factors affecting microenvironmental (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 Staff Paper (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 clinical 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 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 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 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 (Tables 26 and 27 in Langstaff, 2007). 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,
2007, 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 include the 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.\30\ The
current standard uses 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, where the precision would extend to three
instead of two decimal places (in ppm).
---------------------------------------------------------------------------

    \30\ The current O3 standard is 0.08 ppm, but the
current rounding convention specifies that the average of the 4th
daily maximum 8-hour average concentrations over a three-year period
must be at 0.084 ppm or lower to be in attainment of the standard.
When EPA staff selected alternative standards to analyze, it was
presumed that the same type of rounding convention would be used,
and thus alternative standards of 0.084, 0.074, 0.064 ppm were
chosen.
---------------------------------------------------------------------------

    The 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 \31\ corresponding to the
standard being analyzed. The quadratic rollback technique reduces
higher concentrations more than lower concentrations near ambient
background levels.\32\ This procedure was considered in a sensitivity
analysis in the last 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.
---------------------------------------------------------------------------

    \31\ A design value is a statistic that describes the air
quality status of a given area relative to the level of the NAAQS.
Design values are often based on multiple years of data, consistent
with specification of the NAAQS in Part 50 of the CFR. For the
current O3 NAAQS, the 3-year average of the annual 4th-
highest daily maximum 8-hour average concentrations, based on the
monitor within (or downwind of) an urban area yielding the highest
3-year average, is the design value.
    \32\ The quadratic rollback approach and evaluation of this
approach are described by Johnson (1997), Duff et al. (1998) and
Rizzo (2005, 2006).
---------------------------------------------------------------------------

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 \33\ 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 we cannot currently evaluate 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 we know or can reasonably infer that specific
O3-related health effects are occurring. We refer to
exposures at and above these benchmark concentrations as ``exposures of
concern.''
---------------------------------------------------------------------------

    \33\ As discussed above in Section II.A., O3 health
responses observed in human clinical studies are associated with
exposures while engaged in moderate or greater exertion and,
therefore, these are the exposure measures of interest. The level of
exertion of individuals engaged in particular activities is measured
by an equivalent ventilation rate (EVR), ventilation normalized by
body surface area (BSA, in m\2\), which is calculated as VE/BSA,
where VE is the ventilation rate (liters/minute). Moderate and
greater exertion levels were defined as EVR > 13 liters/min-m\2\
(Whitfield et al., 1996) to correspond to the exertion levels
measured in most subjects studied in the controlled human exposure
studies that reported health effects associated with 6.6 hour
O3 exposures.
---------------------------------------------------------------------------

    EPA emphasizes 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. 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 human clinical 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, we first considered the exposure
level of 0.080 ppm, at which there is a substantial amount of clinical
evidence demonstrating a range of O3-related health effects
including lung inflammation and airway responsiveness in healthy
individuals. Thus, as in the last 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 epidemiology 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 epidemiology 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. EPA has not included 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. 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 has chosen 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 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 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.\34\ 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 current
standard.
---------------------------------------------------------------------------

    \34\ The full range of quantitative exposure estimates
associated with just meeting the current and alternative
O3 standards are presented in chapter 4 and Appendix 4A
of the Staff Paper.
---------------------------------------------------------------------------

    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 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 1 or more exposures of concern decline
from simulations of just meeting the current 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 current 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 Data\1, 2\
----------------------------------------------------------------------------------------------------------------
                                     All children, ages 5-18 aggregate for      Asthmatic children, ages 5-18
                       8-Hour air      12 urban areas, number of children   Aggregate for 12 urban areas, number
Benchmark levels of      quality      exposed (% of all) [%reduction from    of children exposed (% of group) [%
    exposures of      standards\3\             current standard]              reduction from current standard]
   concern (ppm)          (ppm)     ----------------------------------------------------------------------------
                                            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%)     100,000 (1%)       330,000 (13%)      10,000 (0%) [75%]
                                      [35%].              [62%].             [36%].
                              0.074  770,000 (4%) [77%]  20,000 (0%) [92%]  120,000 (5%)       0 (0%) [100%]
                                                                             [77%].
                              0.070  270,000 (1%) [92%]  0 (0%) [100%]....  50,000 (2%) [90%]  0 (0%) [100%]
                              0.064  30,000 (0.2%)       0 (0%) [100%]....  10,000 (0.2%)      0 (0%) [100%]
                                      [99%].                                 [98% ].
----------------------------------------------------------------------------------------------------------------
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%)     1,050,000 (6%)     1,020,000 (40%)    150,000 (6%)
                                      [16%].              [42%].             [16%].             [44%]
                              0.074  4,550,000 (25%)     350,000 (2%)       700,000 (27%)      50,000 (2%) [81%]
                                      [43%].              [80%].             [42%].
                              0.070  3,000,000 (16%)     110,000 (1%)       460,000 (18%)      10,000 (1%) [96%]
                                      [62%].              [94%].             [62%].
                              0.064  950,000 (5%) [88%]  10,000 (0%) [99%]  150,000 (6%)       0 (0%) [100%]
                                                                             [88%].
----------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate >= 13 l-min/
  m\2\.
\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, DC).
  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 current 8-hour standard 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 Staff Paper (section 4.5.8), recent O3 air quality
  distributions have been statistically adjusted to simulate just meeting the current 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 the current
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 the current 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, 2007, Exhibit 2, p. 4-48). 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, 2007, Exhibit 8,
p. 4-60).
    (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.\35\ As part of the last 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.\36\ The risk assessment for the last 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.
---------------------------------------------------------------------------

    \35\ The methodology, scope, and results from the risk
assessment conducted in the last review are described in Chapter 6
of the 1996 Staff Paper (EPA, 1996) and in several technical reports
(Whitfield et al., 1996; Whitfield, 1997) and publication (Whitfield
et al., 1998).
    \36\ The 9 urban study areas included in the exposure and risk
analyses conducted during the last review were: Chicago, Denver,
Houston, Los Angeles, Miami, New York City, Philadephia, St. Louis,
and Washington, DC.
---------------------------------------------------------------------------

a. Overview
    The updated health risk assessment conducted as part of this review
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 current 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 the Staff Paper (EPA, 2007, chapter 5) and in a technical
support document (TSD), Ozone Health Risk Assessment for Selected Urban
Areas (Abt Associates, 2006, 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.\37\ 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.
---------------------------------------------------------------------------

    \37\ The general approach used in the current risk assessment
was described in the draft Health Assessment Plan (EPA, 2005a) that
was released to the CASAC and general public in April 2005 and was
the subject of a consultation with the CASAC O3 Panel on
May 5, 2005. In October 2005, OAQPS released the first draft of the
Staff Paper containing a chapter discussing the risk assessment and
first draft of the Risk Assessment TSD for CASAC consultation and
public review on December 8, 2005. In July 2006, OAQPS released the
second draft of the Staff Paper and second draft of the Risk
Assessment TSD for CASAC review and public comment which was held by
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------

    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
current 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 Criteria Document and 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 the current 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 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.
    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 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 the current
and selected 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, 2007, p. 6-20). With respect to
uncertainties about estimated background concentrations, as discussed
below and in the Staff Paper (EPA 2007b, 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, 2007, pp.
6-20--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. EPA recognizes that these credible
intervals do not reflect all of the uncertainties noted above.

b. Scope and Key Components
    The current health risk assessment is based on the information
evaluated in the final Criteria Document. The risk assessment includes
several categories of health effects and estimates risks associated
with just meeting the current 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.\38\ 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 do not meet the current 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.
---------------------------------------------------------------------------

    \38\ The 12 urban areas are the same urban areas evaluated in
the exposure analysis discussed in the prior section. However, for
most of the health endpoints based on findings from epidemiological
studies, the geographic areas and populations examined in the health
risk assessment were limited to those counties included in the
original epidemiological studies that served as the basis for the
concentration-response relationships.
---------------------------------------------------------------------------

    The short-term exposure related health endpoints selected for
inclusion in the quantitative risk assessment include those for which
the final Criteria Document and or 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 the
current and 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 current 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 Staff Paper (EPA, 2007, 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.\39\
---------------------------------------------------------------------------

    \39\ EPA notes that the estimated level of policy-relevant
background O3 used in the prior risk assessment was a
single concentration of 0.04 ppm, which was the midpoint of the
range of levels for policy-relevant background that was provided in
the 1996 Criteria Document.
---------------------------------------------------------------------------

    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 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).
Recognizing these complexities, EPA requests comments on the new
approach used in this review for estimating these levels as an input to
the health risk assessment.\40\
---------------------------------------------------------------------------

    \40\ Recognizing the importance of this issue, EPA intends to
conduct additional sensitivity analyses related to policy-relevant
background and its implications for the risk assessment.
---------------------------------------------------------------------------

    In the first part of the current 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, 2003, 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
Staff Paper (EPA, 2007, 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. 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 current 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). 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 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 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 current 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.\41\ These 12 urban areas
include approximately 18.3 million school age children, of which 2.6
million are asthmatic school age children.\42\
---------------------------------------------------------------------------

    \41\ As discussed above in section II.B.1, the urban areas were
defined using the consolidated statistical areas definition and the
total population residing in the 12 urban areas was approximately
88.5 million people.
    \42\ For 9 of the 12 urban areas, the O3 season is
defined as a period running from March or April to September or
October. In 3 of the urban areas (Houston, Los Angeles, and
Sacramento), the O3 season is defined as the entire year.
---------------------------------------------------------------------------

    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 Staff Paper and in the Risk Assessment
TSD (Abt Associates, 2006).
    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 Criteria Document and Staff Paper, as well as the
criteria discussed in chapter 5 of the 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 current risk assessment. With
respect to nonaccidental and cardiorespiratory mortality, the 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 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.\43\ 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.
---------------------------------------------------------------------------

    \43\ The geographic boundaries for the urban areas included in
this portion of the risk assessment were generally matched to the
geographic boundaries used in the epidemiological studies that
served as the basis for the concentration-response functions. In
most cases, the urban areas were defined as either a single county
or a few counties for this portion of the risk assessment.
---------------------------------------------------------------------------

    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 the current or alternative 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 multi-city and single-city
O3 concentration-response functions. While the Risk
Assessment TSD and chapter 5 of the Staff Paper present a more
comprehensive set of risk estimates, EPA has focused on estimates based
on multi-city studies where available. The advantages of relying more
heavily on concentration-response functions based on multi-city 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 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 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 Criteria Document finds that no definitive conclusion can be
reached with regard to the existence of population thresholds in
epidemiological studies (Criteria Document, pp. 8-44). 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 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
current 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 Staff Paper (chapter 5) and Risk Assessment TSD present risk
estimates associated with just meeting the current 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 has
chosen to include only the 8-hour moderate exertion exposures in the
current risk assessment for this health endpoint. Thus, the risk
estimates presented here and in the 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 current standard and several alternative 8-hour
standard levels with the same form as the current 8-hour standard. The
estimates are for the aggregate number 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 \44\ 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 current 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 the current standard based on 2002 air quality data
compared to 230,000 (1.2 percent of children) associated with just
meeting the current standard based on 2004 air quality data.
---------------------------------------------------------------------------

    \44\ Due to time constraints, lung function risk estimates for
asthmatic school age children were developed for only 5 of the 12
urban areas, and the areas were selected to represent different
geographic regions. The 5 areas were: Atlanta, Chicago, Houston, Los
Angeles, and New York City.

    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 1 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
                                                  Data \1,\ \2\
----------------------------------------------------------------------------------------------------------------
                                    All children, ages 5-18, FEV1 >=15      Asthmatic children, ages 5-18, FEV1
                                  percent, aggregate for 12 urban areas,    >=10 percent, aggregate for 5 urban
                                  number of children affected (% of all)   areas, number of children affected (%
8-Hour air quality standards \3\    [% reduction from current standard]     of group) [% reduction from current
                                 ----------------------------------------                standard]
                                                                         ---------------------------------------
                                         2002                2004                2002                2004]
----------------------------------------------------------------------------------------------------------------
0.084 ppm (Current standard)....  610,000 (3.3%)....  230,000 (1.2%)....  130,000 (7.8%)....  70,000 (4.2%).
0.080 ppm.......................  490,000 (2.7%)      180,000 (1.0%)      NA \4\............  NA.
                                   [20% reduction].    [22% reduction].
0.074 ppm.......................  340,000 (1.9%)      130,000 (0.7%)      90,000 (5.0%) [31   40,000 (2.7%) [43%
                                   [44% reduction].    [43% reduction].    % reduction].       reduction].
0.070 ppm.......................  260,000 (1.5%)      100,000 (0.5%)      NA................  NA.
                                   [57% reduction].    [57% reduction].
0.064 ppm.......................  180,000 (1.0%)      70,000 (0.4%) [70%  50,000 (3.0%) [62%  20,000 (1.5%) [71%
                                   [70% reduction].    reduction].         reduction].         reduction].
----------------------------------------------------------------------------------------------------------------
\1\ Associated with exposures while engaged in moderate or greater exertion which is defined as having an 8-hour
  average equivalent ventilation rate >=13 l-min/m \2\.
\2\ Estimates 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, DC) 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.
\3\ All standards summarized here have the same form as the current 8-hour standard 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
  stated concentration level. As described in the Staff Paper (section 4.5.8), recent O3 air quality
  distributions have been statistically adjusted to simulate just meeting the current and selected alternative
  standards. These simulations do not represent predictions of when, whether, or how areas might meet the
  specified standards
\4\ NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic
  school age children population.

    As discussed in the Staff Paper, a child may experience multiple
occurrences of a lung function response during the O3
season. For example, upon meeting the current 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 the current 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. 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 current and
alternative 8-hour standards are intermediate to the estimates
presented in Table 2 above in this notice and are presented in the
Staff Paper (chapter 5) and Risk Assessment TSD.
    For just meeting the current 8-hour standard, Table 5-8 in the
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 Staff Paper and in the Risk Assessment
TSD.
    For just meeting the current 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 attainment of the current 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 the current and
alternative 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 the current
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 the current
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 the current 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 the current 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 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 the current 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 the current 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 the
current 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 the current 8-hour standard to
3.0 cases per 100,000 under the 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. 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 the current 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 the current standard,
using simulated O3 concentrations that just meet the current
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 the
current 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 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 the current and potential alternative 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 the current 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 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)\45\ 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 current
standard, was significantly less impacted.
---------------------------------------------------------------------------

    \45\ For example, assuming lower background levels resulted in
increased estimates of non-accidental mortality incidence per
100,000 that were often 50 to 100 percent greater than the base case
estimates; assuming higher background levels resulted in decreased
estimates of non-accidental mortality incidence per 100,000 that
were less than the base case estimates by 50 percent or more in many
of the areas.
---------------------------------------------------------------------------

C. Conclusions on the Adequacy of the Current Primary Standard

1. Background
    The initial issue to be addressed in the current review of the
primary O3 standard is whether, in view of the advances in
scientific knowledge and additional information, the existing standard
should be revised. In evaluating whether it is appropriate to retain or
revise the current standard, the Administrator builds upon the last
review and reflects the broader body of evidence and information now
available. The Administrator has taken into account both evidence-based
and quantitative exposure- and risk-based considerations in developing
conclusions on the adequacy of the current primary O3
standard. Evidence-based considerations include the assessment of
evidence from controlled human exposure, animal toxicological, field,
and epidemiological studies for a variety of health endpoints. For
those endpoints based on epidemiological studies, greater weight has
been placed on associations with health endpoints that are causal or
likely causal based on an integrative synthesis of the entire body of
evidence, including not only all available epidemiological evidence but
also evidence from animal toxicological and controlled human exposure
studies. Less weight has been placed on evidence of associations that
were judged to be only suggestive of possible causal relationships.
Consideration of quantitative exposure- and risk-based information
draws from the results of the exposure and risk assessments described
above. More specifically, estimates of the magnitude of O3-
related exposures and risks associated with recent air quality levels,
as well as the exposure and risk reductions likely to be associated
with just meeting the current 8-hour primary O3 NAAQS, have
been considered.
    In this review, a series of general questions frames the approach
to reaching a decision on the adequacy of the current standard, such as
the following: (1) To what extent does newly available information
reinforce or call into question evidence of associations of
O3 exposures with effects identified in the last review?;
(2) to what extent has evidence of new effects and/or at-risk
populations become available since the last review?; (3) to what extent
have important uncertainties identified in the last review been reduced
and have new uncertainties emerged?; (4) to what extent does newly
available information reinforce or call into question any of the basic
elements of the current standards?
    The question of whether the available evidence supports
consideration of a standard that is more protective than the current
standard includes consideration of: (1) Whether there is evidence that
associations, especially likely causal associations, extend to ambient
O3 concentration levels that are as low as or lower than had
previously been observed, and the important uncertainties associated
with that evidence; (2) the extent to which exposures of concern and
health risks are estimated to occur in areas upon meeting the current
standard and the important uncertainties associated with the estimated
exposures and risks; and (3) the extent to which the O3-
related health effects indicated by the evidence and the exposure and
risk assessments are considered important from a public health
perspective, taking into account the nature and severity of the health
effects, the size of the at-risk populations, and the kind and degree
of the uncertainties associated with these considerations.
    The current primary O3 standard is an 8-hour standard,
which was set at a level of 0.08 ppm,\46\ with a form of the annual
fourth-highest daily maximum 8-hour average concentration, averaged
over three years. This standard was chosen to provide protection to the
public, especially children and other at-risk populations, against a
wide range of O3-induced health effects. As an introduction
to this discussion of the adequacy of the current O3
standard, it is useful to summarize the key factors that formed the
basis of the decision in the last review to revise the averaging time,
level, and form of the then current 1-hour standard.
---------------------------------------------------------------------------

    \46\ If the standard were to be specified to the nearest
thousandth ppm, the current 0.08 ppm 8-hour standard would be
equivalent to a standard set at 0.084 ppm, reflecting the data
rounding conventions that are part of the definition of the current
8-hour standard.
---------------------------------------------------------------------------

    In the last review, the key factor in deciding to revise the
averaging time of the primary standard was evidence from controlled
human exposure studies of healthy young adult subjects exposed for 1 to
8 hours to O3. The best documented health endpoints in these
studies were decrements in indices of lung function, such as forced
expiratory volume in 1 second (FEV1), and respiratory
symptoms, such as cough and chest pain on deep inspiration. For short-
term exposures of 1 to 3 hours, group mean FEV1 decrements were
statistically significant for O3 concentrations only at and
above 0.12 ppm, and only when subjects engaged in very heavy exertion.
By contrast, evidence available in the prior review showed that
prolonged exposures of 6 to 8 hours produced statistically significant
group mean FEV1 decrements at the lowest O3
concentrations evaluated in those studies, 0.080 ppm, even when
experimental subjects were engaged in more realistic intermittent
moderate exertion levels. The health significance of this newer
evidence led to the conclusion in the 1997 final decision that the 8-
hour averaging time is more directly associated with health effects of
concern at lower O3 concentrations than is the 1-hour
averaging time.

    Based on the available evidence of O3-related health
effects, the following factors were of particular importance in the
last review in informing the selection of the level and form of a new
8-hour standard: (1) Quantitative estimates of O3-related
risks to active children, who were judged to be an at-risk subgroup of
concern, in terms of transient and reversible respiratory effects
judged to be adverse, including moderate to large decreases in lung
function and moderate to severe pain on deep inspiration, and the
uncertainty and variability in such estimates; (2) consideration of
both the estimated percentages, total numbers of children, and number
of times they were likely to experience such effects; (3)
epidemiological evidence of associations between ambient O3
and increased respiratory hospital admissions, and quantitative
estimates of percentages and total numbers of asthma-related admissions
in one example urban area that were judged to be indicative of a
pyramid of much larger effects, including respiratory-related hospital
admissions, emergency department visits, doctor visits, and asthma
attacks and related increased medication use; (4) quantitative
estimates of the number of ``exposures of concern\47\'' (defined as
exposures >= 0.080 ppm for 6 to 8 hour) that active children are likely
to experience, and the uncertainty and variability in such estimates;
(5) the judgment that such exposures are an important indicator of
public health impacts of O3-related effects for which
information is too limited to develop quantitative risk estimates,
including increased nonspecific bronchial responsiveness (e.g., related
to aggravation of asthma), decreased pulmonary defense mechanisms
(suggestive of increased susceptibility to respiratory infection), and
indicators of pulmonary inflammation (related to potential aggravation
of chronic bronchitis or long-term damage to the lungs); (6) the
broader public health perspective of the number of people living in
areas that would breathe cleaner air as a result of the revised
standard; (7) consideration of the relative seriousness of various
health effects and the relative degree of certainty in both the
likelihood that people will experience various health effects and their
medical significance; (8) the relationship of a standard level to
estimated ``background'' levels associated with nonanthropogenic
sources of O3; and (9) CASAC's advice and recommendations.
Additional factors considered in selecting the form of the standard
included balancing the public health implications of the estimated
number of times in an O3 season that the standard level
might be exceeded in an area that is in attainment with the standard
with the year-to-year stability of the air quality statistic, which can
be particularly affected by years with unusual meteorology. A more
stable air quality statistic serves to avoid disruptions to ongoing
control programs that could result from moving into and out of
attainment, thereby interrupting the public health protection afforded
by such control programs.
---------------------------------------------------------------------------

    \47\ In the last review, ``exposures of concern'' referred to
exposures at and above 0.08 ppm, 8-hour average, at which a range of
health effects have been observed in controlled human studies, but
for which data were too limited to allow for quantitative risk
assessment. (62 FR 38860, July 18, 1997).
---------------------------------------------------------------------------

    In reaching a final decision in the last review, the Administrator
was mindful that O3 exhibits a continuum of effects, such
that there is no discernible threshold above which public health
protection requires that no exposures be allowed or below which all
risks to public health can be avoided. The final decision reflected a
recognition that important uncertainties remained, for example with
regard to interpreting the role of other pollutants co-occurring with
O3 in observed associations, understanding biological
mechanisms of O3-related health effects, and estimating
human exposures and quantitative risks to at-risk populations for these
health effects.
2. Evidence- and Exposure/Risk-Based Considerations in the Staff Paper
    The Staff Paper (section 6.3.1) considers the evidence presented in
the Criteria Document as discussed above in section II.A as a basis for
evaluating the adequacy of the current O3 standard,
recognizing that important uncertainties remain. The extensive body of
human clinical, toxicological, and epidemiological evidence serves as
the basis for the judgments about O3-related health effects
discussed above, including judgments about causal relationships with a
range of respiratory morbidity effects, including lung function
decrements, increased respiratory symptoms, airway inflammation,
increased airway responsiveness, and respiratory-related
hospitalizations and emergency department visits in the warm season,
and about the evidence being highly suggestive that O3
directly or indirectly contributes to non-accidental and
cardiopulmonary-related mortality.
    These judgments take into account important uncertainties that
remain in interpreting this evidence. For example, with regard to the
utility of time-series epidemiological studies to inform judgments
about a NAAQS for an individual pollutant, such as O3,
within a mix of highly correlated pollutants, such as the mix of
oxidants produced in photochemical reactions in the atmosphere, the
Staff Paper notes that there are limitations especially at ambient
O3 concentrations below levels at which O3-
related effects have been observed in controlled human exposure
studies. The Staff Paper (section 3.4.5) also recognizes that the
available epidemiological evidence neither supports nor refutes the
existence of thresholds at the population level for effects such as
increased hospital admissions and premature mortality. 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 variability in susceptibility to O3-related
effects in populations.
    While noting these limitations in the interpretation of the
findings from the epidemiological studies, the Staff Paper (section
3.4.5) concludes that if a population threshold level does exist, it
would likely be well below the level of the current O3
standard and possibly within the range of background levels. As
discussed above in section II.A.3.a, this conclusion is supported by
several epidemiological studies that have explored the question of
potential thresholds directly, either using a statistical curve-fitting
approach to evaluate whether linear or non-linear models fit the data
better using sub-sets of the data, where days over or under a specific
cutpoint (e.g., 0.080 ppm or even lower O3 levels) were
excluded and then evaluating the association for statistical
significance. In addition to direct consideration of the
epidemiological studies, findings from controlled human exposure
studies discussed above in section II.A.2.a.i(a)(i) indicate that
prolonged exposures produced statistically significant group mean
FEV1 decrements and symptoms in healthy adult subjects at
levels down to at least 0.060 ppm, with a small percentage of subjects
experiencing notable effects (e.g., >10 percent FEV1
decrement, pain on deep inspiration). Controlled human exposure studies
evaluated in the last review also found significant responses in
indicators of lung inflammation and cell injury at 0.080 ppm in healthy
adult subjects. The effects in these controlled human exposure studies
were observed in healthy young adult subjects, and it is likely that
more serious responses, and

responses at lower levels, would occur in people with asthma and other
respiratory diseases. 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. The
observations provide additional support for the conclusion in the Staff
Paper that the associations observed in the epidemiological studies,
particularly for respiratory-related effects and potentially for
cardiovascular effects, extend down to O3 levels well below
the current standard (i.e., 0.084 ppm) (EPA, 2007, p. 6-7).
    As discussed above in section II.A and in the Staff Paper (section
3.7), the newly available information reinforces the judgments about
the likelihood of causal relationships between O3 exposure
and respiratory effects observed in the last review and broadens the
evidence of O3-related associations to include additional
respiratory-related endpoints, newly identified cardiovascular-related
health endpoints, and mortality. Newly available evidence also has
shown that people with asthma are likely to experience more serious
effects than people who do not have asthma (section II.A.4.b.ii above).
The Staff Paper also concludes that substantial progress has been made
since the last review in advancing the understanding of potential
mechanisms by which ambient O3, alone and in combination
with other pollutants, is causally linked to a range of respiratory-
related health endpoints, and may be causally linked to a range of
cardiovascular-related health endpoints. Thus, the Staff Paper (section
6.3.6) finds strong support in the evidence developed since the last
review, for consideration of an O3 standard that is at least
as protective as the current standard and finds no support for
consideration of an O3 standard that is less protective than
the current standard. This conclusion is consistent with the advice and
recommendations of CASAC and with the views expressed by all interested
parties who provided comments on drafts of the Staff Paper. While CASAC
and some commenters supported revising the current standard to provide
increased public health protection and other commenters supported
retaining the current standard, no one who provided comments supported
a standard that would be less protective than the current standard.
a. Evidence-Based Considerations
    In looking more specifically at the controlled human exposure and
epidemiological evidence (which is summarized in chapter 3 and Appendix
3B of the Staff Paper), the Staff Paper first notes that controlled
human exposure studies provide the clearest and most compelling
evidence for an array of human health effects that are directly
attributable to acute exposures to O3 per se. Evidence from
such human studies, together with animal toxicological studies, help to
provide biological plausibility for health effects observed in
epidemiological studies. In considering the available evidence, the
Staff Paper focuses on studies that examined health effects that have
been demonstrated to be caused by exposure to O3, or for
which the Criteria Document judges associations with O3 to
be causal or likely causal, or for which the evidence is highly
suggestive that O3 contributes to the reported effects. In
considering the epidemiological evidence as a basis for reaching
conclusions about the adequacy of the current standard, the Staff Paper
focuses on studies reporting effects in the warm season, for which the
effect estimates are more consistently positive and statistically
significant than those from all-year studies. The Staff Paper (section
<IP_ADDRESS>) considers the extent to which such studies provide evidence of
associations that extend down to ambient O3 concentrations
below the level of the current standard, which would thereby call into
question the adequacy of the current standard. In so doing, the Staff
Paper notes, as discussed above, that if a population threshold level
does exist for an effect observed in such studies, it would likely be
at a level well below the level of the current standard. The Staff
Paper (section <IP_ADDRESS>) also attempts to characterize whether the area
in which a study was conducted likely would or would not have met the
current standard during the time of the study, although it recognizes
that the confidence that would appropriately be placed on the
associations observed in any given study, or on the extent to which the
association would likely extend down to relatively low O3
concentrations, is not dependent on this distinction. Further, the
Staff Paper considered studies that examined subsets of data that
include only days with ambient O3 concentrations below the
level of the current O3 standard, or below even lower
O3 concentrations, and continue to report statistically
significant associations. The Staff Paper (section <IP_ADDRESS>) judges that
such studies are directly relevant to considering the adequacy of the
current standard, particularly in light of reported responses to
O3 at levels below the current standard found in controlled
human exposure studies.
i. Lung Function, Respiratory Symptoms, and Other Respiratory Effects
    Health effects for which the Criteria Document continues to find
clear evidence of causal associations with short-term O3
exposures include lung function decrements, respiratory symptoms,
pulmonary inflammation, and increased airway responsiveness. In the
last review, these O3-induced effects were demonstrated with
statistical significance down to the lowest level tested in controlled
human exposure studies at that time (i.e., 0.080 ppm). As discussed in
chapter 3 of the Staff Paper, and in section II.A.2.a.i.(a)(i) above,
two new studies are notable in that they are the only controlled human
exposure studies that examined respiratory effects, including lung
function decrements and respiratory symptoms, in healthy adults at
lower exposure levels than had previously been examined. EPA's
reanalysis of the data from the most recent study shows small group
mean decrements in lung function responses to be statistically
significant at the 0.060 ppm exposure level, while the author's
analysis did not yield statistically significant lung function
responses but did yield some statistically significant respiratory
symptom responses toward the end of the exposure period. Notably, these
studies report a small percentage of subjects experiencing lung
function decrements (>= 10 percent) at the 0.060 ppm exposure level.
These studies provide very limited evidence of O3-related
lung function decrements and respiratory symptoms at this lower
exposure level.
    The Staff Paper (section <IP_ADDRESS>.1) notes that evidence from
controlled human exposures studies indicates that people with moderate-
to-severe asthma have somewhat larger decreases in lung function in
response to O3 relative to healthy individuals and that lung
function responses in people with asthma appear to be affected by
baseline lung function (i.e., magnitude of responses increases with
increasing disease severity). As discussed in the Criteria Document
(p.8-80), this newer information expands our understanding of the
physiological basis for increased sensitivity in people with asthma and
other airway diseases, recognizing that

people with asthma present a different response profile for cellular,
molecular, and biochemical responses than people who do not have
asthma. New evidence indicates that some people with asthma have
increased occurrence and duration of nonspecific airway responsiveness,
which is an increased bronchoconstrictive response to airway irritants.
Controlled human exposure studies also indicate that some people with
allergic asthma and rhinitis have increased airway responsiveness to
allergens following O3 exposure. Exposures to O3
exacerbated lung function decrements in people with pre-existing
allergic airway disease, with and without asthma. Ozone-induced
exacerbation of airway responsiveness persists longer and attenuates
more slowly than O3-induced lung function decrements and
respiratory symptom responses and can have important clinical
implications for asthmatics.
    The Staff Paper (p.6-10) also concludes that newly available human
exposure studies suggest that some people with asthma also have
increased inflammatory responses, relative to non-asthmatic subjects,
and that this inflammation may take longer to resolve. The new data on
airway responsiveness, inflammation, and various molecular markers of
inflammation and bronchoconstriction indicate that people with asthma
and allergic rhinitis (with or without asthma) comprise susceptible
groups for O3-induced adverse effects. This body of evidence
qualitatively informs the Staff Paper's (pp.6-10 to 6-11) evaluation of
the adequacy of the current O3 standard in that it indicates
that human clinical and epidemiological panel 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.
    The Staff Paper (p.6-11) notes that in addition to the experimental
evidence of lung function decrements, respiratory symptoms, and other
respiratory effects in healthy and asthmatic populations discussed
above, epidemiological studies have reported associations of lung
function decrements and respiratory symptoms in several locations
(Appendix 3B; also Figure 3-4 for respiratory symptoms). As discussed
in the Staff Paper (section <IP_ADDRESS>.1) and above, two large U.S. panel
studies which together followed over 1000 asthmatic children on a daily
basis (Mortimer et al., 2002, the National Cooperative Inner-City
Asthma Study, or NCICAS; and Gent et al., 2003), as well as several
smaller U.S. and international studies, have reported robust
associations between ambient O3 concentrations and measures
of lung function and daily symptoms (e.g., chest tightness, wheeze,
shortness of breath) in children with moderate to severe asthma and
between O3 and increased asthma medication use. Overall, the
multi-city NCICAS (2002), Gent et al. (2003), and several other single-
city studies indicate a robust positive association between ambient
O3 concentrations and increased respiratory symptoms and
increased medication use in asthmatics.
    In considering the large number of single-city epidemiological
studies reporting lung function or respiratory symptoms in healthy or
asthmatic populations (Staff Paper, Appendix 3B), the Staff Paper (p.6-
11) notes that most such studies that reported positive and often
statistically significant associations in the warm season were
conducted in areas that likely would not have met the current standard.
In considering the large multi-city NCICAS (Mortimer et al., 2002), the
Staff Paper notes that the 98th percentile 8-hour daily maximum
O3 concentrations at the monitor reporting the highest
O3 concentrations in each of the study areas ranged from
0.084 ppm to >0.10 ppm. However, the authors indicate that less than 5
percent of the days in the eight urban areas had 8-hour daily
O3 concentrations exceeding 0.080 ppm. Moreover, the authors
observed that when days with 8-hour average O3 levels
greater than 0.080 ppm were excluded, similar effect estimates were
seen compared to estimates which included all of the days. There are
also a few other studies in which the relevant air quality statistics
provide some indication that lung function and respiratory symptom
effects may be occurring in areas that likely would have met the
current standard (EPA, 2007, p.6-12).
ii. Respiratory Hospital Admissions and Emergency Department Visits
    At the time of the last review, many time-series studies indicated
positive associations between ambient O3 and increased
respiratory hospital admissions and emergency room visits, providing
strong evidence for a relationship between O3 exposure and
increased exacerbations of preexisting lung disease at O3
levels below the level of the then current 1-hour standard (EPA 2007,
section <IP_ADDRESS>.6). Analyses of data from studies conducted in the
northeastern U.S. indicated that O3 air pollution was
consistently and strongly associated with summertime respiratory
hospital admissions.
    Since the last review, new epidemiological studies have evaluated
the association between short-term exposures to O3 and
unscheduled hospital admissions for respiratory causes. Large multi-
city studies, as well as many studies from individual cities, have
reported positive and often statistically significant O3
associations with total respiratory hospitalizations as well as asthma-
and COPD-related hospitalizations, especially in studies analyzing the
O3 effect during the summer or warm season. Analyses using
multipollutant regression models generally indicate that copollutants
do not confound the association between O3 and respiratory
hospitalizations and that the O3 effect estimates were
robust to PM adjustment in all-year and warm-season only data. The
Criteria Document (p.8-77) concludes that the evidence supports a
causal relationship between acute O3 exposures and increased
respiratory-related hospitalizations during the warm season.
    In looking specifically at U.S. and Canadian respiratory
hospitalization studies that reported positive and often statistically
significant associations (and that either did not use GAM or were
reanalyzed to address GAM-related problems), the Staff Paper (p.6-12)
notes that many such studies were conducted in areas that likely would
not have met the current O3 standard, with many providing
only all-year effect estimates, and with some reporting a statistically
significant association in the warm season. Of the studies that provide
some indication that O3-related respiratory hospitalizations
may be occurring in areas that likely would have met the current
standard, the Staff Paper notes that some are all-year studies, whereas
others reported statistically significant warm-season associations.
    Emergency department visits for respiratory causes have been the
focus of a number of new studies that have examined visits related to
asthma, COPD, bronchitis, pneumonia, and other upper and lower
respiratory infections, such as influenza, with asthma visits typically
dominating the daily incidence counts. Among studies with adequate
controls for seasonal patterns, many reported at least one significant
positive association involving O3. However, inconsistencies
were observed which were at least partially attributable to differences
in model specifications and analysis approach among various studies. In
general, O3 effect estimates from summer-only analyses
tended to be positive and larger compared to results from cool season
or all-year analyses. Almost all of the studies that reported

statistically significant effect estimates were conducted in areas that
likely would not have met the current standard. The Criteria Document
(section 7.3.2) concluded that analyses stratified by season generally
supported a positive association between O3 concentrations
and emergency department visits for asthma in the warm season. These
studies provide evidence of effects in areas that likely would not have
met the current standard and evidence of associations that likely
extend down to relatively low ambient O3 concentrations.
iii. Mortality
    The 1996 Criteria Document concluded that an association between
daily mortality and O3 concentrations for areas with high
O3 levels (e.g., Los Angeles) was suggested. However, due to
a very limited number of studies available at that time, there was
insufficient evidence to conclude that the observed association was
likely causal, and thus the possibility that O3 exposure may
be associated with mortality was not relied upon in the 1997 decision
on the O3 primary standard.
    Since the last review, as described above, the body of evidence
with regard to O3-related health effects has been expanded
by animal, human clinical, and epidemiological studies and now includes
biologically plausible mechanisms by which O3 may affect the
cardiovascular system. In addition, there is stronger information
linking O3 to serious morbidity outcomes, such as
hospitalization, that are associated with increased mortality. Thus,
there is now a coherent body of evidence that describes a range of
health outcomes from lung function decrements to hospitalization and
premature mortality.
    Newly available large multi-city studies (Bell et al., 2004; Huang
et al.,2005; and Schwartz 2005) designed specifically to examine the
effect of O3 and other pollutants on mortality have provided
much more robust and credible information. Together these studies have
reported significant associations between O3 and mortality
that were robust to adjustment for PM and different adjustment methods
for temperature and suggest that the effect of O3 on
mortality is immediate but also persists for several days. One recent
multi-city study (Bell et al., 2006) examined the shape of the
concentration-response function for the O3-mortality
relationship in 98 U.S. urban communities for the period 1987 to 2000
specifically to evaluate whether a ``safe'' threshold level exists.
Results from various analytic methods all indicated that any threshold,
if it exists, would likely occur at very low concentrations, far below
the level of the current O3 NAAQS and nearing background
levels.
    New data are also available from several single-city studies
conducted world-wide, as well as from several meta-analyses that have
combined information from multiple studies. Three recent meta-analyses
evaluated potential sources of heterogeneity in O3-mortality
associations. All three analyses reported common findings, including
effect estimates that were statistically significant and larger in warm
season analyses. Reanalysis of results using default GAM criteria did
not change the effect estimates, and there was no strong evidence of
confounding by PM. The Criteria Document (p.7-175) finds that the
majority of these studies suggest that there is an elevated risk of
total nonaccidental mortality associated with acute exposure to
O3, especially in the summer or warm season when
O3 levels are typically high, with somewhat larger effect
estimate sizes for associations with cardiovascular mortality.
    Overall, the Criteria Document (p.8-78) finds that the results from
U.S. multi-city time-series studies, along with the meta-analyses,
provide relatively strong evidence for associations between short-term
O3 exposure and all-cause mortality even after adjustment
for the influence of season and PM. The results of these analyses
indicate that copollutants generally do not appear to substantially
confound the association between O3 and mortality. In
addition, several single-city studies observed positive associations of
ambient O3 concentrations with total nonaccidental and
cardiopulmonary mortality.
    Finally, from those studies that included assessment of
associations with specific causes of death, it appears that effect
estimates for associations with cardiovascular mortality are larger
than those for total mortality; effect estimates for respiratory
mortality are less consistent in size, possibly due to reduced
statistical power in this subcategory of mortality. For cardiovascular
mortality, the Criteria Document (p.7-106) suggests that effect
estimates are consistently positive and more likely to be larger and
statistically significant in warm season analyses. The Criteria
Document (p.8-78) concludes that these findings are highly suggestive
that short-term O3 exposure directly or indirectly
contributes to nonaccidental and cardiopulmonary-related mortality, but
additional research is needed to more fully establish underlying
mechanisms by which such effects occur.
b. Exposure- and Risk-Based Considerations
    As discussed above in section II.B, the Staff Paper also estimated
quantitative exposures and health risks associated with recent air
quality levels and with air quality that meets the current standard to
help inform judgments about whether or not the current standard
provides adequate protection of public health. In so doing, it
presented the important uncertainties and limitations associated with
the exposure and risk assessments (discussed above in section II.B and
more fully in chapters 4 and 5 of the Staff Paper).
    The 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
Staff Paper 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 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 recent air quality or air quality that just meets the
current 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.
    As described above in section II.B, the Staff Paper estimated
exposures and risks for the three most recent years (2002-2004) for
which data were available at the time of the analyses. Within this 3-
year period, 2002 was a year with relatively higher O3
levels in most, but not all, areas and simulation of just meeting the
current standard based on 2002 air quality data provides a generally
more upper-end estimate of exposures and risks, while 2004 was a year
with relatively lower O3 levels in

[[Continued on page 37867]]

]

[[pp. 37867-37916]] National Ambient Air Quality Standards for Ozone

[[Continued from page 37866]]

most, but not all, areas and simulation of just meeting the current
standard using 2004 air quality data provides a generally more lower-
end estimate of exposures and risks.
i. Exposure Assessment Results
    As discussed above in section II.B.1, the Staff Paper estimates
personal exposures to ambient O3 levels at and above
specific benchmark levels to 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 current air quality
levels, and the extent to which such impacts might be reduced by
meeting the current and alternative standards. As described in greater
detail in section II.B.1.c above, the Staff Paper refers to exposures
at and above these benchmark levels as ``exposures of concern.'' The
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
relevant public health concerns. Therefore, with the concurrence of the
CASAC, the Staff Paper estimated exposures of concern not only at 0.080
ppm O3, a level at which there are demonstrated effects, but
also at 0.070 and 0.060 ppm O3. The Staff Paper recognized
that there will be varying degrees of concern about exposures at each
of these levels, based in part on the population subgroups 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 O3 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 Staff Paper, and the discussion
below, focuses on exposures of concern at or above benchmark levels of
0.070 and 0.060 ppm O3 for purposes of evaluating the
adequacy of the current standard.
    The exposure estimates presented in the Staff Paper are for the
number and percent of all school age children and asthmatic school age
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. As
shown in the Table 1 in this notice, the percent of population exposed
at any given level is very similar for all and asthmatic school age
children. Substantial year-to-year variability in exposure estimates is
observed, ranging to over an order of magnitude at the current standard
level, in estimates of the number of children and, as shown in Table 6-
1a and b of the Staff Paper, the number of occurrences of exposures of
concern at both of these benchmark levels. The Staff Paper states that
it is appropriate to consider not just the average estimates across all
years, but also to consider public health impacts in year with
relatively higher O3 levels. The 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 upon meeting
the current standard.
    As discussed in the Staff Paper (EPA, 2007b, see section <IP_ADDRESS>),
about 50 percent of asthmatic or all school age children, representing
nearly 1.3 million asthmatic children and about 8.5 million school age
children in the 12 urban areas examined, are estimated to experience
exposures of concern at or above the 0.070 ppm benchmark level (i.e.,
these individuals are estimated to experience 8-hour O3
exposures at or above 0.070 ppm while engaged in moderate or greater
exertion 1 or more times during the O3 season) associated
with 2002 O3 air quality levels. In contrast, about 17
percent of asthmatic and all school age children are estimated to
experience exposures of concern at or above the 0.070 ppm benchmark
level associated with 2004 O3 air quality levels. Just
meeting the current standard results in an aggregate estimate of about
20 percent of asthmatic or 18 percent or all school age children likely
to experience exposures of concern at or above the 0.070 ppm benchmark
level using the 2002 simulation. The exposure estimates for this
benchmark level range up to about 40 percent of asthmatic or all school
age children in the single city with the least degree of protection
from this standard. Just meeting the current standard based on the 2004
simulation, results in an aggregate estimate of about 1 percent of
asthmatic or all school age children experiencing exposures at the 0.07
ppm benchmark level.
    At the benchmark level of 0.060 ppm, about 70 percent of all or
asthmatic school age children are estimated to experience exposures of
concern at this benchmark level for the aggregate of the 12 urban areas
associated with 2002 O3 levels. Just meeting the current
standard would result in an aggregate estimate of about 45 percent of
asthmatic or all school age children likely to experience exposures of
concern at or above the 0.060 ppm benchmark level using the 2002
simulation. The exposure estimates for this benchmark level range up to
nearly 70 percent of all or asthmatic school age children in the single
city with the least degree of protection associated with just meeting
the current standard using the 2002 simulation. The Staff Paper
indicates an aggregate estimate of about 10 percent of asthmatic or all
school age children would experience exposures at or above the 0.06 ppm
benchmark level associated with just meeting the current standard using
the 2004 simulation.
ii. Risk Assessment Results
    As described in more detail in section II.B.2 above and in chapters
5 and 6 of the Staff Paper, risk estimates have been developed for
several important health endpoints, including: (1) Lung function
decrements (i.e., >=15 percent and >=20 percent reductions in
FEV1) in all school age children for 12 urban areas; (2)
lung function decrements (i.e., >=10 percent and >=20 percent
reductions in FEV1) in asthmatic school age children for 5
urban areas (a subset of the 12 urban areas); (3) respiratory symptoms
(i.e., chest tightness, shortness of breath, wheeze) in moderate to
severe asthmatic children for the Boston area; (4) respiratory-related
hospital admissions for 3 urban areas; and (5) nonaccidental and
cardiorespiratory mortality for 12 urban areas for three recent years
(2002 to 2004) and for just meeting the current standard using a 2002
simulation and a 2004 simulation.
    With regard to estimates of moderate lung function decrements, as
shown in Tables 6-2 of the Staff Paper, meeting the current standard
substantially reduces the estimated number of school age children
experiencing one or more occurrences of FEV1 decrements >=15
percent for the 12 urban areas, going from about 1.3 million children
(7 percent of children) under 2002 air quality to about 610,000 (3
percent of children) based on the 2002 simulation, and from about
620,000 children (3 percent of children) to about 230,000 (1 percent of
children) using the 2004 simulation. In asthmatic children, the
estimated number of children experiencing one or more occurrences of
FEV1 decrements >=10 percent for the 5 urban areas goes from
about 250,000 children (16 percent of asthmatic children) under 2002
air quality to about 130,000 (8 percent of asthmatic children) using
the 2002 simulation, and from about 160,000 (10 percent of asthmatic
children) to about 70,000 (4 percent of asthmatic children) using the
2004 simulation. Thus, even when the

current standard is met, about 4 to 8 percent of asthmatic school age
children are estimated to experience one or more occurrences of
moderate lung function decrements, resulting in about 1 million
occurrences (using the 2002 simulation) and nearly 700,000 occurrence
(using the 2004 simulation) in just 5 urban areas. Moreover, the
estimated number of occurrences of moderate or greater lung function
decrements per child is on average approximately 6 to 7 in all children
and 8 to 10 in asthmatic children in an O3 season, even when
the current standard is met, depending on the year used to simulate
meeting the current standard. In the 1997 review of the O3
standard a general consensus view of the adversity of such moderate
responses emerged as the frequency of occurrences increases, with the
judgment that repeated occurrences of moderate responses, even in
otherwise healthy individuals, may be considered adverse since they may
well set the stage for more serious illness.
    With regard to estimates of large lung function decrements, the
Staff Paper notes that FEV1 decrements 20 percent
would likely interfere with normal activities in many healthy
individuals, therefore single occurrences would be considered to be
adverse. In people with asthma, large lung function responses would
likely interfere with normal activities for most individuals and would
also increase the likelihood that these individuals would use
additional medication or seek medical treatment. Not only would single
occurrences be considered to be adverse to asthmatic individuals under
the ATS definition, but they also would be cause for medical concern.
While the current standard reduces the occurrences of large lung
function decrements in all children and asthmatic children from about