects.  Moreover,
these studies also report a small percentage of subjects (7 to 20
percent) experienced moderate lung function decrements (> 10 percent) at
the 0.060 ppm exposure level.  While for active healthy people, moderate
levels of functional responses (e.g., FEV1 decrements of > 10% but <
20%) and/or moderate respiratory symptom responses would likely
interfere with normal activity for relatively few responsive
individuals, the Administrator notes that for people with lung disease,
even moderate functional or symptomatic responses would likely interfere
with normal activity for many individuals, and would likely result in
more frequent use of medication.  Further, she notes that CASAC
indicated that a focus on the lower end of the range of moderate levels
of functional responses (e.g., FEV1 decrements ( 10%) is most
appropriate for estimating potentially adverse lung function decrements
in people with lung disease (Henderson, 2006c).

The Administrator also notes that many public commenters on the 2007
proposed rule raised a number of questions about the weight that should
be placed on the Adams studies and EPA’s reanalysis of data from the
Adams (2006) study.  Some commenters expressed the view that the results
of these studies and EPA’s reanalysis provided support for setting a
standard level below the proposed range, while others raised questions
about EPA’s reanalysis and generally expressed the view that the study
results were not robust enough to reach conclusions about respiratory
effects at the 0.060 ppm exposure level.

Based on all the abovethese considerations, the Administrator concludes
that the Adams studies provide limited but important evidence which adds
to the overall body of evidence that to informs her proposed decision on
the range of levels within which a standard could be set that would be
requisite to protect public health with an adequate margin of safety,
including the health of at-risk populations such as people with lung
disease.

In considering controlled human exposure studies reporting O3-induced
pulmonary inflammation, airway responsiveness, and impaired host defense
capabilities at exposure levels down to 0.080 ppm, the lowest level at
which these effects have been tested, the Administrator notes that these
physiological effects have been linked to aggravation of asthma and
increased susceptibility to respiratory infection, potentially leading