air quality standard for PM2.5. In light of the degree of
sensitivity of the ACS-based relative risk estimates to model
specifications and the significant research underway, in this view, it
would be wiser to consider modification of the annual standard with a
fuller body of information in hand rather than initiate a change in the
annual standard at this time.
    The Administrator solicits comment on this view and on the issues
raised in interpreting the results of the ACS-based

studies. For example, comment is solicited on the extent to which the
associations reported in the ACS-based studies suggest that
SO2 should be considered as a surrogate for fine particles
and/or the broader mix of air pollutants or as an independent pollutant
exhibiting separate effects. Comment is also solicited on relevant
research that would improve our understanding of issues related to
model specification and alternative analytic approaches that would
better inform judgments based on such epidemiologic studies in the
future.

H. Proposed Decisions on Primary PM2.5 Standards

    For the reasons discussed above, and taking into account the
information and assessments presented in the Criteria Document and
Staff Paper, the advice and recommendations of CASAC, and public
comments to date, the Administrator proposes to revise the current
primary PM2.5 standards. Specifically, the Administrator
proposes to revise (1) the level of the 24-hour PM2.5
standard to 35 [mu]g/m3, and (2) the form of the annual
PM2.5 standard by changing the constraints on the use of
spatial averaging to include the criterion that the minimum correlation
coefficient between monitor pairs to be averaged be 0.9 or greater,
determined on a seasonal basis, and the criterion that differences
between monitor values not exceed 10 percent. Data handling conventions
are specified in proposed revisions to Appendix N, as discussed in
Section V below, and the reference method for monitoring PM as
PM2.5 is specified in proposed minor revisions to Appendix
L, as discussed in Section VI below.
    In recognition of alternative views of the science and the
appropriate policy response based on the currently available
information, the Administrator also solicits comments on (1)
alternative levels of the 24-hour PM2.5 standard within the
range of 35 to 30 [mu]g/m3, and alternative approaches for
selecting the level of the 24-hour PM2.5 standard, and
related levels (such as approaches that suggest retaining the current
level of 65 [mu]g/m3, setting a level no higher than 25
[mu]g/m3, or setting a level within the range of 65 down to
35 [mu]g/m3); (2) alternative levels of the annual
PM2.5 standard below 15 [mu]g/m3 down to12 [mu]g/
m3; (3) issues related to consideration of alternative
indicators of fine particle components; and (4) an alternative form of
the annual PM2.5 standard based on the highest community-
oriented monitor in an area. Based on the comments received and the
accompanying rationales, the Administrator may adopt other standards
within the range of the alternatives identified above in lieu of the
standards he is proposing today.
    The Administrator solicits comment on all aspects of this proposed
decision. Comment is specifically invited on the methodology for
evaluating the uncertainty and significance of risks to public health.
The Administrator believes that it is important to further develop ways
of addressing uncertainty when estimating such risk, recognizing the
wide variety of information available in the underlying health effects
and other studies. The Agency seeks comment on methods and approaches
for conducting a more formalized uncertainty analysis. In addition, the
Agency seeks comment on how to evaluate the results from a formalized
uncertainty analysis or from the Staff Paper's risk assessment, which
addresses multiple health effects across multiple populations, in the
context of judging the public health importance of such risks and
determining the requisite level of public health protection for the PM
standards.
    To address issues related to the transition from the current
PM2.5 standards to revised PM2.5 standards, the
Administrator intends to seek public comment on EPA's implementation
plans for the revised PM2.5 standards, including its plans
for assuring an effective transition, as part of an advance notice of
proposed rulemaking (ANPR) on NAAQS implementation that will be
published in an early in 2006. In this ANPR, EPA will be discussing
issues related to the timing and regulatory implications of this
transition. The EPA intends to present and take comment on the need and
potential approaches for revocation of the current 24-hour
PM2.5 standard, and on issues related to the establishment
of no-backsliding requirements, such as those adopted by the Agency in
1997 with respect to the ozone NAAQS. The EPA also expects to address a
variety of implementation issues concerning revised PM2.5
standards in the ANPR. The ANPR will explain the designation process
and its timing, and the timing of SIP submittals for both attainment
and nonattainment areas. The EPA also expects to address issues
regarding the attainment dates for areas designated nonattainment. The
EPA will also discuss new source permitting requirements for both
attainment and nonattainment areas, i.e., the PSD and Part D NSR
programs. If the Administrator promulgates a revised PM2.5
standard, EPA will determine the final implementation approach for that
standard.

III. Rationale for Proposed Decisions on Primary PM10
Standards

    This action presents the Administrator's proposed decisions on
revision to the primary NAAQS for PM10. The rationale for
the proposed revisions of the primary PM10 NAAQS includes
consideration of: (1) Evidence of health effects related to short- and
long-term exposures to thoracic coarse particles; (2) insights gained
from a quantitative risk assessment prepared by EPA; and (3) specific
conclusions regarding the need for revisions to the current standards
and the elements of PM10 standards (i.e., indicator,
averaging time, form, and level) that, taken together, would be
requisite to protect public health with an adequate margin of safety.
    In developing this rationale, EPA has taken into account the
information available from a growing, but still limited, body of
evidence on health effects associated with thoracic coarse particles
from studies that use PM10-2.5 as a measure of thoracic
coarse particles. The EPA has drawn upon an integrative synthesis of
the body of evidence on associations between exposure to ambient
thoracic coarse particles and a range of health endpoints (EPA, 2004,
Chapter 9), focusing on those health endpoints for which the Criteria
Document concludes that the associations are suggestive of possible
causal relationships. In its policy assessment of the evidence judged
to be most relevant to making decisions on elements of the standards,
EPA has placed greater weight on U.S. and Canadian epidemiological
studies using thoracic coarse particles measurements, since studies
conducted in other countries may well reflect different demographic and
air pollution characteristics.
    While there is little question that particles in the thoracic
coarse particle size range can present a risk of adverse effects to the
most sensitive regions of the respiratory tract, the characterization
of health effects attributable to various levels of exposure to ambient
thoracic coarse particles is subject to uncertainties that are markedly
greater than is the case for fine particles. As discussed below,
however, there is a growing body of evidence available since the last
review of the PM NAAQS, with important new information coming from
epidemiologic, toxicologic, and dosimetric studies. Moreover, the newly
available research studies have undergone intensive scrutiny through
multiple layers of peer review and extended opportunities for public
review and comment. While

important uncertainties remain, the review of the health effects
information has been extensive and deliberate. In the judgment of the
Administrator, this intensive evaluation of the scientific evidence has
provided an adequate basis for proposing regulatory decisions at this
time. This review also provides important input to EPA's research plan
for improving our future understanding of the relationships between
exposures to ambient thoracic coarse particles and health effects.

A. Evidence of Health Effects Related to Thoracic Coarse Particle
Exposure

    The first PM NAAQS (36 FR 8186) used an indicator based solely on a
preexisting monitor for total suspended particles (TSP) that was not
designed to focus on particles of greatest risk to health. In preparing
for the initial review of those standards, EPA placed a major emphasis
on developing a new indicator that considered the significant amount of
evidence on particle size, composition, and relative risk of effects
from penetration and deposition to the major regions of the respiratory
tract (Miller et al., 1979). The development and assessment of these
lines of evidence in the PM Criteria Document and PM Staff Paper
published between 1979 and 1986 culminated in revised standards for PM
that used PM10 as the indicator (52 FR 24634). The major
conclusion from that review, which remained unchanged in the 1997
review, was that ambient particles smaller than or equal to 10 [mu]m in
aerodynamic diameter are capable of penetrating to the deeper
``thoracic'' \45\ regions of the respiratory tract and present the
greatest concern to health (61 FR 65648). While considerable advances
have been made, the available evidence in this review continues to
support the basic conclusions reached in the 1987 and 1997 reviews
regarding penetration and deposition of fine and thoracic coarse
particles. As discussed in the Criteria Document, both fine and
thoracic coarse particles penetrate to and deposit in the alveolar and
tracheobronchial regions. For a range of typical ambient size
distributions, the total deposition of thoracic coarse particles to the
alveolar region can be comparable to or even larger than that for fine
particles. For areas with appreciable coarse particle concentrations,
thoracic coarse particles would tend to dominate particle deposition to
the tracheobronchial region for mouth breathers (EPA, 2004, p. 6-16).
Deposition of particles to the tracheobronchial region is of particular
concern with respect to aggravation of asthma.
---------------------------------------------------------------------------

    \45\ The `thoracic' regions of the respiratory tract are located
in the chest (thorax) and are comprised of the tracheo-bronchial
region with connecting airways and the alveolar, or gas-exchange
region of the lung. For ease of communications, `thoracic' particles
penetrating to these regions are often called `inhalable' particles.
---------------------------------------------------------------------------

    In the last review, little new toxicologic evidence was available
on potential effects of thoracic coarse particles and there were few
epidemiologic studies that had included direct measurements of thoracic
coarse particles. Evidence of associations between health outcomes and
PM10 that were conducted in areas where PM10 was
predominantly composed of thoracic coarse particles was an important
part of the basis for reaching conclusions about the requisite level of
protection provided against coarse particles for the final standards.
The new studies available in this review include a number of
epidemiologic studies that have reported associations with health
effects using direct measurements of PM10-2.5, as well as a
number of new toxicologic studies.
    This section outlines key information contained in the Criteria
Document (Chapters 6-9 and the Staff Paper (Chapter 3) on known or
potential effects associated with exposure to thoracic coarse particles
and their major constituents. The information highlighted here
summarizes: (1) New information available on potential mechanisms for
health effects associated with exposure to thoracic coarse particles or
their constituents; (2) the nature of the effects that have been
associated with ambient thoracic coarse particles or their
constituents; (3) an integrative assessment of the evidence on health
effects related to thoracic coarse particles; (4) subpopulations that
appear to be sensitive to effects of exposure to thoracic coarse
particles; and (5) the public health impact of exposure to ambient
thoracic coarse particles.
1. Mechanisms
    As summarized above, the first review of the PM NAAQS found a
strong basis for concluding that thoracic coarse particles could be
plausibly linked to health effects. This was based on an integrated
assessment of the physical and chemical characteristics of ambient
coarse particles, the evidence regarding health effects that could be
associated with deposition of coarse particulate substances in the
different regions of the respiratory tract, and the relative potential
for penetration and deposition of ambient distributions of coarse
particles in the human respiratory tract (52 FR 24634). In the 1987
review, EPA found that occupational and toxicologic studies provided
ample cause for concern related to higher levels of thoracic coarse
particles. Such findings indicated that elevated levels of thoracic
coarse particles were linked with effects such as aggravation of asthma
and increases in upper respiratory illness, which was consistent with
dosimetric evidence of enhanced deposition of thoracic coarse particles
in the respiratory tract (61 FR 65649).
    Toxicologic and controlled human exposure studies available in
previous reviews have generally used particle exposures at levels
higher than ambient levels, relying on various particle components or
surrogates. Such studies reported some effects on the respiratory
tract, indicative of inflammatory or irritant effects for particles in
both the fine and thoracic coarse particle size range (EPA, 1982,
chapters 12 and 13; EPA, 1996, chapters 10 and 11). As discussed above
in section II.A, the results of numerous new toxicologic and controlled
human exposure studies have implicated a number of potential mechanisms
or pathways for effects associated with PM. Many of these studies have
used particle exposures that are generally more relevant to studying
the effects of fine particles than those of thoracic coarse particles.
However, several studies, discussed more fully below, have suggested
mechanisms or pathways for thoracic coarse particles to cause
inflammatory and other effects on the respiratory system. This evidence
generally supports previous conclusions that thoracic coarse particles
can affect the respiratory system.
    Some limited evidence is available from recent toxicologic studies
on effects of exposure to thoracic coarse particles, specifically using
PM10-2.5, for either acute or chronic exposures (EPA, 2004,
p. 9-55). This toxicologic evidence includes results from studies where
respiratory cell cultures were exposed to ambient particles, thus
providing insight into potential mechanisms for respiratory effects of
thoracic coarse particles. The types of effects reported include
inflammatory and allergic effects. For example, two recent studies
report inflammatory responses in cells exposed to extracts of water-
soluble and water-insoluble materials from thoracic coarse particles
and fine particles collected in Chapel Hill, NC (Monn and Becker, 1999;
Soukup and Becker, 2001). One study focused on water-soluble materials,
and reported significant immune system effects with water-soluble
extracts of ambient PM10-2.5, in contrast to the lack of
effects observed with extracts from

ambient PM2.5 as well as indoor-collected
PM10-2.5 and PM2.5. The authors report that
different components of PM10-2.5 appeared to have different
effects, with endotoxin implicated in inflammatory effects, while
coarse particulate metals appeared to have a role in cytotoxicity
effects (Monn and Becker, 1999). A followup study in the same
laboratory (Soukup and Becker, 2001) reports that the insoluble
materials from thoracic coarse particles resulted in several effects on
immune system cells.\46\ In this extract of thoracic coarse particles,
endotoxin appeared to be the most pro-inflammatory component, but
components other than endotoxin or metals appeared to contribute to
other effects. Using particles collected in two urban areas in the
Netherlands, Becker et al. (2003) reported that thoracic coarse
particles, but not fine or ultrafine particles, resulted in effects
related to inflammation and decreased pulmonary defenses. This small
group of studies thus suggests that exposure to thoracic coarse
particles may cause pro-inflammatory effects, as well as cytotoxicity
and oxidant generation (EPA, 2004, section 7.4.2). While still limited,
these emerging new studies provide additional insight into potential
mechanisms for respiratory effects of thoracic coarse particles. The
results also indicate that different health responses may be linked
with different components of thoracic coarse particles.
---------------------------------------------------------------------------

    \46\ Examples of such effects include cytokine production,
decreased phagocytic ability and oxidant generation.
---------------------------------------------------------------------------

    In contrast, one recent study exposed human red blood cell cultures
to ambient coarse particles collected in Italy and found only limited
effects on blood cells (Diociaiuti et al., 2001). The addition of
thoracic coarse particles that were collected in Italy to human
respiratory tract cell cultures produced only limited evidence of
carcinogenic effects; some response was seen with thoracic coarse
particles but greater response was reported with fine particle
exposures (Hornberg et al., 1998). These latter results are consistent
with the evidence from epidemiologic studies, which provide no direct
evidence for carcinogenicity of thoracic coarse particles.
    As noted in past reviews (EPA, 1981b, 1996b), deposition of a
variety of particle types in the tracheobronchial region, including
resuspended urban dust and coarse-fraction organic materials, has the
potential to affect lung function and aggravate symptoms, particularly
in asthmatics. Of particular note are limited toxicologic studies that
found urban road dust can produce cellular and immunological effects
(e.g., Kleinman et al., 1995; Steerenberg et al., 2003). Road dust is a
major source of thoracic coarse particles in urban areas and is
therefore representative of the components expected to be found in
resuspended thoracic coarse particles. In the 1996 Staff Paper, results
from the study by Kleinman and colleagues (1995) were highlighted in
which effects were observed in rats with inhalation exposure to road
dust. These effects included changes in the structure of the rat
airways as well as effects on immune cells. Higher concentrations of
road dust were needed to cause effects, compared with exposures to fine
particle components (e.g., sulfates, nitrates), in part because of the
limited penetration of coarse-sized particles past the nose of the rats
studied (EPA, 1996b, p. V-70).\47\ Another study used a standard
toxicologic approach to studying allergic responses, and the authors
concluded that exposure to road tunnel dust particles resulted in
greater allergy-related effects than did exposure to several other
particle samples, including residual oil fly ash and diesel exhaust
particles (Steerenberg et al., 2003).\48\ In this study, the particles
were collected in a road tunnel and placed directly in the animal
respiratory tract, so differences in inhalability of larger particles
in rodents was not an issue. In contrast, a number of studies have
reported that Mt. St. Helens volcanic ash, which is generally in the
size range of thoracic coarse particles, has very little toxicity in
animal or in vitro toxicologic studies (EPA, 2004, p. 7-216).
---------------------------------------------------------------------------

    \47\ The particles used in this study were collected by vacuum
sweeping of freeway surfaces in California, and were generally 5
[mu]m in diameter or lower (Kleinman et al., 1995).
    \48\ This approach, using ovalbumin-sensitized mice, is commonly
used for comparing allergic potency of air pollutants. The authors
also tested responses in an additional toxicologic model, based on
pollen-sensitized rats, and reported responses only with diesel
exhaust particles (Steerenberg et al., 2003, p. 1436).
---------------------------------------------------------------------------

    The Criteria Document finds that the limited number of recent
toxicologic studies using PM10-2.5 provide some evidence
that coarse fraction particle exposures can result in effects primarily
linked to the respiratory system, related to inflammation or
aggravation of allergic effects. Toxicologic studies have suggested
potential pathways for effects from a few sources or components of
thoracic coarse particles, such as road dust particles, metals or
organic constituents. The need to better understand the relationship
between different components or sources of thoracic coarse particles
remains a key area of uncertainty with regard to the effects of
thoracic coarse particles.
2. Nature of Effects
    In the last review, EPA considered a substantial number of
epidemiological studies using PM10, which contains both fine
and coarse particles, as a measure of exposure to PM. In many such
studies in which fine and coarse particles occur at similar levels, it
is difficult or impossible to determine whether fine and coarse
particles both played major roles in the associations. Accordingly,
considerable emphasis was placed on the more limited body of evidence
from PM10 studies in locations where coarse particles were a
much greater fraction of PM10 than were fine particles.
These findings indicated that short-term exposure to thoracic coarse
particles in such areas was linked with respiratory morbidity effects,
such as aggravation of asthma, increases in respiratory symptoms and
respiratory infections (62 FR 38677). The single available short-term
exposure study that compared associations between mortality and fine
and coarse particles reported a significant association between short-
term exposure to PM10-2.5 and mortality in one of six cities
(Steubenville, OH). In this location, an unusually high correlation
between high levels of fine and thoracic coarse particles suggested a
common industrial source, and a clear conclusion about the relative
contribution was not possible. The study found no association with
thoracic coarse particles in a combined multi-city analysis (Schwartz
et al., 1996; CD, p. 8-40 to 8-41).\49\ No studies in the past review
provided clear epidemiologic evidence of mortality or morbidity effects
related to long-term exposure to PM10-2.5. EPA observed that
toxicologic studies offered some qualitative evidence suggesting the
potential for effects on the respiratory system with long-term exposure
to coarse particles or coarse particle constituents (62 FR 38678).
---------------------------------------------------------------------------

    \49\ Note that in more recent reanalyses of this study to
investigate statistical modeling issues, the association for
Steubenville was not statistically significant in most models
reported in the two reanalyses (Klemm and Mason, 2003; Schwartz,
2003a).
---------------------------------------------------------------------------

    In this review, epidemiologic studies have continued to support a
relationship between short-term exposure to thoracic coarse particles
and respiratory morbidity, with effects ranging from increased
respiratory symptoms to hospitalization for respiratory diseases. As
discussed below, the new studies also suggest associations with effects
on the cardiovascular system and possibly with

mortality. Figure 2 summarizes results from both multi-city and single-
city epidemiologic studies using short-term exposures to
PM10-2.5, including all U.S. and Canadian studies that used
direct measurements of PM10-2.5\50\ and for which effect
estimates and confidence intervals were reported. Consistent with the
presentation of fine particle study results in Figure 1, the central
effect estimate is indicated by a diamond for each study result, with
the vertical bar representing the 95 percent confidence interval around
the estimate. The results of these epidemiologic studies are discussed
below.
---------------------------------------------------------------------------

    \50\ All epidemiologic studies discussed below included
measurements of thoracic coarse particles either through monitors
that collected thoracic coarse particles separately (e.g.,
dichotomous monitors) or using data from side-by-side (co-located)
monitors for fine particles and PM10. Investigators have
sometimes also used prediction models to ``fill'' or estimate PM
concentrations where measurements are not available (most often
where data are collected less frequently than daily). In one
particular study in Coachella Valley, measurements were made of fine
and thoracic coarse particle concentrations for two and a half
years. The investigators predicted PM10-2.5
concentrations for a longer time series, based on a ten-year data
set for PM10 for use in the health study (Ostro et al.,
2003).

BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP17JA06.049

BILLING CODE 6560-50-C

a. Effects Associated With Short-Term Exposure to Thoracic Coarse
Particles

    The discussion below focuses first on evidence related to
respiratory morbidity effects, since information available in the
previous review provided plausible evidence that short-term exposure to
thoracic coarse particles was associated with such effects. This is
followed by a discussion of new findings on potential cardiovascular
effects of thoracic coarse particles, as well as new evidence from
studies of mortality.
i. Morbidity

(a) Effects on the Respiratory System

    Evidence available in the last review suggested that aggravation of
asthma

and respiratory infections and symptoms were associated with
PM10 in areas where thoracic coarse particles were a much
greater fraction of PM10 than were fine particles, such as
Anchorage, AK, and southeast Washington (62 FR 38679). Only one
epidemiologic study had used PM10-2.5 data; it reported a
positive, but not statistically significant, association between
respiratory hospital admissions and PM10-2.5 in Toronto
(Thurston et al., 1994).
    Several new studies of respiratory symptoms and lung function have
included both PM10-2.5 and PM2.5 data, and these
results suggest a role for thoracic coarse particles as well as for
fine particles in associations with respiratory symptoms (EPA, 2004, p.
8-311). In the Six Cities study, a statistically significant increase
in cough for children was found with PM10-2.5 but not with
PM2.5, while the reverse was true for lower respiratory
symptoms. When both PM10-2.5 and PM2.5 were
included in models, the effect estimates were reduced for each, but
PM10-2.5 retained significance in the association with cough
and PM2.5 retained significance in the association with
lower respiratory symptoms (Schwartz and Neas, 2000).\51\ Changes in
lung function were evaluated in three cities in Pennsylvania, and in
all three, short-term exposure to thoracic coarse particles was not
significantly associated with peak flow rate, although some
statistically significant associations were found with exposure to fine
particles (EPA, 2004, p. 8-312).
---------------------------------------------------------------------------

    \51\ The authors conclude that for acute asthma-related
responses as well as daily mortality, fine particles are a stronger
predictor of health response that are thoracic coarse particles
(Schwartz and Neas, 2000, p. 8).
---------------------------------------------------------------------------

    Three new U.S. and Canadian epidemiologic studies have reported
associations between short-term exposure to PM10-2.5 with
hospital admissions for respiratory diseases, including asthma,
pneumonia and COPD (Burnett et al., 1997; Ito, 2003; Sheppard et al.,
2003). As shown in Figure 2, the effect estimates for these
associations are positive and some are statistically significant. In
these associations with respiratory hospitalization, the risk estimates
tend to fall in the range of 5 to 15 percent per 25 [mu]g/m3
PM10-2.5 (EPA, 2004, p. 8-193).
    Because fine particles and ozone, as well as other gaseous air
pollutants, are known to cause respiratory effects, a key consideration
for assessing this body of studies is assessment of potential
confounding by these co-pollutants, as discussed in detail in Section
8.4.3 of the Criteria Document. The associations reported between
respiratory hospital admissions and short-term exposure to
PM10-2.5 were largely unchanged in most cases when gaseous
co-pollutants were included in the models (EPA, 2004, Figure 8-18;
Burnett et al., 1997; Ito, 2003).\52\ Few investigators have evaluated
potential confounding of PM10-2.5 effects with adjustment
for PM2.5 in multi-pollutant models. Only the study
conducted in Detroit included such multi-pollutant models for
respiratory hospitalization and was reanalyzed to address potential
statistical modeling questions. In this study, the simultaneous
consideration of PM10-2.5 and PM2.5 resulted in
reduction in the size of the effect estimate, as well as loss of
statistical significance, for both pollutants. The authors report that
the correlation between the two pollutants was ``modest'' (correlation
coefficient of 0.42) (Lippmann et al., 2000, p. 33). The results in
this study vary by health outcome; for example, for pneumonia
hospitalization, effect estimates for PM2.5 were little
changed but those for PM10-2.5 decreased substantially in
magnitude in two-pollutant models. In contrast, effect estimates for
PM2.5 with COPD hospitalization decreased dramatically,
whereas those for PM10-2.5 were only slightly decreased in
size in two-pollutant models (Ito, 2003, pp. 152, 153).
---------------------------------------------------------------------------

    \52\ More specifically, the effect estimates for associations
between PM10-2.5 and hospitalization for COPD and
pneumonia in Detroit are largely unchanged with the addition of
gaseous co-pollutants to the models, except in one case where the
PM10-2.5 effect estimate for COPD hospitalization is
substantially reduced in size with the inclusion of O3 in
the model (Ito, 2003). Results for the study in Toronto also show
relatively consistent effect estimate size for associations between
PM10-2.5 and respiratory hospitalization, except for the
models including NO2 and all four gaseous pollutants
(Burnett et al., 1997).
---------------------------------------------------------------------------

    Additional insight into the respiratory effects of coarse particles
is provided by studies using PM10 in locations where
thoracic coarse particles were a much greater fraction of
PM10 than were fine particles. This review includes new
PM10 studies in such relatively high coarse-fraction areas,
such as Reno, NV and Anchorage, AK.\53\ In these areas, statistically
significant associations have been reported between PM10 and
hospitalization for respiratory diseases (Chen et al., 2000) and
outpatient medical visits for asthma (Choudhury et al., 1997). These
findings support the evidence from the limited group of studies
discussed above that have reported associations between measured
PM10-2.5 and respiratory morbidity.
---------------------------------------------------------------------------

    \53\ For example, Anchorage, AK and Reno, NV do not currently
attain the PM10 24-hour standard which is set at 150
[mu]g/m3. Based on 2002-2004 data, the 98th percentile
PM2.5 concentrations in these areas were 21 and 25 [mu]g/
m3, respectively. As noted in the fine particle
discussion above, no short-term exposure studies to date have shown
statistically significant associations between fine particles and
effects with 98th percentile values this low. This suggests that
coarse particles either caused or contributed to the observed
PM10 associations.
---------------------------------------------------------------------------

    Considering evidence from across a range of respiratory morbidity
health outcomes, the Criteria Document concludes that the epidemiologic
evidence indicates that both fine and thoracic coarse particles impact
respiratory health (EPA, 2004, p. 8-311).

(b) Effects on the Cardiovascular System

    Two new studies conducted in the U.S. and Canada have also reported
associations between short-term exposure to PM10-2.5 and
hospital admissions for various cardiovascular diseases. The results of
these studies are included in Figure 2, where it can be seen that the
associations are generally positive and the results of the larger
studies with more statistical power are statistically significant
(Burnett et al., 1997, cardiovascular disease hospitalization; Ito,
2003, ischemic heart disease hospitalization). The excess risks for
hospital admissions for cardiovascular diseases range from about 1 to
10 percent per 25 [mu]g/m3 PM10-2.5, as seen in
the Detroit study (EPA, 2004, p. 8-310). In addition, a statistically
significant association was reported between PM10 and
increased hospitalization for cardiovascular diseases in Tucson, AZ, an
urban area where thoracic coarse particles are a much greater fraction
of PM10 than are fine particles (Schwartz, 1997).\54\ The
Criteria Document finds that associations between cardiovascular
hospitalization and short-term PM10-2.5 exposure were
relatively unchanged when gaseous co-pollutants were included in the
models (EPA, 2004, Figure 8-17; Burnett et al., 1997; Ito, 2003).\55\
In assessing potential confounding between PM2.5 and
PM10-2.5, one new study in Detroit reported that
simultaneous consideration of PM10-2.5 and PM2.5
resulted in a reduction in effect estimate

size and a lack of statistical significance for both PM indicators
(Ito, 2003). In the reanalysis for this study, for example, a
significant association was reported between PM10-2.5 and
hospitalization for ischemic heart disease in a single-pollutant model,
and in a two-pollutant model the effect estimates for PM2.5
and PM10-2.5 were both reduced in magnitude and neither
remained statistically significant (Ito, 2003, pp. 152, 153).
---------------------------------------------------------------------------

    \54\ Tucson currently attains the PM10 standard, and
the 98th percentile 24-hour average concentrations reported for
PM2.5 are 15 and 17[mu]g/m3 at two monitoring
sites in the area.
    \55\ The effect estimates for associations between
PM10-2.5 and hospitalization for ischemic heart disease
and heart failure in Detroit are largely unchanged with the addition
of gaseous co-pollutants to the models (Ito, 2003). Results
presented for the study in Toronto also show relatively consistent
effect estimate size for associations between PM10-2.5
and cardiovascular hospitalization, except for the models including
NO2 and all four gaseous pollutants (Burnett et al.,
1997).
---------------------------------------------------------------------------

    Epidemiologic studies have also reported associations between
short-term exposures to ambient PM (generally using PM10 or
PM2.5) and more subtle cardiovascular health outcomes (e.g.,
changes in heart rhythm or cardiovascular biomarkers) (EPA, 2004, p. 8-
169). Only one of this new set of epidemiologic studies included
PM10-2.5, and no significant associations were reported
between onset of myocardial infarction and short-term
PM10-2.5 exposures (EPA, 2005a, p. 8-165; Peters et al.,
2001).
ii. Mortality
    In the few epidemiologic studies available for the last review,
only the Six City study summarized above evaluated the relationship
between short-term exposure to PM10-2.5 and mortality. That
study provided a suggestion of a potential effect of thoracic coarse
particles only in the city with the highest coarse and fine particle
concentrations, but it was not possible to separate fine and thoracic
coarse particle contributions.
    As shown in Figure 2 for U.S. and Canadian studies, effect
estimates for associations between mortality and short-term exposure to
PM10-2.5 are generally positive and similar in magnitude to
those for PM2.5 and PM10 though most are not
statistically significant. In general, the confidence intervals
(indicating uncertainty) are greater for associations between mortality
and PM10-2.5 than for associations with PM2.5, as
is apparent when directly comparing results from numerous studies as
shown in Figure 8-5 of the Criteria Document (EPA, 2004, p. 8-61). In
the same comparison, it can be seen that the size of the effect
estimates for the associations are in the same range. In general,
effect estimates are somewhat larger for respiratory and cardiovascular
mortality than for total mortality. Two of the five effect estimates
for cardiovascular mortality with short-term PM10-2.5
exposure are positive and statistically significant (Mar et al., 2003;
Ostro et al., 2003) while none of the effect estimates for total
mortality reach statistical significance. The new studies include a
multi-city study that uses data from the eight largest Canadian cities
and reported associations between total mortality and
PM10-2.5 as well as PM2.5 and PM10.
The effect estimates were of similar magnitude for each PM indicator
(Burnett and Goldberg, 2003), but the association with
PM10-2.5 did not reach statistical significance. The
magnitude of the effect estimates for PM10-2.5 are similar
to those for PM2.5, generally falling in the range of 3 to 8
percent for cardiovascular mortality per 25 [mu]g/m3
PM10-2.5.
    Potential confounding by co-pollutant gases has been assessed in
some of these mortality studies. As shown in Figures 8-16 through 8-18
of the Criteria Document, the associations reported with
PM10-2.5 are generally unchanged in effect size when co-
pollutant gases are included in multi-pollutant models. The evidence
available on potential confounding between PM2.5 and
PM10-2.5 is limited, but the Criteria Document includes
results from two studies that showed effects of the two PM indicators
to be relatively independent in multi-pollutant models, however, these
particular analyses were not included in reanalyses to address
statistical modeling questions.\56\
---------------------------------------------------------------------------

    \56\ One study was the Canadian 8-city study, in which multi-
pollutant models included PM2.5 and PM10-2.5
and gaseous co-pollutants, with moderate reductions in the effect
estimate size for both PM indicators (Burnett et al., 2000).
Moolgavkar (2000) presented results of two-pollutant models for
PM2.5 and PM10-2.5 with COPD hospitalization
in Los Angeles, and again, effect estimates for both pollutants were
generally reduced somewhat in size. The author also reports that
associations with PM10-2.5 were generally reduced in size
and lost statistical significance in two-pollutant models including
CO. These two studies were reanalyzed to address potential issues
with statistical model specification, but these multi-pollutant
model results were not included in the reanalysis reports.
---------------------------------------------------------------------------

iii. Effects of Thoracic Coarse Particle Components or Sources in
Epidemiologic Studies
    In considering the epidemiologic evidence on morbidity or mortality
associations with short-term exposure to thoracic coarse particles, EPA
recognizes that the issue of the relative toxicity of different PM
components, discussed above in section II.A.1 for fine particles, is an
important uncertainty for thoracic coarse particles as well. Several
toxicologic studies, discussed above in section III.A.1, have reported
evidence of effects with different components or sources of thoracic
coarse particles. However, the available epidemiologic studies that
have used PM10-2.5 did not evaluate associations with
specific components of thoracic coarse particles (EPA, 2004, section
<IP_ADDRESS>.2). As discussed in section II.A, several studies have reported
that PM2.5 from combustion-related sources is more strongly
linked with mortality than PM2.5 of crustal origin. However,
these findings are not directly relevant to findings related to
thoracic coarse particles. Combustion sources are a major contributor
to PM2.5 emissions, but not to emissions of
PM10-2.5, while crustal material is an important component
of PM10-2.5 but only a small portion of PM2.5
(EPA, 2005a, Table 2-2).
    One study that does have relevance to considering the effects of
PM10-2.5 from different sources assessed the contribution of
dust storms to PM10-related mortality. The authors focused
on days when dust storms or high wind events occurred in Spokane,
during which thoracic coarse particles from surrounding rural soils are
the dominant fraction of PM10. No evidence was reported of
increased mortality on days with high PM10 levels related to
these dust storms (average PM10 level was 221 [mu]g/
m3 higher on dust storm days than on other study days)
(Schwartz, et al., 1999), suggesting that PM10-2.5 from
wind-blown rural dust is also not likely associated with mortality.\57\
EPA has also observed that the available epidemiologic studies using
PM10-2.5 have been conducted in urban areas, such as
Phoenix, Detroit and Seattle. Coarse particles are generally not
distributed over broad areas, but rather reflect contributions from
more localized sources, thus it is more difficult than for fine
particles to generalize the results of these studies to areas with
other types of sources.
---------------------------------------------------------------------------

    \57\ In addition, studies conducted in several areas in the
western U.S. have reported that associations between PM10
and mortality or morbidity remained unchanged or became larger and
more precise when days indicative of wind-blown dust or high
PM10 concentration days were excluded from the analyses
(Pope et al., 1999; Schwartz, 1997; Chen et al., 2000; Hefflin et
al., 1994). This group of studies does not provide conclusive
evidence of any effects or lack of effects associated with wind-
blown dust or high concentration days, nor were the studies designed
specifically for that purpose. The results do, however, indicate
that associations between PM10 and health outcomes in
these western areas are not overly influenced or ``driven by'' such
days.
---------------------------------------------------------------------------

    The Criteria Document finds that the new epidemiologic studies
support the conclusions drawn in the previous review, and indicate that
short-term exposure to thoracic coarse particles is likely associated
with respiratory morbidity. The epidemiologic studies report
statistically significant associations between short-term
PM10-2.5 exposure and outcomes ranging from respiratory
symptoms to hospitalization for respiratory diseases (EPA, 2004, p. 8-
312). A limited body of new

epidemiologic evidence suggests that short-term exposure to thoracic
coarse particles is associated with effects on the cardiovascular
system. Finally, the Criteria Document finds that evidence from health
studies on associations between short-term exposure to
PM10-2.5 and mortality is ``limited and clearly not as
strong'' as evidence for associations with PM2.5 or
PM10 but nonetheless is suggestive of associations with
mortality (EPA, 2004, p. 9-28, 9-32). As discussed briefly above, some
epidemiologic evidence suggests that there are components of thoracic
coarse particles (e.g., crustal material in non-urban areas) that are
less likely to have adverse effects, at least at lower concentrations,
than other components. Based on the epidemiologic evidence, the
Criteria Document concluded that the limited body of evidence provided
suggestive evidence for associations between throacic coarse particles
and various mortality and morbidity effects ``in some locations'' (EPA,
2004, p. 8-338).

b. Effects Related to Long-Term Exposure to Thoracic Coarse Particles

    In the last review, the available prospective cohort study results
had shown no evidence of associations between long-term exposure to
thoracic coarse particles and either mortality (Dockery et al., 1993;
Pope et al., 1995) or morbidity (Dockery et al., 1996; Raizenne et al.,
1996). As discussed above for PM2.5, new studies available
in this review include the reanalyses and extended analyses for the Six
Cities and ACS cohort studies of mortality, and new analyses from the
southern California children's cohorts of morbidity effects.
    In both the reanalyses and extended analyses of the ACS cohort
study, long-term exposure to PM10-2.5 was not significantly
associated with mortality (CD, p. 8-105; Krewski et al., 2000; Pope et
al., 2002). Based on evidence from reanalyses and extended analyses
using ACS cohort data, the Criteria Document concludes that the long-
term exposure studies find no associations between long-term exposure
to thoracic coarse particles and mortality (EPA, 2004, p. 8-307).
    In the previous review, results from the Harvard 24-city study had
shown associations between respiratory illness prevalence and decreased
lung function in children with fine particles or fine particle
indicators, but not with the larger size fractions (Dockery et al.,
1996; Raizenne et al., 1996). Further EPA staff evaluation of the data
from this study that suggested that lung function decrements were not
associated with long-term exposure to thoracic coarse particles (EPA,
1996b, p. V-67a) . In this group of cities, mean thoracic coarse
particle concentrations ranged from approximately 4 to 15 [mu]g/
m3. Several new studies have used data from the Southern
California children's cohorts, one of which included
PM10-2.5 data; in these cities, mean thoracic coarse
particle concentrations ranged from 6 to 39 [mu]g/m3. In
this study, decreases in several measures of lung function growth were
associated with long-term exposure to PM10-2.5 (as well as
PM10 and PM2.5) though not all associations
reached statistical significance (Gauderman et al., 2000). Further, in
analyses for a second cohort of children, no statistically significant
associations were reported between lung function growth and long-term
PM10-2.5 exposure (Gauderman et al., 2002, p. 81). The
correlation reported between PM10-2.5 and PM2.5
in this area was unusually high (r=0.76); in two-pollutant models, the
authors observe that the effects reported with both pollutants were
reduced in magnitude, and did not remain statistically significant,
with somewhat larger reductions for PM10-2.5 associations
than for PM2.5 (Gauderman et al., 2000, p. 1387). Thus,
results from one children's cohort study provide no evidence of
associations between long-term to exposure to PM10-2.5 and
respiratory morbidity, while findings from a more recent cohort study
provide only very limited evidence for such effects. Overall, EPA finds
that the available evidence provides little support to link long-term
exposures to thoracic coarse particles with respiratory morbidity (EPA,
2004, p. 9-34).
3. Integration and Interpretation of the Health Evidence
    As discussed in section II.A.3, the Criteria Document and Staff
Paper focused on well-recognized criteria in evaluating the
epidemiologic evidence, including the strength of associations;
robustness of reported associations to the use of alternative model
specifications, potential confounding by co-pollutants, and exposure
misclassification related to measurement error; consistency of findings
in multiple studies of adequate power, and in different persons,
places, circumstances and times; and the nature of concentration-
response relationships. These evaluations addressed key methodological
issues that are relevant to interpretation of evidence from
epidemiologic studies. Further, findings from epidemiologic studies
were integrated with available experimental evidence (e.g., dosimetric
and toxicologic), in considering the extent of coherence and biological
plausibility of effects observed in epidemiologic studies. This
integrative assessment formed the basis for the Criteria Document and
Staff Paper to draw judgments about the extent to which causal
inferences can be made about observed associations between health
endpoints and thoracic coarse particles combination with other
pollutants. The key elements of these evaluations are summarized below.
Many of these issues are discussed in section II.A.3 above for fine
particles, and are thus only briefly summarized here with regard to
implications for thoracic coarse particles.
    (1) Effect estimates from associations between short-term exposures
to thoracic coarse particles and various health outcomes are generally
small in size. The Criteria Document observes that the associations are
similar in size to those reported for PM2.5, but with less
precision as the measurement error for PM10-2.5 is greater
than that for PM2.5. Thus, the Criteria Document concludes
that the magnitude of PM10-2.5 associations is similar to
those for fine particles, but the lesser precision of the associations
reduces the strength of the evidence for thoracic coarse particles
(EPA, 2004, p. 9-41).
    (2) EPA has evaluated the robustness of epidemiologic associations
in part by considering the effect of differences in statistical model
specification, exposure error on PM-health associations, and potential
confounding by co-pollutants.
    Sensitivity to model specification was discussed above for fine
particles, and, in general, similar conclusions apply to studies using
PM10-2.5. Section 8.4.2 of the Criteria Document discusses a
series of reanalyses that address issues related to a specific type of
statistical model (``generalized additive methods'') used in some
recent epidemiologic studies. The results of the reanalyses showed
little change in effect estimates for some studies; in others the
effect estimates were reduced in size though it was observed that the
reductions were often not substantial (EPA, 2004, p. 9-35). Overall,
the Criteria Document concludes that associations between short-term
exposure to PM and various health outcomes are generally robust to the
use of alternative modeling strategies, recognizing that further
evaluation of alternative modeling strategies is warranted. It was also
observed that the results of reanalyses indicated that effect estimates
were more sensitive to the modeling approach used to account for
temporal effects and weather variables than to the specific model
specifications, and thus

recommended further exploration of alternative modeling approaches for
time-series analyses (EPA, 2004, pp. 8-236 to 8-237).
    Recent epidemiologic studies have also evaluated the influence of
exposure error on PM-health associations. This includes both
consideration of error in measurements of PM, and the degree to which
measurements from an individual monitor reflect exposures to the
surrounding community. As discussed in section 8.4.5 of the Criteria
Document, several studies have shown that fairly extreme conditions
(e.g., very high correlation between pollutants and no measurement
error in the ``false'' pollutant) are needed for complete ``transfer of
causality'' of effects from one pollutant to another (EPA, 2004, p. 9-
38). Exposure error is likely to be more important for associations
with PM10-2.5 than with PM2.5, since there is
generally greater error in PM10-2.5 measurements,
PM10-2.5 concentrations are less evenly distributed across a
community, and thoracic coarse particles are less likely to penetrate
into buildings (EPA, 2004, p. 9-38). Thus, factors related to exposure
error likely result in reduced precision for epidemiologic associations
with PM10-2.5.
    There are two key implications of this uncertainty for this review.
First, for an individual epidemiologic association, the increased
uncertainty in measurements would tend to increase the standard error
about the effect estimate, possibly reducing statistical significance
of the findings. This would mean that a set of positive but generally
not statistically significant associations between PM10-2.5
and a health outcome could be reflecting a true association that is
measured with error (EPA, 2004, p. 5-126). Second, this uncertainty
about measurements is an important consideration in evaluating the air
quality concentrations with which a statistical association is
reported. The air quality levels reported in these studies, as measured
by ambient concentrations at monitoring sites within the study areas,
are not necessarily good surrogates for the population exposures that
are likely associated with the observed effects in the study areas or
that would likely be associated with effects in other urban areas
across the country. The concentrations measured at one particular site
may over-or under-estimate air quality levels in other parts of the
area. In evaluating the air quality data from the locations in which
epidemiologic associations were reported, as discussed in the Staff
Paper and below in section III.G, examples of both cases are seen. For
example, in Coachella Valley, mortality was statistically significantly
associated with PM10-2.5 measurements made at one site
(Ostro et al., 2003), but these air quality measurements appear to
represent concentrations on the high end of PM10-2.5 levels
for Coachella Valley communities. In contrast, statistically
significant associations were reported with PM10-2.5
measurements in Detroit (Ito, 2003), and in this case the data appear
to represent concentrations on the low end of PM10-2.5
levels for the Detroit area (EPA, 2005a, p. 5-65, 5-66).
    Finally, some investigators have assessed the robustness of
associations between health outcomes and short-term exposures to
PM10-2.5 in multi-pollutant models to potential confounding
by the gaseous co-pollutants or fine particles. A high degree of
correlation between the concentrations of thoracic coarse particles and
other pollutants (either gaseous co-pollutants or fine particles) can
make interpretation of the study results difficult. Multi-pollutant
models including PM10-2.5 and gaseous co-pollutants are
included in Figures 8-16 through 8-18 of the Criteria Document, where
it can be seen that associations with PM10-2.5 are largely
unchanged when gaseous co-pollutants are added to the models (EPA,
2004, section 8.4.3). Further, in the available epidemiologic studies,
it can be seen that correlations between the gaseous co-pollutants (CO,
NO2, O3, SO2) and PM10-2.5
concentrations are often lower than correlations between the gases and
fine particles.\58\ While recognizing that disentangling the effects
attributable to various pollutants within an air pollution mixture is
challenging, the Criteria Document concludes that effect estimates for
associations between PM, including PM10-2.5, and health
endpoints are generally robust to confounding by gaseous co-pollutants
(EPA, 2004, p. 9-37).
---------------------------------------------------------------------------

    \58\ For example, from the studies included in Figures 8-16
through 8-18, correlation coefficients reported in Detroit between
PM10-2.5 and the four gaseous co-pollutants ranged from
0.13 to 0.32, whereas the correlation coefficients between
PM2.5 and the gaseous co-pollutants range from 0.38-0.49
(Ito, 2003).
---------------------------------------------------------------------------

    Less information is available from studies that specifically
assessed potential confounding between fine and thoracic coarse
particles, as noted above. The reported correlation coefficients
between PM10-2.5 and PM2.5 are in the low to
moderate range for most such studies, i.e., generally in a range of
below 0.3 to 0.5, with some notably higher correlation coefficients
reported in Phoenix (0.59) and Steubenville (0.69). As observed
previously, one study in Detroit evaluated the effects of both
PM2.5 and PM10-2.5 simultaneously where the
correlation between the two pollutants was ``modest'' (correlation
coefficient of 0.42). The authors report a reduction in coefficients
for both PM10-2.5 and PM2.5 in associations with
mortality and hospital admissions for respiratory or cardiovascular
diseases (Ito, 2003, pp. 152-153); the degree of reduction in size
varied for different health outcomes. Similarly, Schwartz and Neas
(2000) report some reduction in effect estimate size for both
PM10-2.5 and PM2.5 associations across six cities
in two-pollutant models, but the association reported between
PM10-2.5 and cough remains statistically significant.\59\
Two studies reported associations between PM10-2.5 and
mortality (Ostro et al., 2003, Coachella Valley; Mar et al., 2003,
Phoenix); stronger associations were reported with PM10-2.5
than PM2.5 by Ostro et al., although the authors note the
reduced sample size for PM2.5 may have influenced the
statistical power (Ostro et al., 2003). Both areas have relatively low
fine particle concentrations, with 98th percentile PM2.5
concentrations of about 32 [mu]g/m3 in Phoenix and 34 [mu]g/
m3 in Coachella Valley, while the correlation coefficient
reported between PM2.5 and PM10-2.5 was low in
Coachella Valley (0.28) and fairly high in Phoenix (0.59). This limited
body of evidence suggests that PM10-2.5 and PM2.5
have associations with health outcomes that are likely independent of
one another, but further work is needed to help distinguish the
contributions of thoracic coarse particles on health outcomes from
those of fine particles.
---------------------------------------------------------------------------

    \59\ The correlation coefficients between PM10-2.5
and PM2.5 range from 0.23 to 0.45 in five of the six
cities (Boston, Knoxville, Portage, Topeka, and St. Louis), with a
correlation coefficient of 0.69 in Steubenville.
---------------------------------------------------------------------------

    Overall, the Criteria Document concludes that associations reported
between health outcomes and short-term exposure to PM10-2.5
are generally robust to the use of alternative modeling strategies, to
adjustment for the potential confounding effects of gaseous co-
pollutants, and in terms of exposure error (EPA, 2004, p. 9-46).
However, the remaining uncertainties are larger in assessing the degree
to which effects observed with thoracic coarse particle exposures are
independent from effects of fine particles. In addition, in
interpreting the results of epidemiologic studies, it is difficult to
determine how well PM10-2.5 concentrations measured at
ambient monitoring stations

characterize the magnitude of population exposures to thoracic coarse
particles.
    (3) In assessing consistency in effect estimates, the epidemiologic
study results suggest that effect estimates may differ from one
location to another, but the extent of variation is not clear. For
example, in one multi-city study, some limited evidence was reported in
the reanalysis to address model specification issues that suggested
some heterogeneity among the 8 largest Canadian cities for associations
with PM10-2.5, although there had been no evidence of
heterogeneity in initial study findings (Burnett and Goldberg, 2003;
EPA, 2004, p. 9-39). As was observed for fine particles, there are a
number of factors that would be likely to cause variation in PM-health
outcomes in different populations and geographic areas. The Criteria
Document discusses such factors, including the mix of PM sources and
composition, the mix of other gaseous pollutants, geographic features
that would affect the spatial distribution of ambient PM, and
population characteristics that affect susceptibility or exposure
levels (EPA, 2004, p. 9-41). In addition, the use of data collected on
a 1-in-6 or 1-in-3 day schedule results in reduced statistical power,
resulting in less precision for estimated effect estimates for the
individual cities and increased potential variability in results (EPA,
2004, p. 9-40). Overall, the Criteria Document concludes that there is
some consistency in effect estimates for hospitalization for
respiratory and cardiovascular causes with short-term exposure to
thoracic coarse particles, though fewer studies are available on which
to make such an assessment than are available for fine particles (EPA,
2004, p. 9-47).
    (4) Of the group of new epidemiologic studies that have evaluated
the shape of concentration-response functions, many (generally using
PM10) have been unable to detect threshold levels in the
relationship between short-term PM exposure and mortality. One single-
city study used PM10-2.5 and PM2.5 measurements
in Phoenix and reported that there was no indication of a threshold in
the association between PM10-2.5 and mortality (Smith et
al., 2000; EPA, 2004, p. 8-322). However, a few analyses have provided
suggestions of some potential threshold levels, generally at fairly low
ambient concentrations. Thus, the Criteria Document concludes that the
evidence did not support selecting any particular population threshold
for PM10-2.5, recognizing that there may be thresholds for
specific health responses in individuals, and that it is possible that
such thresholds exist toward the lower end of the range of air quality
measurements in the health studies, but cannot be detected due to
variability in susceptibility across a population. Even in those few
studies with suggestive evidence of such thresholds, the potential
thresholds are at fairly low concentrations (EPA, 2004, sections 8.4.7
and <IP_ADDRESS>).
    (5) Several issues related to exposure time periods were assessed
in the Criteria Document, as summarized in section 3.6.5 of the Staff
Paper. One key issue is the lag period between thoracic coarse particle
exposure and health outcome in short-term exposure studies. In many
epidemiologic studies, the authors have reported a pattern of positive
associations across several consecutive lag periods for thoracic coarse
particles, such that an effect estimate for any individual lag day for
thoracic coarse particles likely underestimates the magnitude of the
PM-health response. A number of recent studies that have investigated
associations with distributed lags provide effect estimates for health
responses that persist over a period of time (days to weeks) after the
exposure period and the effect estimates are often, but not always,
larger in size that those for single-day lag periods; however,
available studies have generally not included PM10-2.5 (EPA,
2004, p. 8-281). As reported for fine particles, the Criteria Document
concludes that it is likely that the most appropriate lag period for a
study will vary, depending on the health outcome and the specific
pollutant under study. (EPA, 2004, p. 8-279).
    (6) In integrating evidence from across scientific disciplines, the
Criteria Document and Staff Paper observed that the body of
epidemiologic evidence on thoracic coarse particles is smaller than
that for fine particles and the evidence available from toxicologic
studies is also more limited. The clearest case for a causal
relationship for coarse particles is for effects on the respiratory
system. The epidemiologic results showing respiratory effects is
consistent with the assessment of regional particle penetration and
deposition, as well the observations from more limited toxicologic
studies. The fractional deposition of elevated coarse particle
concentrations is significant in the tracheobronchial region, which is
particularly sensitive in asthmatic individuals. From the limited
number of toxicologic studies using PM10-2.5, as noted above
in section III.A.1, there is some evidence that exposure to thoracic
coarse particles results in respiratory-related effects such as
inflammation or oxidative stress. In addition, allergic adjuvant
effects were linked with road dust exposures. These findings are
generally consistent with epidemiologic evidence linking
PM10-2.5 with respiratory morbidity, such as increased
respiratory symptoms and hospitalization for respiratory diseases such
as asthma or COPD.
    The evidence is less coherent for effects on the cardiovascular
system. Some epidemiologic studies have reported significant
associations with hospital admissions for cardiovascular diseases, and
associations reported with cardiovascular mortality are positive and
some are statistically significant (see Figure 2). However, the very
limited available evidence from toxicologic studies or epidemiologic
studies on more subtle cardiovascular effects has not provided evidence
that demonstrates plausible mechanisms or pathways for these effects.
    Based on an integrative assessment of the evidence, the Criteria
Document concludes that this growing but still limited body of health
evidence is suggestive of causality in associations between short-term
(but not long-term) exposures to thoracic coarse particles and health
effects, particularly for associations with respiratory morbidity.
    (7) In summary, based on the available evidence and the evaluation
of that evidence in the Criteria Document and Staff Paper, the Criteria
Document concludes that the body of evidence on effects related to
exposure to thoracic coarse particles is less strong than that for fine
particles, but provides suggestive evidence of causality for short-term
exposure to PM10-2.5 and morbidity, including
hospitalization for respiratory diseases, increased respiratory
symptoms and decreased lung function, and possibly mortality (EPA,
2004, pp. 9-79, 9-80). The Staff Paper recognizes, however, that the
substantial uncertainties associated with this limited body of evidence
suggest that it should be interpreted with a high degree of caution
(EPA, 2005a, p. 5-70).
4. Sensitive Subgroups for Effects of Thoracic Coarse Particle Exposure
    As described in section II.A.4, there are several population groups
that may be susceptible or vulnerable to PM-related effects. These
groups include those with preexisting lung diseases, such as asthma,
and children and older adults. Emerging evidence indicates that people
from lower socioeconomic strata or who have particularly elevated
exposures may be more vulnerable to PM-related effects. However, the
available evidence does not generally

allow distinctions to be drawn between the PM indicators, in terms of
which groups might have greater susceptibility or vulnerability to
PM2.5 or PM10-2.5 (EPA, 2005a pp. 3-35 to 36).
5. Impacts on Public Health From Thoracic Coarse Particle Exposure
    While recognizing that the health evidence regarding effects of
thoracic coarse particles is more limited, the Criteria Document has
concluded that the evidence suggests causal associations between short-
term exposure to thoracic coarse particles and morbidity effects, such
as respiratory symptoms or hospital admissions for respiratory
diseases, and possibly mortality. As observed above, the potentially
susceptible populations for such effects include people with
preexisting respiratory diseases, including asthma, and children and
older adults. In focusing on respiratory effects likely associated with
PM10-2.5, it can be observed that population groups with
respiratory diseases such as asthma or COPD include tens of millions of
people (EPA, 2004; Tables 9-4 and 9-5). Considering the magnitude of
these subpopulations and risks identified in health studies, the
Criteria Document concludes that exposure to thoracic coarse particles
can have an important public health impact.

B. Quantitative Risk Assessment

    The general overview and discussion of key components of the risk
assessment used to develop risk estimates for PM2.5
presented in section II.B above is also applicable to the assessment
done for PM10-2.5 in this review. However, the scope of the
risk assessment for PM10-2.5 is much more limited than that
for PM2.5, reflecting the much more limited body of
epidemiologic evidence and air quality information available for
PM10-2.5. As discussed in chapter 4 of the Staff Paper, the
PM10-2.5 risk assessment includes risk estimates for just
three urban areas for two categories of health endpoints related to
short-term exposure to PM10-2.5: hospital admissions for
cardiovascular and respiratory causes and respiratory symptoms.
    Consistent with the approach used in the PM2.5 risk
assessment, discussed above in section II.B, PM10-2.5-
related health risks attributable to anthropogenic sources and
activities (i.e., risk associated with concentrations above background
or above various selected higher cutpoints intended as surrogates for
alternative assumed population thresholds) were estimated by using the
reported linear or log-linear concentration-response functions from
epidemiologic studies and available air quality data from the locations
in which the studies had been conducted. A series of base case analyses
were conducted, using the same assumed cutpoints as were used in the
assessment of short-term exposures to PM2.5.
    Estimates of hospital admissions attributable to short-term
exposure to PM10-2.5 have been developed for Detroit
(cardiovascular and respiratory admissions) and Seattle (respiratory
admissions), and estimates of respiratory symptoms have been developed
for St. Louis.\60\ Base case estimates of respiratory-related hospital
admissions under recent air quality levels in Detroit are on the order
of several hundred admissions per year across the range of assumed
cutpoints considered in this assessment. The Detroit estimates are
roughly one to two orders of magnitude greater than the range of
estimated asthma-related admissions in Seattle, which can be attributed
in part to differences in baseline risks related to respiratory-related
health endpoints as well as to differences in PM10-2.5 air
quality levels in these two areas. More specifically, recent (e.g.,
2001-2003) PM10-2.5 concentrations are substantially higher
in Detroit, where the current 24-hour PM10 standard is not
met, than they are in Seattle (where the 24-hour PM10 design
value is well below the level of the current PM10 standard).
In considering risk estimates for respiratory symptoms in St. Louis,
the number of days of cough in children living in St. Louis associated
with recent PM10-2.5 levels range from approximately 27,000
days per year \61\ at the lowest assumed cutpoint to almost 3,000 days
per year at the highest assumed cutpoint. For the same time period,
PM10-2.5 air quality levels in St. Louis are high, where,
like Detroit, the current 24-hour PM10 standard is not met.
---------------------------------------------------------------------------

    \60\ Quantitative risk estimates associated with recent air
quality levels for these three cities are presented in Figures 4-11
and 4-12 in Chapter 4 of the Staff Paper.
    \61\ This represents roughly 1100 days of cough per 100,000
people in the general population, of which approximately 12 percent
are children.
---------------------------------------------------------------------------

    While one of the goals of the PM10-2.5 risk assessment
was to provide estimates of the risk reductions associated with just
meeting alternative PM10-2.5 standards, the nature and
magnitude of the uncertainties and concerns associated with this
portion of the risk assessment weigh against use of these risk
estimates as a basis for recommending specific standard levels (EPA,
2005a, p. 5-69). These uncertainties and concerns include, but are not
limited to the following:
    (1) As noted above in section II.A and discussed more fully below
in section III.G, the PM10-2.5 levels measured at ambient
monitoring sites in recent years may be quite different from the levels
used to characterize exposure in the original epidemiologic studies
based on monitoring sites in different location, thus possibly over- or
underestimating population risk levels.
    (2) There is greater uncertainty about the reasonableness of the
use of proportional rollback to simulate just meeting alternative
PM10-2.5 standards in any urban area relative to that for
PM2.5 due to the limited availability of historic
PM10-2.5 air quality data.
    (3) The locations used in the PM10-2.5 risk assessment
are not representative of urban areas in the U.S. that experience the
most significant 24-hour peak PM10-2.5 concentrations, and
thus, observations about relative risk reductions associated with
alternative standards may not be relevant to the areas expected to have
the greatest health risks associated with elevated ambient
PM10-2.5 levels.
    (4) The health effects database that supplies the concentration-
response relationships used in the PM10-2.5 risk assessment
is much smaller than that available for PM2.5, which limits
EPA's ability to evaluate the robustness of the risk estimates for the
same health endpoints across different locations.

C. Need for Revision of the Current Primary PM10 Standards

    The initial issue to be addressed in the current review of the
primary PM10 standards is whether, in view of the advances
in scientific knowledge reflected in the Criteria Document and Staff
Paper, the existing standards should be revised. The Staff Paper
addresses this question by first considering the conclusions reached in
the last review, the subsequent litigation of that decision, and the
nature of the new information available in this review.
    In 1997, in conjunction with establishing new PM2.5
standards, EPA concluded that continued protection against potential
effects associated with thoracic coarse particles in the size range of
2.5 to 10 [mu]m was warranted based on particle dosimetry, toxicologic
information, and limited epidemiologic evidence (62 FR 38,677). This
information indicated that thoracic coarse particles can deposit in the
sensitive regions of the lung of most concern (e.g., the
tracheobronchial and alveolar regions, which together make

up the thoracic region),\62\ and that they can be expected to aggravate
effects in individuals with asthma and contribute to increased upper
respiratory illness (62 FR 38,666-8).
---------------------------------------------------------------------------

    \62\ EPA further concluded at that time that the risks of
adverse health effects associated with deposition of particles in
the thoracic region are ``markedly greater than for deposition in
the extrathoracic (head) region,'' and that risks from extrathoracic
deposition are ``sufficiently low that particles which deposit only
in that region can safely be excluded from the standard indicator''
(62 FR 38,666).
---------------------------------------------------------------------------

    Further, EPA decided that the new function of PM10
standard(s) would be to provide such protection against effects
associated with particles in this narrower size range between 2.5 to 10
[mu]m. Although some consideration had been given to a more narrowly
defined indicator that did not include fine particles (e.g.,
PM10-2.5), EPA decided that it was more appropriate to
continue to use PM10 as the indicator for standards to
control thoracic coarse particles. This decision was based in part on
the recognition that the only studies of clear quantitative relevance
to health effects most likely associated with thoracic coarse particles
used PM10 in areas where the coarse fraction was the
dominant fraction of PM10, namely two studies conducted in
areas that substantially exceeded the 24-hour PM10 standard
(62 FR 38,679). The decision also reflected the fact that there were
only very limited ambient air quality data then available specifically
on thoracic coarse particles, in contrast to the extensive monitoring
network already in place for PM10. In essence, EPA concluded
at that time that it was appropriate to continue to control thoracic
coarse particles, but that the only information available upon which to
base such standards was indexed in terms of PM10.
    In subsequent litigation regarding the 1997 PM NAAQS revisions,
however, the court held in part that PM10 is a ``poorly
matched indicator'' for thoracic coarse particles in the context of a
rule that also includes PM2.5 standards because
PM10 includes PM2.5. American Trucking
Associations v. EPA, 175 F.3d. at 1054. Although the court found
``ample support'' (id.) for EPA's decision to regulate thoracic coarse
particles, it vacated the 1997 revised PM10 standards for
that reason. The result of subsequent EPA actions, discussed above in
section I.C, is that the 1987 PM10 standards remain in place
(65 FR 80776, 80777, Dec. 22, 2000) and the present review is
consequently of those 1987 standards.
    In this review, the Staff Paper focuses on the information now
available from a growing, but still limited, body of evidence on health
effects associated with thoracic coarse particles from studies that use
PM10-2.5 as the measure of thoracic coarse particles. In
addition, there is now much more information available to characterize
air quality in terms of PM10-2.5 than was available in the
last review.\63\ In considering this information, the Staff Paper finds
that the major considerations that formed the basis for EPA's 1997
decision to retain PM10 as the indicator for thoracic coarse
particles, rather than a more narrowly defined indicator that does not
include fine particles, no longer apply. More specifically, the
continued use of PM10 as an indicator for standards intended
to protect against health effects associated with thoracic coarse
particles is no longer appropriate since information is now available
that supports the use of a more directly relevant indicator,
PM10-2.5. Further, continuing to rely principally on health
effects evidence indexed by PM10 to determine the
appropriate averaging time, form, and level of a standard is no longer
necessary or appropriate since a number of more directly relevant
studies, indexed by PM10-2.5, are also now available. Thus,
separate from any legal considerations, the Staff Paper concludes it is
appropriate to revise the current PM10 standards in part by
revising the indicator for thoracic coarse particles, and by basing any
such revised standard principally on the currently available evidence
and air quality information indexed by PM10-2.5, but also
considering evidence from studies using PM10 in locations
where PM10-2.5 is the predominant fraction (EPA, 2005a,
section 5.4.1).
---------------------------------------------------------------------------

    \63\ Coarse particle concentrations from EPA's monitoring
network are currently determined using a difference method in
locations with same-day data from co-located PM10 and
PM2.5 FRM monitors.
---------------------------------------------------------------------------

    Recognizing that dosimetric evidence formed the principal basis for
the initial establishment of the PM10 indicator in 1987, and
supported the decision in 1997 to retain the PM10 indicator,
the Staff Paper also considers whether currently available dosimetric
evidence continues to support the basic conclusions reached in those
reviews of the standards. In particular, consideration is given to
available information about patterns of penetration and deposition of
thoracic coarse particles in the sensitive thoracic region of the lung
and to whether an aerodynamic size of 10 [mu]m remains a reasonable
separation point for particles that penetrate and potentially deposit
in the thoracic regions. The Staff Paper concludes that while
considerable advances have been made in understanding particle
dosimetry, the available evidence continues to support those basic
conclusions from past reviews. More specifically, both fine particles,
indexed by PM2.5, and thoracic coarse particles, indexed by
PM10-2.5, penetrate to and deposit in the thoracic regions.
Further, for a range of typical ambient size distributions, the total
deposition of thoracic coarse particles to the alveolar region can be
comparable to or even larger than that for fine particles (EPA, 2004,
p. 6-16).
    Beyond the dosimetric evidence, as noted in past reviews (EPA,
1981b, 1996b), toxicologic studies show that the deposition of a
variety of particle types in the tracheobronchial region, including
resuspended urban dust and coarse-fraction organic materials, has the
potential to affect lung function and aggravate respiratory symptoms,
particularly in asthmatics. Of particular note are limited toxicologic
studies that found urban road dust can produce cellular and
immunological effects (e.g., Kleinman, et al., 1995; Steerenberg et
al., 2003).\64\ In addition, some very limited in vitro toxicologic
studies show some evidence that coarse particles may elicit pro-
inflammatory effects (EPA, 2004, section 7.4.4). Further, the Staff
Paper assessment of the physicochemical properties and occurrence of
ambient coarse particles suggests that both the chemical makeup and the
spatial distribution of coarse particles are likely to be more
heterogeneous than for fine particles (EPA, 2005a, chapter 2). In
particular, as discussed below in section III.D, coarse particles in
urban areas can contain all of the components found in more rural
areas, but be contaminated by a number of additional materials, from
motor vehicle-related emissions to metals and transition elements
associated with industrial operations. The Staff Paper concludes that
the weight of the dosimetric, limited toxicologic, and atmospheric
science evidence, taken together, lends support to the plausibility of
the PM10-2.5-related effects reported in urban epidemiologic
studies, and provides support for retaining some standard for thoracic
coarse particles so as to continue programs to protect public health
from such effects (EPA, 2005a, p. 5-49).
---------------------------------------------------------------------------

    \64\ The Criteria Document notes that toxicologic studies, in
general, use exposure concentrations that are generally much higher
than ambient concentrations (EPA, 2004, p. 9-51).
---------------------------------------------------------------------------

    The available epidemiologic evidence, discussed above in section
III.A, includes studies of associations between short-term exposure to
thoracic coarse particles, indexed by PM10-2.5, and

health endpoints, as well as evidence from PM10 studies
conducted in areas in which the coarse fraction is dominant. More
specifically, several U.S. and Canadian studies now provide evidence of
associations between short-term exposure to PM10-2.5 and
various morbidity endpoints. Three such studies conducted in Toronto
(Burnett et al., 1997), Seattle (Sheppard et al., 2003), and Detroit
(Ito, 2003) report statistically significant associations between
short-term PM10-2.5 exposure and respiratory- and cardiac-
related hospital admissions, and a fourth study (Schwartz and Neas,
2000) conducted in six U.S. cities including Boston, St. Louis,
Knoxville, Topeka, Portage, and Steubenville reports statistically
significant associations across these six areas with respiratory
symptoms in children. These studies were mostly done in areas in which
PM2.5, rather than PM10-2.5, is the larger
fraction of ambient PM10, and they are not representative of
areas with relatively high levels of thoracic coarse particles (EPA,
2005a, p. 5-49).
    In evaluating the epidemiologic evidence from health studies on
associations between short-term exposure to PM10-2.5 and
mortality, the Criteria Document concluded that such evidence was
``limited and clearly not as strong'' as that for associations with
PM2.5 or PM10 but nonetheless was suggestive of
associations with mortality (EPA, 2004, p. 9-28, 9-32). Statistically
significant mortality associations were reported in short-term exposure
studies conducted in areas with relatively high PM10-2.5
concentrations, including Phoenix (Mar et al., 2003), Coachella Valley,
CA (Ostro et al., 2003), and in the initial analysis of data from
Steubenville (as part of the Six Cities study, Schwartz et al., 1996),
although in a reanalysis of this study, the results were generally not
statistically significant (Klemm and Mason, 2003). In areas with lower
PM10-2.5 concentrations, no statistically significant
associations were reported with mortality, though most were positive.
    The Staff Paper also considers relevant epidemiologic studies
indexed by PM10 that were conducted in areas where the
coarse fraction of PM10 is typically much greater than the
fine fraction. Such studies include findings of associations between
short-term exposure to PM10 and hospitalization for
cardiovascular diseases in Tucson, AZ (Schwartz, 1997), hospitalization
for COPD in Reno/Sparks, NV (Chen et al., 2000), and medical visits for
asthma or respiratory diseases in Anchorage, AK (Gordian et al., 1996;
Choudhury et al., 1997). In addition, a number of epidemiologic studies
have reported significant associations with mortality, respiratory
hospital admissions and respiratory symptoms in the Utah Valley area
(e.g., Pope et al., 1989; 1991; 1992). This group of studies provides
additional supportive evidence for associations between short-term
exposure to thoracic coarse particles and health effects, particularly
morbidity effects, generally in areas not meeting the PM10
standards (EPA, 2005a, p. 5-50).\65\
---------------------------------------------------------------------------

    \65\ Based on recent air quality data, as well as the summary
information provided for PM concentrations used in the studies, the
existing PM10 standards are not met in any of these study
cities except Tucson, AZ. Based on 2002-2004 air quality data, the
98th percentile PM2.5 concentrations in three of these
areas range from 15 to 25 [mu]g/m3, while in Utah Valley
the concentrations range from 37 to 54 [mu]g/m3.
---------------------------------------------------------------------------

    In contrast to the findings from the short-term exposure studies
discussed above, available epidemiologic studies do not provide
evidence that long-term exposure to thoracic coarse particles is
associated with mortality or morbidity (EPA, 2005a, p. 3-25). More
specifically, no association is found between long-term exposure to
thoracic coarse particles and mortality in the reanalyses and extended
analysis of the ACS cohort (EPA, 2005a, p. 8-307). Further, little
evidence is available on potential respiratory and cardiovascular
morbidity effects of long-term exposure to thoracic coarse particles
(EPA, 2005a, p. 3-23-24).
    Taken together, the Staff Paper concludes that the health evidence,
including dosimetric, toxicologic and epidemiologic study findings,
supports retaining some standard to protect against effects associated
with short-term exposure to thoracic coarse particles. However, the
substantial uncertainties associated with this limited body of
epidemiologic evidence on health effects related to exposure to
PM10-2.5, including the difficulty in separating the effects
of fine and thoracic coarse particles, suggest a high degree of caution
in interpreting this evidence, especially at the lower levels of
ambient particle concentrations in the morbidity studies discussed
above (EPA, 2004, p. 5-50).
    Beyond this evidence-based evaluation, the Staff Paper also
considers the extent to which PM10-2.5-related health risks
estimated to occur at current levels of ambient air quality may be
judged to be important from a public health perspective, taking into
account key uncertainties associated with the estimated risks.
Consistent with the approach used to address this issue for
PM2.5-related health risks, discussed above in section II.B,
the Staff Paper considers the results of a series of base case analyses
that reflect in part the uncertainty associated with the form of the
concentration-response functions drawn from the studies used in the
assessment. In this assessment, which is much more limited than the
risk assessment conducted for PM2.5, health risks were
estimated for three urban areas by using the reported linear or log-
linear concentration-response functions as well as modified functions
that incorporate alternative assumed cutpoints as surrogates for
potential population thresholds (discussed above in section III.B). In
considering the risk estimates from this limited assessment, and
recognizing the very substantial uncertainties inherent in basing an
assessment on such limited information, the Staff Paper concludes that
the results for the two areas in the assessment that did not meet the
current PM10 standards are indicative of risks that can
reasonably be judged to be important from a public health perspective,
in contrast to the appreciably lower risks estimated for the area that
did meet the current standards (EPA, 2005a, p. 5-52).
    The Staff Paper recognizes the substantial uncertainties associated
with the limited available epidemiologic evidence and the inherent
difficulties in interpreting the evidence for purposes of setting
appropriate standards for thoracic coarse particles. Nonetheless, in
considering the available evidence, the public health implications of
estimated risks associated with current levels of air quality, and the
related limitations and uncertainties, the Staff Paper concludes that
this information supports (1) revising the current PM10
standards in part by revising the indicator for thoracic coarse
particles, and (2) consideration of a standard that will continue to
provide public health protection from short-term exposure to thoracic
coarse particles of concern that have been associated with morbidity
effects and possibly mortality at current levels in some urban areas
(EPA, 2005a, p. 5-52).
    In CASAC's review of these Staff Paper recommendations, there was
general concurrence among CASAC Panel members that there is a need to
revise the current PM10 standards and establish a primary
standard specifically targeted to address particles in the size range
of 2.5 to 10 [mu]m (Henderson, 2005b). In making this recommendation,
CASAC indicated its agreement with the summary of the scientific data
regarding the potential adverse health effects from exposures to
thoracic coarse particles in

section 5.4 of the Staff Paper upon which the EPA staff recommendations
were based.
    In considering whether the primary PM10 standards should
be revised, the Administrator has carefully considered the rationale
and recommendations contained in the Staff Paper, the advice and
recommendations of CASAC, and public comments to date on this issue.
The Administrator provisionally concludes that the health evidence,
including dosimetric, toxicologic and epidemiologic study findings,
supports retaining a standard to protect against effects associated
with short-term exposure to thoracic coarse particles. Further, the
Administrator believes that the new evidence on health effects from
studies that use PM10-2.5 as a measure of thoracic coarse
particles, together with the much more extensive data now available to
characterize air quality in terms of PM10-2.5, provide an
appropriate basis for revising the current PM10 standards in
part by revising the indicator to focus more narrowly on particles
between 2.5 and 10 [mu]m. The Administrator also notes that the need
for a standard for thoracic coarse particles has already been upheld
based upon evidence of health effects considerably more limited than
now available. American Trucking Associations v. EPA, 175 F. 3d at
1054. Based on these considerations, the Administrator provisionally
concludes that the current suite of PM10 standards should be
revised, and that the revised standard(s) should provide more targeted
protection from short-term exposure to those thoracic coarse particles
that are of concern to public health.

D. Indicator of Thoracic Coarse Particles

    In considering an appropriate indicator for a standard intended to
afford protection from health effects associated with exposure to
thoracic coarse particles of concern, the Staff Paper starts by making
the following observations:
    (1) The most obvious choice for a thoracic coarse particle standard
is the size-differentiated, mass-based indicator used in the
epidemiologic studies that provide the most direct evidence of such
health effects, PM10-2.5.
    (2) The upper size cut of a PM10-2.5 indicator is
consistent with dosimetric evidence that continues to reinforce the
finding from past reviews that an aerodynamic size of 10 [mu]m is a
reasonable separation point for particles that penetrate to and
potentially deposit in the thoracic regions of the respiratory tract.
    (3) The lower size cut of such an indicator is consistent with the
choice of 2.5 [mu]m as a reasonable separation point between fine and
coarse fraction particles.
    (4) Further, the limited available information is not sufficient to
define an indicator for thoracic coarse particles solely in terms of
metrics other than size-differentiated mass, such as specific chemical
components.
    (5) The available epidemiologic evidence for effects of
PM10-2.5 exposure is quite limited and is inherently
characterized by large uncertainties, reflective in part of the more
heterogeneous nature of the spatial distribution and chemical
composition of thoracic coarse particles and the more limited and
generally uncertain measurement methods that have historically been
used to characterize their ambient concentrations.
    In evaluating relevant information from atmospheric sciences,
toxicology, and epidemiology related to thoracic coarse particles, the
Staff Paper notes that there appears to be clear distinctions between
(1) the character of the ambient mix of particles generally found in
urban areas as compared to that found in nonurban and, more
specifically, rural areas, and (2) the nature of the evidence
concerning health effects associated with thoracic coarse particles
generally found in urban versus rural areas. Based on such information,
and on specific initial advice from CASAC (Henderson, 2005a), the Staff
Paper considers a more narrowly defined indicator for thoracic coarse
particles that focuses on the mix of such particles that is
characteristic of that generally found in urban areas where thoracic
coarse particles are strongly influenced by traffic-related or
industrial sources. In so doing, the Staff Paper focuses on comparing
the potential health effects associated with thoracic coarse particles
in urban and rural settings, as discussed below.
    Atmospheric science and monitoring information indicates that
exposures to thoracic coarse particles tend to be higher in urban areas
than in nearby rural locations. Further, the mix of thoracic coarse
particles typically found in urban areas contains a number of
contaminants that are not commonly present to the same degree in the
mix of natural crustal particles that is typical of rural areas. The
elevation of PM10-2.5 levels in urban locations as compared
to those at nearby rural sites suggests that sources located within
urban areas are generally the cause of elevated urban concentrations;
conversely, PM10-2.5 concentrations in such urban areas are
not largely composed of particles blown in from more distant regions
(EPA, 2005a, sections 2.4.5 and <IP_ADDRESS>). Important sources of thoracic
coarse particles in urban areas include dense traffic that suspends
significant quantities of dust from paved roads, as well as industrial
and combustion sources and construction activities that contribute to
ambient coarse particles both directly and through deposition to soils
and roads (EPA, 2005a, Table 2-2). It follows that the mix of thoracic
coarse particles in urban areas would differ in composition from that
in rural areas, being influenced to a relatively greater degree by
components from urban mobile and stationary source emissions.
    While detailed composition data are more limited for
PM10-2.5 than for PM2.5, available measurements
from some areas as well as studies of road dust components do show a
significant influence of urban sources on both the composition and mass
of thoracic coarse particles generally found in urban areas. Although
crustal elements and natural biological materials represent a
significant fraction of thoracic coarse particles in urban areas, both
their relative quantity and character may be altered by urban sources.
For example, in industrial cities, primary particle emissions from
industrial sources and resuspended road dust can increase the relative
amount of iron in the mix of PM10-2.5, one of the metals
that has been noted as being of some interest in the studies of
mechanisms of toxicity for PM, as well as other industrial process-
related and potentially toxic materials such as nickel, cadmium, and
chromium (EPA, 2005a, p. 5-54). Traffic-related activities can also
grind and resuspend vegetative materials into forms not as common in
more natural areas (Rogge et al., 1993). Studies of urban road dusts
find that levels of a variety of components are increased from traffic
as well as from other anthropogenic urban sources, including products
of incomplete combustion (e.g. polycyclic aromatic hydrocarbons) from
motor vehicle emissions and other sources, brake and tire wear, rust,
salt and biological materials (EPA, 2004, p. 3D-3). Limited ambient
coarse fraction composition data from various comparisons find that
metals and sometimes elemental carbon contribute a greater proportion
of thoracic coarse particle mass in urban areas than in nearby rural
areas. In addition, while large uncertainties exist in emissions
inventory data, the Staff Paper observes that major sources of
PM10-2.5 emissions in the urban counties in which
epidemiologic studies have been conducted are paved roads and ``other''

sources (largely construction), and that such areas also have larger
contributions from industrial emissions, whereas unpaved roads and
agriculture are the main sources of PM10-2.5 emissions
outside of urban areas.
    Toxicologic studies, although quite limited, support the view that
thoracic coarse particles from sources common in urban areas are of
greater concern than uncontaminated materials of geologic origin. One
major source of thoracic coarse particles in urban areas is paved road
dust; the Criteria Document discusses results from a recent toxicologic
study in which road tunnel dust particles had greater allergic adjuvant
activity than several other particle samples (Steerenberg et al., 2003;
EPA, 2004, pp. 7-136, 137). This study supports evidence available in
the last review regarding potential effects of road dust particles
(EPA, 1996b, p. V-70). In contrast, a number of studies have reported
that Mt. St. Helens volcanic ash, an example of natural crustal
material of geologic origin, has very little toxicity in animal or in
vitro toxicologic studies (EPA, 2004, p. 7-216).
    A few toxicologic studies have used ambient thoracic coarse
particles from urban/suburban locations (PM10-2.5), and the
results suggest that effects can be linked with several components of
PM10-2.5. These in vitro toxicologic studies linked thoracic
coarse particles with effects including cytotoxicity, oxidant
formation, and inflammatory effects (EPA, 2005a, sections 3.2 and
5.4.1). These studies suggest that several components (e.g., metals,
endotoxin, other materials) may have roles in various health responses
but do not suggest a focus on any individual component.
    Although largely focused on undifferentiated PM10, the
series of epidemiologic observations and toxicologic experiments
related to the Utah Valley suggest that directly emitted (fine and
coarse) and resuspended (coarse) urban industrial emissions are of
concern. Of particular interest are area studies spanning a 13-month
period when a major source of PM10 in the area, a steel
mill, was not operating. Observational studies found that respiratory
hospital admissions for children were lower when the plant was shut
down (Pope et al., 1989). More recently, a set of toxicologic and
controlled human exposure studies have used particles extracted from
filters from ambient PM10 monitors from periods when the
plant did and did not operate. In both human volunteers and animals,
greater lung inflammatory responses were reported with particles
collected when the source was operating, as compared to the period when
the plant was closed (EPA, 2004, p. 9-73). In addition, in some studies
it was suggested that the metal content of the particles was most
closely related to the effects reported (EPA, 2004, p. 9-74). While
peak days in the Utah Valley occur in conditions that enhance fine
particle concentrations, over the long run, over half of the
PM10 was in the coarse fraction. The aggregation of
particles collected on the filters during the study period reflect this
long-term composition and represent the kinds of industrial components
that would be incorporated in road dusts in the area.
    Epidemiologic studies that have examined exposures to thoracic
coarse particles generally found in urban environments, together with
studies that have taken into account exposures to natural crustal
materials typical of rural areas, generally support the view that the
mix of thoracic coarse particles generally found in urban areas is of
concern to public health, in contrast to natural crustal dusts of
geologic origin. With respect to the urban results, several recent
studies have shown associations between PM10-2.5 and health
outcomes in a few sites across the U.S. and Canada. Associations have
been reported with morbidity in a few urban areas, some of which had
relatively low PM10-2.5 concentrations. For mortality,
statistically significant associations have been reported only for two
urban areas that have notably higher ambient PM10-2.5
concentrations. These associations are with short-term exposures to
aggregated PM10-2.5 mass, and no epidemiologic evidence is
available on associations with different components or sources of
PM10-2.5. However, these studies have all been conducted in
urban areas of the U.S., and thus reflect effects associated with the
ambient mix of thoracic coarse particles generally present in urban
environments.
    In contrast, recent evidence from epidemiologic studies has
suggested that mortality and possibly other health effects are not
associated with thoracic coarse particles from dust storms or other
such wind-related events that result in suspension of natural crustal
materials of geologic origin. The clearest example is provided by a
study in Spokane, WA, which specifically assessed whether mortality was
increased on dust-storm days using case-control analysis methods. The
average PM10 level was more than 200 [mu]g/m3
higher on dust storm days than on control days, and the authors report
no evidence of increased mortality on these specific days (Schwartz et
al., 1999). One caveat of note is the possibility that people may
reduce their exposure to ambient particles on the most dusty days
(e.g., Gordian et al., 1996; Ostro et al., 2000). Nevertheless, these
studies provide no suggestion of significant health effects from
uncontaminated natural crustal materials that would typically form a
major fraction of coarse particles in non-urban or rural areas.
    Beyond the urban and rural distinctions discussed above, the Staff
Paper also considers the extent to which there is evidence of effects
with exposure to the ambient thoracic coarse particles in communities
predominantly influenced by agricultural or mining sources.\66\ For
example, in the last review, EPA considered health evidence related to
long-term silica exposures from mining activities, but found that there
was a lack of evidence that such emissions contribute to effects linked
with ambient PM exposures (EPA, 1996b, p. V-28). Similarly in this
review, there is an absence of evidence related to such community
exposures. While crustal and organic dusts generated from agricultural
activity can include a variety of biological materials, and some
occupational studies discussed in the Criteria Document report effects
at occupational exposure levels (EPA, 2004, Table 7B-3, p. 7B-11), such
studies do not provide relevant evidence for effects at much lower
levels of community exposures. Further, it is unlikely that such
sources contribute to the effects that have been observed in the recent
urban epidemiologic studies.
---------------------------------------------------------------------------

    \66\ Mining sources are intended to include all activities that
encompass extraction and/or mechanical handling of natural geologic
crustal materials.
---------------------------------------------------------------------------

    The Criteria Document concludes its integrated assessment of the
effects of natural crustal materials as follows:

    Certain classes of ambient particles appear to be distinctly
less toxic than others and are unlikely to exert human health
effects at typical ambient exposure concentrations (or perhaps only
under special circumstances). For example, particles of crustal
origin, which are predominately in the coarse fraction, are
relatively non-toxic under most circumstances, compared to
combustion-related particles (such as from coal and oil combustion,
wood burning, etc.) However, under some conditions, crustal
particles may become sufficiently toxic to cause human health
effects. (EPA, 2004, p. 8-344)

    The Staff Paper assessment of the available evidence relevant to
the appropriate scope of an indicator for coarse particles can be
summarized as follows. Ambient concentrations of thoracic coarse
particles generally

reflect contributions from local sources, and the limited information
available from speciation of thoracic coarse particles and emissions
inventory data indicate that the sources of thoracic coarse particles
in urban areas generally differ from those found in nonurban areas. As
a result, the mix of thoracic coarse particles people are typically
exposed to in urban areas can be expected to differ appreciably from
the mix typically found in non-urban or rural areas. Ambient
PM10-2.5 exposure is associated with health effects in
studies conducted in urban areas, and the limited available health
evidence more strongly implicates the ambient mix of thoracic coarse
particles that is dominated by traffic-related and industrial sources
than that from uncontaminated soil or geologic sources. The limited
evidence does not support either the existence or the lack of causative
associations for community exposures to thoracic coarse particles from
agricultural or mining industries. Given the apparent differences in
composition and in the epidemiologic evidence, the Staff Paper
concludes that it is not appropriate to generalize the available
evidence of associations with health effects that have been related to
thoracic coarse particles generally found in urban areas and apply it
to the mix of particles typically found in nonurban or rural areas
(EPA, 2005a, p. 5-57).
    Collectively, this evidence suggests that a more narrowly defined
indicator for thoracic coarse particles should be considered that would
protect public health against effects that have been linked with the
mix of thoracic coarse particles generally present in urban areas. Such
an indicator would be principally based on particle size, but also
reflect a focus on the mix of thoracic coarse particles that is
generally present in urban environments and the sources that
principally generate that mix. The Staff Paper recommends consideration
of thoracic coarse urban particulate matter \67\ as an indicator for a
thoracic coarse particle standard, referring to the mix of airborne
particles between 2.5 and 10 [mu]m in diameter that are generally
present in urban environments, which, as discussed above, are
principally comprised of resuspended road dust typical of high traffic-
density areas and emissions from industrial sources and construction
activities (EPA, 2005a, p. 5-54, 5-57-58). The Staff Paper concludes
that such an indicator would more likely be an effective indicator for
standards to protect against health effects that have been associated
with thoracic coarse particles than a more broadly focused
PM10-2.5 indicator. This indicator would also be consistent
with an appropriately cautious interpretation of the epidemiologic
evidence that does not potentially over-generalize the results of the
limited available studies.
---------------------------------------------------------------------------

    \67\ The acronym ``UPM10-2.5'' is used in the Staff
Paper to refer to this indicator.
---------------------------------------------------------------------------

    In conjunction with this recommendation of an indicator defined in
terms of the mix of thoracic coarse particles that are generally
present in urban areas, the Staff Paper also discusses the importance
of a monitoring network designed so as to be consistent with the intent
of such an indicator and that would facilitate implementation of such a
standard. EPA has historically used implementation policies to address
elevations in thoracic coarse particle levels that may occur in urban
areas as a result of dust storms or other such events for which this
staff-recommended indicator is not intended to apply. Both new criteria
for monitor network design and revised natural/exceptional events
policies should work in concert with a revised thoracic coarse particle
indicator to ensure the most effective application of a thoracic coarse
particle standard.
    In its review of the Staff Paper recommendation for a thoracic
coarse particle indicator (Henderson, 2005b), the CASAC generally
agreed that ``thoracic coarse particles in urban areas can be expected
to differ in composition from those in rural areas;'' that ``coarse
particles in urban or industrial areas are likely to be enriched by
anthropogenic pollutants that tend to be inherently more toxic than the
windblown crustal material which typically dominates coarse particle
mass in arid rural areas;'' and that ``evidence of associations with
health effects related to urban coarse-mode particles would not
necessarily apply to non-urban or rural coarse particles.'' Further,
most CASAC Panel members concurred that ``the current scarcity of
information on the toxicity of rural dusts makes it necessary'' for EPA
to base its standard for thoracic coarse particles ``on the known
toxicity of urban-derived coarse particles.'' While most Panel members
concurred with the thoracic coarse particle indicator recommended in
the Staff Paper, a few members recommended specifying a
PM10-2.5 indicator in conjunction with monitoring network
design criteria and natural/exceptional events policies that would
emphasize urban influences. In either case, CASAC indicated that the
intent of any such indicator should be to ``provide protection against
those components of PM10-2.5 that arise from anthropogenic
activities occurring in or near urban and industrial areas.''
    In considering an appropriate indicator for a standard intended to
afford protection from health effects associated with exposure to
thoracic coarse particles of concern, the Administrator has carefully
considered the rationale and recommendations contained in the Staff
Paper, the advice and recommendations from CASAC, and public comments
to date on this issue. In so doing, the Administrator believes, despite
the substantial limitations and uncertainties in the relevant
information available, that it is appropriate to propose a new
indicator for such particles at this time. Further, the Administrator
believes that any such indicator should be defined not only by particle
size, to generally include those particles between 2.5 and 10 [mu]m in
diameter, but also by qualifications that narrow the scope of the
indicator. In considering an indicator that is intended to focus on the
mix of thoracic coarse particles generally present in urban
environments and commonly derived from sources typically found in urban
environments, consistent with Staff Paper and CASAC recommendations,
the Administrator notes that identifying it as an ``urban'' thoracic
coarse particle indicator could be misconstrued as meaning that the
standard is limited to certain geographic locations and, thus, not a
national standard. To avoid this semantic problem, the Administrator
has sought to define the indicator in a way that more clearly focuses
on the nature of the mix of thoracic coarse particles intended to be
included and the sources that principally generate that mix, rather
than just where they are found, and that also explicitly focuses on
what would be excluded from such an indicator. In so doing, the
Administrator intends the proposed indicator to be equivalent to the
one recommended in the Staff Paper and endorsed by CASAC, but to do so
in a manner that will be more clearly understood and less likely to be
misinterpreted.
    Taking into account the considerations discussed above, the
Administrator proposes to establish a new indicator for thoracic coarse
particles in terms of PM10-2.5, the definition of which
includes qualifications that identify both the mix of such particles
that are of concern to public health, and are thus included in the
indicator, and those for which currently available information is not
sufficient to infer a public health concern, and are thus excluded.
More specifically, the proposed PM10-2.5 indicator is
qualified so as to include any ambient mix of PM10-2.5 that
is

dominated by resuspended dust from high-density traffic on paved roads
and PM generated by industrial sources and construction sources, and
excludes any ambient mix of PM10-2.5 that is dominated by
rural windblown dust and soils and PM generated by agricultural and
mining sources. In short, the indicator is not defined by nor limited
to any specific geographic area, but includes the mix of
PM10-2.5 in any location that is dominated by these sources.
    With the indicator as defined above, each area in the country would
fall into one or the other of these two categories: (1) Either the
majority of the ambient mix of PM10-2.5 in an area is
resuspended dust from high-density traffic on paved roads and PM
generated by industrial sources and construction sources, or (2) the
majority of the ambient mix is rural windblown dust and soils and PM
generated by agricultural and mining sources. The indicator would apply
when PM10-2.5 generated by one or more of these named
sources in the first category constitutes a majority of the ambient mix
of PM10-2.5. The EPA recognizes that in many cases it will
be clear which of these two categories applies, while in other cases it
may be difficult to determine the appropriate category. As described in
more detail in the preamble to EPA's proposed monitor network design
rule, published elsewhere in today's Federal Register, the proposed
minimum monitor siting criteria would provide guidance on
distinguishing between areas where the mix of PM10-2.5 of
concern would likely be dominated by the named sources in the first
category and those areas where it would not. Consequently, all
PM10-2.5 captured by a monitor that is properly sited in
light of the indicator described above, as discussed in the proposed
monitoring rule, would be considered in applying the standard, since
the monitor would be capturing the mix of ambient PM10-2.5
covered by the proposed indicator. As such, the proposed indicator does
not present the type of over-inclusion or under-inclusion problems
noted by the court with respect to a PM10 indicator (see
American Trucking Associations v. EPA, 175 F.3d at 1054), since the
application of the proposed indicator would result in compliance being
based on measurement of the mix of ambient PM10-2.5 at which
the standard is directed.
    The regulation for the proposed thoracic coarse particle indicator
states that ``[a]gricultural sources, mining sources, and other similar
sources of crustal material shall not be subject to control in meeting
this standard.'' This proposed language reflects that the information
supporting the proposed standard for thoracic coarse particles does not
support extending controls to thoracic coarse particles from
agricultural, mining sources, and other similar sources of crustal
material. This statement in the regulations therefore is designed to
make clear that there is no need nor basis to control these sources to
obtain the public health benefits intended by the proposed indicator.
    Although the Administrator believes that an indicator qualified
through reference to these categories and named sources appropriately
identifies the ambient mixes that the epidemiologic studies indicate
are of concern to public health, he solicits comment as to whether
there may be other classes of sources which should also be included or
excluded from the indicator. More generally, comment is also solicited
on the approach of defining the indicator in terms of both particle
size and categories of named sources.
    The Administrator recognizes that the proposed indicator, which
includes considerations beyond particle size in its definition,
represents a shift in the way in which PM indicators have been defined
historically, and thus poses new challenges in ensuring a common
understanding of how it can be appropriately and consistently
implemented in areas across the country. In the Administrator's view,
the application of this proposed indicator in conjunction with the
proposed monitoring network design criteria, published elsewhere in
today's Federal Register, and proposed rules for the treatment of air
quality data influenced by exceptional events that will be published in
the near future, will facilitate appropriate and consistent
implementation.

E. Averaging Time of Primary PM10-2.5 Standard

    In the last review, EPA retained both 24-hour and annual
PM10 standards to provide protection against the known and
potential effects of short- and long-term exposures to thoracic coarse
particles (62 FR at 38,677-79). That decision was based in part on
qualitative considerations related to the expectation that deposition
of thoracic coarse particles in the respiratory system could aggravate
effects in individuals with asthma. In addition, quantitative support
for retaining a 24-hour standard came from limited epidemiologic
evidence suggesting that aggravation of asthma and respiratory
infection and symptoms may be associated with daily or episodic
increases in PM10, where dominated by thoracic coarse
particles including fugitive dust. The decision to retain an annual
standard as well was generally based on considerations of the
plausibility of the potential build-up of insoluble thoracic coarse
particles in the lung after long-term exposures to high levels of such
particles.
    New information available in this review on thoracic coarse
particles, discussed above, includes several epidemiologic studies that
report statistically significant associations between short-term (24-
hour) exposure to PM10-2.5 and various morbidity effects and
mortality. With regard to long-term exposure studies, while one recent
study conducted in southern California reported a link between reduced
lung function growth and long-term exposure to PM10-2.5 and
PM2.5, other such studies reported no associations (EPA,
2005a, p. 3-19, 3-23-24). Thus, the Criteria Document concludes that
the available evidence does not suggest an association with long-term
exposure to PM10-2.5 (EPA, 2004, p. 9-79).
    Based on these considerations, the Staff Paper concludes that the
newly available evidence continues to support a 24-hour averaging time
for a standard intended to control thoracic coarse particles, based
primarily on evidence suggestive of associations between short-term
(24-hour) exposure and morbidity effects and, to a lesser degree,
mortality. Noting the absence of evidence judged to be suggestive of an
association with long-term exposures, the Staff Paper concludes that
there is no quantitative evidence that directly supports an annual
standard, while recognizing that it could be appropriate to consider an
annual standard to provide a margin of safety against possible effects
related to long-term exposure to thoracic coarse particles that future
research may reveal. The Staff Paper observes, however, that a 24-hour
standard that would reduce 24-hour exposures would also likely reduce
long-term average exposures, thus providing some margin of safety
against the possibility of health effects associated with long-term
exposures (EPA, 2005a, p. 5-61).
    Based on its review of the Staff Paper, CASAC recommends retention
of a 24-hour averaging time and agrees that an annual averaging time
for PM10-2.5 is not currently warranted (Henderson, 2005b).
Based on these considerations, the Administrator concurs with staff and
CASAC recommendations, and provisionally concludes that the newly
available evidence continues to support a 24-hour averaging time for a
PM10-2.5 standard, based primarily on evidence suggestive of
associations between

short-term (24-hour) exposure and morbidity effects and, to a lesser
degree, mortality. Further, the Administrator agrees that an annual
PM10-2.5 standard is not warranted at this time. Thus, the
Administrator proposes to revoke the annual PM10 standard
and is not proposing an annual PM10-2.5 standard.

F. Form of Primary PM10-2.5 Standard

    For reasons similar to those discussed above in section II.F.2 on
the form of the 24-hour PM2.5 standard, the Staff Paper also
recommends consideration of either the 98th or 99th percentile form for
a 24-hour PM10-2.5 standard. The relative year-to-year
stability of the air quality statistic to be used as the basis for the
form of a PM10-2.5 standard is of particular importance for
a PM10-2.5 standard, since the nature and magnitude of the
uncertainties in the risk assessment conducted for thoracic coarse
particles weighed against considering risk estimates as a basis for
comparing alternative combinations of specific forms and levels of
standards.
    In considering the information provided in the Staff Paper, CASAC
strongly recommends use of the 98th percentile form because it is more
statistically robust than the 99th percentile form, together with the
use of a three-year average of this statistic (Henderson 2005b). In
making this recommendation, CASAC notes that the use of this statistic
will tend to minimize ``measurement error and spatial variability,
which are larger for coarse-mode particles than for fine PM'' as well
as ``the influence in arid areas of occasional but extreme excursion
contributions from rural, coarse-mode dust sources that are thought to
be inherently less toxic than coarse-mode particles heavily enriched
with urban source contaminants'' (Henderson, 2005b).
    In considering the available information, the Administrator concurs
with the CASAC recommendation and proposes that the form of the 24-hour
PM10-2.5 standard be based on the annual 98th percentile
statistic, averaged over three years.

G. Level of Primary PM10-2.5 Standard

    In considering the available evidence on associations between
short-term PM10-2.5 concentrations and morbidity and
mortality effects as a basis for setting a 24-hour standard for
thoracic coarse particles, the Staff Paper focuses on relevant U.S. and
Canadian epidemiologic studies, as discussed above in section II.A. As
an initial matter, the Staff Paper recognizes that these individual
short-term exposure studies provide no evidence of clear population
thresholds, or lowest-observed-effects levels, in terms of 24-hour
average concentrations. As a consequence, this body of evidence is
difficult to translate directly into a specific 24-hour standard that
would protect against the range of effects that have been associated
with short-term exposures.
    In considering the evidence, the Staff Paper notes the significant
uncertainties and the limited nature of the available evidence. In
examining the available evidence to identify a basis for a range of
standard levels that would be appropriate for consideration, the Staff
Paper focuses on the upper end of the distributions of daily
PM10-2.5 concentrations in the relevant studies in terms of
the 98th and 99th percentile values.\68\
---------------------------------------------------------------------------

    \68\ This examination of the evidence is based on air quality
information and analyses presented in two staff memos which were
part of the materials reviewed by CASAC (Ross and Langstaff, 2005;
Ross, 2005).
---------------------------------------------------------------------------

    In looking first at the morbidity studies that report statistically
significant associations with respiratory- and cardiac-related hospital
admissions in Toronto (Burnett et al., 1997), Seattle (Sheppard et al.,
2003), and Detroit (Ito, 2003), the 98th percentile values reported in
these studies range from approximately 30 to 36 [mu]g/m\3\. To provide
some perspective on these PM10-2.5 levels, the Staff Paper
notes that the level of the 24-hour PM10 standard was
exceeded only on a few occasions during the time periods of the studies
in Detroit and Seattle.\69\ In looking also at the mortality studies
that report statistically significant and generally robust associations