[Federal Register: January 17, 2006 (Volume 71, Number 10)]
[Proposed Rules]
[Page 2619-2708]
[DOCID:fr17ja06-21]

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Part II

Environmental Protection Agency

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40 CFR Part 50

National Ambient Air Quality Standards for Particulate Matter; Proposed
Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[OAR-2001-0017; FRL-8015-8]
RIN 2060-AI44

National Ambient Air Quality Standards for Particulate Matter

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Based on its review of the air quality criteria and national
ambient air quality standards (NAAQS) for particulate matter (PM), EPA
proposes to make revisions to the primary and secondary NAAQS for PM to
provide requisite protection of public health and welfare,
respectively, and to make corresponding revisions in monitoring
reference methods and data handling conventions for PM.
    With regard to primary standards for fine particles (particles
generally less than or equal to 2.5 micrometers ([mu]m) in diameter,
PM2.5), EPA proposes to revise the level of the 24-hour
PM2.5 standard to 35 micrograms per cubic meter ([mu]g/
m3), providing increased protection against health effects
associated with short-term exposure (including premature mortality and
increased hospital admissions and emergency room visits) and to retain
the level of the annual PM2.5 standard at 15 [mu]g/
m3, continuing protection against health effects associated
with long-term exposure (including premature mortality and development
of chronic respiratory disease). The EPA solicits comment on
alternative levels of the 24-hour PM2.5 standard (down to 25
[mu]g/m3 and up to 65 [mu]g/m3) and the annual
PM2.5 standard (down to 12 [mu]g/m3), and on
alternative approaches for selecting the standard levels.
    With regard to primary standards for particles generally less than
or equal to 10 [mu]m in diameter (PM10), EPA proposes to
revise the 24-hour PM10 standard in part by establishing a
new indicator for thoracic coarse particles (particles generally
between 2.5 and 10 [mu]m in diameter, PM10-2.5), 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. The EPA proposes to set the new PM10-2.5
standard at a level of 70 [mu]g/m3, continuing to provide a
generally equivalent level of protection against health effects
associated with short-term exposure (including hospital admissions for
cardiopulmonary diseases, increased respiratory symptoms and possibly
premature mortality). Also, EPA proposes to revoke, upon finalization
of a primary 24-hour standard for PM10-2.5, the current 24-
hour PM10 standard in all areas of the country except in
areas where there is at least one monitor located in an urbanized area
(as defined by the U.S. Bureau of the Census) with a minimum population
of 100,000 that violates the current 24-hour PM10 standard
based on the most recent three years of data. In addition, EPA proposes
to revoke the current annual PM10 standard upon promulgation
of this rule. The EPA solicits comment on alternative approaches for
selecting the level of a 24-hour PM10-2.5 standard, on
alternative approaches based on retaining the current 24-hour
PM10 standard, and on revoking and not replacing the 24-hour
PM10 standard.
    With regard to secondary PM standards, EPA proposes to revise the
current standards by making them identical to the suite of proposed
primary standards for fine and coarse particles, providing protection
against PM-related public welfare effects including visibility
impairment, effects on vegetation and ecosystems, and materials damage
and soiling. Also, EPA solicits comment on adding a new sub-daily
PM2.5 standard to address visibility impairment.

DATES: Written comments on this proposed decision must be received by
April 17, 2006.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2001-0017 by one of the following methods:
     http://www.regulations.gov: Follow the on-line

instructions for submitting comments.
     E-mail<EMAIL_ADDRESS>     Fax:<PHONE_NUMBER>.
     Mail: Docket ID No. EPA-HQ-OAR-2001-0017, Environmental
Protection Agency, Mailcode: 6102T, 1200 Pennsylvania Avenue, NW.,
Washington, DC 20460. Please include a total of two copies.
     Hand Delivery: Environmental Protection Agency, EPA West
Building, Room B102, 1301 Constitution Avenue, NW., Washington, DC.
Such deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2001-0017. The EPA's policy is that all comments received will be
included in the public docket without change and may be made available
online at http://www.regulations.gov, including any personal

information provided, unless the comment includes information claimed
to be Confidential Business Information (CBI) or other information
whose disclosure is restricted by statute. Do not submit information
that you consider to be CBI or otherwise protected through http://www.regulations.gov or e-mail. The http://www.regulations.gov Web site

is an ``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through http://www.regulations.gov your e-mail address will be

automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses. For additional information about EPA's public
docket visit the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm
.

    Docket: All documents in the docket are listed in the http://www.regulations.gov
 index. Although listed in the index, some

information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the Air and Radiation

Docket and Information Center, EPA/DC, EPA West, Room B102, 1301
Constitution Ave., NW., Washington, DC. The Public Reading Room is open
from 8:30 a.m. to 4:30 p.m. Monday through Friday, excluding legal
holidays. The telephone number for the Public Reading Room is 202-566-
1744 and the telephone number for the Air and Radiation Docket and
Information Center is<PHONE_NUMBER>.
    Public Hearings: The EPA intends to hold public hearings around the
end of

February in Philadelphia, Chicago, and San Francisco, and will announce
in a separate Federal Register notice the date, time, and address of
the public hearings on this proposed decision.

FOR FURTHER INFORMATION CONTACT: Dr. Erika Sasser, mail code C539-01,
Air Quality Strategies and Standards Division, Office of Air Quality
Planning and Standards, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711, telephone:<PHONE_NUMBER>, e-mail:
<EMAIL_ADDRESS>

SUPPLEMENTARY INFORMATION:

General Information

A. What Should I Consider As I Prepare My Comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through
http://www.regulations.gov or e-mail. Clearly mark the part or all of

the information that you claim to be CBI. For CBI information in a disk
or CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM
as CBI and then identify electronically within the disk or CD-ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments,
remember to:
     Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
     Follow directions--The agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree; suggest alternatives
and substitute language for your requested changes.
     Describe any assumptions and provide any technical
information and/or data that you used.
     If you estimate potential costs or burdens, explain how
you arrived at your estimate in sufficient detail to allow for it to be
reproduced.
     Provide specific examples to illustrate your concerns, and
suggest alternatives.
     Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
     Make sure to submit your comments by the comment period
deadline identified.

Availability of Related Information

    A number of documents are available on EPA Web sites. The Air
Quality Criteria for Particulate Matter (Criteria Document) (two
volumes, EPA/600/P-99/002aF and EPA/600/P-99/002bF, October 2004) is
available on EPA's National Center for Environmental Assessment Web
site. To obtain this document, go to http://www.epa.gov/ncea, and click

on ``Particulate Matter''. The Staff Paper, human health risk
assessment, and several other related technical documents are available
on EPA's Office of Air Quality Planning and Standards (OAQPS)
Technology Transfer Network (TTN) Web site. The Staff Paper is
available at http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html
, and the risk assessment and technical documents are available

at http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_td.html. These

and other related documents are also available for inspection and
copying in the EPA docket identified above.

Table of Contents

    The following topics are discussed in today's preamble:

I. Background
    A. Legislative Requirements
    B. Review of Air Quality Criteria and Standards for PM
    C. Related Control Programs to Implement PM Standards
    D. Overview of Current PM NAAQS Review
II. Rationale for Proposed Decisions on Primary PM2.5
Standards
    A. Health Effects Related to Exposure to Fine Particles
    1. Mechanisms
    2. Nature of Effects
    3. Integration and Interpretation of the Health Evidence
    4. Sensitive Subgroups for PM2.5-Related Effects
    5. PM2.5-Related Impacts on Public Health
    B. Quantitative Risk Assessment
    1. Overview
    2. Scope and Key Components
    3. Risk Estimates and Key Observations
    C. Need for Revision of the Current Primary PM2.5
Standards
    D. Indicator of Fine Particles
    E. Averaging Time of Primary PM2.5 Standards
    F. Form of Primary PM2.5 Standards
    1. 24-Hour PM2.5 Standard
    2. Annual PM2.5 Standard
    G. Level of Primary PM2.5 Standards
    1. 24-Hour PM2.5 Standard
    2. Annual PM2.5 Standard
    H. Proposed Decisions on Primary PM2.5 Standards
III. Rationale for Proposed Decisions on the Primary PM10
Standards
    A. Health Effects Related to Exposure to Thoracic Coarse
Particles
    1. Mechanisms
    2. Nature of Effects
    3. Integration and Interpretation of the Health Evidence
    4. Sensitive Subgroups for Effects of Thoracic Coarse Particle
Exposure
    5. Impacts on Public Health from Thoracic Coarse Particle
Exposure
    B. Quantitative Risk Assessment
    C. Need for Revision of the Current Primary PM10
Standards
    D. Indicator of Thoracic Coarse Particles
    E. Averaging Time of Primary PM10-2.5 Standard
    F. Form of Primary PM10-2.5 Standard
    G. Level of Primary PM10-2.5 Standard
    H. Proposed Decisions on Primary PM10-2.5 Standard
IV. Rationale for Proposed Decisions on Secondary PM Standards
    A. Visibility Impairment
    1. Visibility Impairment Related to Ambient PM
    2. Need for Revision of the Current Secondary PM Standards for
Visibility Protection
    3. Indicator of PM for Secondary Standard to Address Visibility
Impairment
    4. Averaging Time of a Secondary PM2.5 Standard for
Visibility Protection
    5. Elements of a Secondary PM2.5 Standard for
Visibility Protection
    B. Other PM-related Welfare Effects
    1. Nature of Effects
    2. Need for Revision of Current Secondary PM Standards to
Address Other PM-related Welfare Effects
    C. Proposed Decision on Secondary PM Standards
V. Interpretation of the NAAQS for PM
    A. Proposed Amendments to Appendix N--Interpretation of the
National Ambient Air Quality Standards for PM2.5
    1. General
    2. PM2.5 Monitoring and Data Reporting Considerations
    3. PM2.5 Computations and Data Handling Conventions
    4. Secondary Standard
    5. Conforming Revisions
    B. Proposed Appendix P--Interpretation of the National Ambient
Air Quality Standards for PM10-2.5
    1. General
    2. PM2.5 Data Reporting Considerations
    3. PM10-2.5 Computations and Data Handling
Conventions
    4. Exceptional Events
VI. Reference Methods for the Determination of Particulate Matter as
PM2.5 and PM10-2.5
    A. Proposed Appendix O: Reference Method for the Determination
of Coarse Particulate Matter (as PM10-2.5) in the
Atmosphere
    1. Purpose of the New Reference Method
    2. Rationale for Selection of the New Reference Method
    3. Consideration of Other Methods for the Federal Reference
Method
    4. Consideration of Automated Method
    5. Relationship of Proposed FRM to Transportation Equity Act
Requirements
    6. Use of the Proposed Federal Reference Method

    7. Basic Requirements of the Proposed Federal Reference Method
Sampler
    8. Other Important Aspects of the Proposed Federal Reference
Method Sampler
    B. Proposed Amendments to Appendix L--Reference Method for the
Determination of Fine Particulate Matter (as PM2.5) in
the Atmosphere
    VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children from
Environmental Health and Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution or Use
    I. National Technology Transfer Advancement Act
    J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
References

I. Background

A. Legislative Requirements

    Two sections of the Clean Air Act (CAA) govern the establishment
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list ``air pollutants'' that ``in his
judgment, may reasonably be anticipated to endanger public health and
welfare'' and whose ``presence * * * in the ambient air results from
numerous or diverse mobile or stationary sources'' and to issue air
quality criteria for those that are listed. Air quality criteria are
intended to ``accurately reflect the latest scientific knowledge useful
in indicating the kind and extent of identifiable effects on public
health or welfare which may be expected from the presence of [a]
pollutant in ambient air * * *.''
    Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants
listed under section 108. Section 109(b)(1) defines a primary standard
as one ``the attainment and maintenance of which in the judgment of the
Administrator, based on such criteria and allowing an adequate margin
of safety, are requisite to protect the public health.'' \1\ A
secondary standard, as defined in section 109(b)(2), must ``specify a
level of air quality the attainment and maintenance of which, in the
judgment of the Administrator, based on such criteria, is requisite to
protect the public welfare from any known or anticipated adverse
effects associated with the presence of [the] pollutant in the ambient
air.'' \2\
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    \1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level * * * which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group'' [S.
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
    \2\ Welfare effects as defined in section 302(h) [42 U.S.C.
7602(h)] include, but are not limited to, ``effects on soils, water,
crops, vegetation, man-made materials, animals, wildlife, weather,
visibility and climate, damage to and deterioration of property, and
hazards to transportation, as well as effects on economic values and
on personal comfort and well-being.''
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    In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. In establishing ``requisite'' primary and
secondary standards, EPA may not consider the costs of implementing the
standards. See generally Whitman v. American Trucking Associations, 531
U.S. 457, 465-472, 475-76 (2001).
    The requirement that primary standards include an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert.
denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are
components of the risk associated with pollution at levels below those
at which human health effects can be said to occur with reasonable
scientific certainty. Thus, in selecting primary standards that include
an adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollutant levels that may pose an unacceptable
risk of harm, even if the risk is not precisely identified as to nature
or degree. The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration
levels (see Lead Industries Association v. EPA, supra, 647 F.2d at 1156
n. 51), but rather at a level that reduces risk sufficiently so as to
protect public health with an adequate margin of safety.
    In addressing the requirement for an adequate margin of safety, EPA
considers such factors as the nature and severity of the health effects
involved, the size of the sensitive population(s) at risk, and the kind
and degree of the uncertainties that must be addressed. The selection
of any particular approach to providing an adequate margin of safety is
a policy choice left specifically to the Administrator's judgment. Lead
Industries Association v. EPA, supra, 647 F.2d at 1161-62.
    Section 109(d)(1) of the CAA requires that ``not later than
December 31, 1980, and at 5-year intervals thereafter, the
Administrator shall complete a thorough review of the criteria
published under section 108 and the national ambient air quality
standards * * * and shall make such revisions in such criteria and
standards and promulgate such new standards as may be appropriate * *
*.'' Section 109(d)(2) requires that an independent scientific review
committee ``shall complete a review of the criteria * * * and the
national primary and secondary ambient air quality standards * * * and
shall recommend to the Administrator any new * * * standards and
revisions of existing criteria and standards as may be appropriate * *
*.'' This independent review function is performed by the Clean Air
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.

B. Review of Air Quality Criteria and Standards for PM

    Particulate matter is the generic term for a broad class of
chemically and physically diverse substances that exist as discrete
particles (liquid droplets or solids) over a wide range of sizes.
Particles originate from a variety of anthropogenic stationary and
mobile sources as well as from natural sources. Particles may be
emitted directly or formed in the atmosphere by transformations of
gaseous emissions such as sulfur oxides (SOX), nitrogen
oxides (NOX), and volatile organic compounds (VOC). The
chemical and physical properties of PM vary greatly with time, region,
meteorology, and source category, thus complicating the assessment of
health and welfare effects.
    The last review of PM air quality criteria and standards was
completed in July 1997 with notice of a final decision to revise the
existing standards (62 FR 38652, July 18, 1997). In that decision, EPA
revised the PM NAAQS in several respects. While EPA determined that the
PM NAAQS should continue to focus on particles less than or equal to 10
[mu]m in

diameter (PM10), EPA also determined that the fine and
coarse fractions of PM10 should be considered separately.
The EPA added new standards, using PM2.5 as the indicator
for fine particles (with PM2.5 referring to particles with a
nominal mean aerodynamic diameter less than or equal to 2.5 [mu]m), and
retained PM10 standards for the purpose of regulating the
coarse fraction of PM10 (referred to as thoracic coarse
particles or coarse-fraction particles; generally including particles
with a nominal mean aerodynamic diameter greater than 2.5 [mu]m and
less than or equal to 10 [mu]m, or PM10-2.5). The EPA
established two new PM2.5 standards: an annual standard of
15 [mu]g/m3, based on the 3-year average of annual
arithmetic mean PM2.5 concentrations from single or multiple
community-oriented monitors; and a 24-hour standard of 65 [mu]g/
m3, based on the 3-year average of the 98th percentile of
24-hour PM2.5 concentrations at each population-oriented
monitor within an area. Also, EPA established a new reference method
for the measurement of PM2.5 in the ambient air and adopted
rules for determining attainment of the new standards. To continue to
address thoracic coarse particles, EPA retained the annual
PM10 standard, while revising the form, but not the level,
of the 24-hour PM10 standard to be based on the 99th
percentile of 24-hour PM10 concentrations at each monitor in
an area. The EPA revised the secondary standards by making them
identical in all respects to the primary standards.
    Following promulgation of the revised PM NAAQS, petitions for
review were filed by a large number of parties, addressing a broad
range of issues. In May 1999, a three-judge panel of the U.S. Court of
Appeals for the District of Columbia Circuit issued an initial decision
that upheld EPA's decision to establish fine particle standards,
holding that ``the growing empirical evidence demonstrating a
relationship between fine particle pollution and adverse health effects
amply justifies establishment of new fine particle standards.''
American Trucking Associations v. EPA, 175 F.3d 1027, 1055-56 (D.C.
Cir. 1999) (rehearing granted in part and denied in part, 195 F.3d 4
(D.C. Cir. 1999), affirmed in part and reversed in part, Whitman v.
American Trucking Associations, 531 U.S. 457 (2001). The Panel also
found ``ample support'' for EPA's decision to regulate coarse particle
pollution, but vacated the 1997 PM10 standards, concluding
in part that PM10 is a ``poorly matched indicator for coarse
particulate pollution'' because it includes fine particles. Id. at
1053-55. Pursuant to the court's decision, EPA removed the vacated 1997
PM10 standards from the Code of Federal Regulations (CFR)
(69 FR 45592, July 30, 2004) and deleted the regulatory provision (at
40 CFR 50.6(d)) that controlled the transition from the pre-existing
1987 PM10 standards to the 1997 PM10 standards
(65 FR 80776, December 22, 2000). The pre-existing 1987 PM10
standards remained in place. Id. at 80777.
    More generally, the three-judge panel held (with one dissenting
opinion) that EPA's approach to establishing the level of the standards
in 1997, both for PM and for ozone NAAQS promulgated on the same day,
effected ``an unconstitutional delegation of legislative authority.''
Id. at 1034-40. Although the panel stated that ``the factors EPA uses
in determining the degree of public health concern associated with
different levels of ozone and PM are reasonable,'' it remanded the rule
to EPA, stating that when EPA considers these factors for potential
non-threshold pollutants ``what EPA lacks is any determinate criterion
for drawing lines'' to determine where the standards should be set.
Consistent with EPA's long-standing interpretation, the panel also
reaffirmed prior rulings holding that in setting NAAQS EPA is ``not
permitted to consider the cost of implementing those standards.'' Id.
at 1040-41.
    Both sides filed cross appeals on these issues to the United States
Supreme Court, and the Court granted certiorari. In February 2001, the
Supreme Court issued a unanimous decision upholding EPA's position on
both the constitutional and cost issues. Whitman v. American Trucking
Associations, 531 U.S. 457, 464, 475-76. On the constitutional issue,
the Court held that the statutory requirement that NAAQS be
``requisite'' to protect public health with an adequate margin of
safety sufficiently guided EPA's discretion, affirming EPA's approach
of setting standards that are neither more nor less stringent than
necessary. The Supreme Court remanded the case to the Court of Appeals
for resolution of any remaining issues that had not been addressed in
that court's earlier rulings. Id. at 475-76. In March 2002, the Court
of Appeals rejected all remaining challenges to the standards, holding
under the traditional standard of judicial review that EPA's
PM2.5 standards were reasonably supported by the
administrative record and were not ``arbitrary and capricious.''
American Trucking Associations v. EPA, 283 F.3d 355, 369-72 (D.C. Cir.
2002).
    In October 1997, EPA published its plans for the current periodic
review of the PM criteria and NAAQS (62 FR 55201, October 23, 1997),
including the 1997 PM2.5 standards and the 1987
PM10 standards. As part of the process of preparing an
updated Air Quality Criteria Document for Particulate Matter
(henceforth, the ``Criteria Document''), EPA's National Center for
Environmental Assessment (NCEA) hosted a peer review workshop in April
1999 on drafts of key Criteria Document chapters. The first external
review draft Criteria Document was reviewed by CASAC and the public at
a meeting held in December 1999. Based on CASAC and public comment,
NCEA revised the draft Criteria Document and released a second draft in
March 2001 for review by CASAC and the public at a meeting held in July
2001. A preliminary draft of a staff paper, Review of the National
Ambient Air Quality Standards for Particulate Matter: Assessment of
Scientific and Technical Information (henceforth, the ``Staff Paper'')
prepared by EPA's Office of Air Quality Planning and Standards (OAQPS)
was released in June 2001 for public comment and for consultation with
CASAC at the same public meeting. Taking into account CASAC and public
comments, a third draft Criteria Document was released in May 2002 for
review at a meeting held in July 2002.
    Shortly after the release of the third draft Criteria Document, the
Health Effects Institute (HEI) \3\ announced that researchers at Johns
Hopkins University had discovered problems with applications of
statistical software used in a number of important epidemiological
studies that had been discussed in that draft Criteria Document. In
response to this significant issue, EPA took steps in consultation with
CASAC to encourage researchers to reanalyze affected studies and to
submit them expeditiously for peer review by a special expert panel
convened at EPA's request by HEI. The results of this reanalysis and
peer-review process were subsequently incorporated into a fourth draft
Criteria Document, which was released in June 2003 and reviewed by
CASAC and the public at a meeting held in August 2003.
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    \3\ The HEI is an independent research institute, jointly
sponsored by EPA and a group of U.S. manufacturers and marketers of
motor vehicles and engines, that conducts health effects research on
major air pollutants related to motor vehicle emissions.
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    The first draft Staff Paper, based on the fourth draft Criteria
Document, was released at the end of August 2003, and was reviewed by
CASAC and the public at a meeting held in November 2003.

During that meeting, EPA also consulted with CASAC on a new framework
for the final chapter (integrative synthesis) of the Criteria Document
and on ongoing revisions to other Criteria Document chapters to address
previous CASAC comments. The EPA held additional consultations with
CASAC at public meetings held in February, July, and September 2004,
leading to publication of the final Criteria Document in October 2004.
The second draft Staff Paper, based on the final Criteria Document, was
released at the end of January 2005, and was reviewed by CASAC and the
public at a meeting held in April 2005. The CASAC's advice and
recommendations to the Administrator, based on its review of the second
draft Staff Paper, were further discussed during a public
teleconference held in May 2005 and are provided in a June 6, 2005
letter to the Administrator (Henderson, 2005a). The final Staff Paper,
issued in June, 2005, takes into account the advice and recommendations
of CASAC and public comments received on the earlier drafts of this
document. The Administrator subsequently received additional advice and
recommendations from the CASAC, specifically on potential standards for
thoracic coarse particles in a teleconference on August 11, 2005, and
in a letter to the Administrator dated September 15, 2005 (Henderson,
2005b).\4\
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    \4\ The EPA has posted on its Web site (http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html
) a second edition of the Staff

Paper which was prepared for the purpose of including as an
attachment this September 2005 letter from CASAC.
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    The schedule for completion of this review is governed by a consent
decree resolving a lawsuit filed in March 2003 by a group of plaintiffs
representing national environmental organizations. The lawsuit alleged
that EPA had failed to perform its mandatory duty, under section
109(d)(1), of completing the current review within the period provided
by statute. American Lung Association v. Whitman (No. 1:03CV00778,
D.D.C. 2003). An initial consent decree was entered by the court in
July 2003 after an opportunity for public comment. The consent decree,
as modified by the court, provides that EPA will sign for publication
notices of proposed and final rulemaking concerning its review of the
PM NAAQS no later than December 20, 2005 and September 27, 2006,
respectively.

C. Related Control Programs to Implement PM Standards

    States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the CAA (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA approval, State
implementation plans (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to
sources of the pollutants involved. The States, in conjunction with
EPA, also administer the prevention of significant deterioration (PSD)
program (42 U.S.C. 7470-7479) for these pollutants. In addition,
Federal programs provide for nationwide reductions in emissions of
these and other air pollutants through the Federal Mobile Source
Control Program under title II of the CAA (42 U.S.C. 7521-7574), which
involves controls for automobile, truck, bus, motorcycle, nonroad or
off-highway, and aircraft emissions; the new source performance
standards under section 111 (42 U.S.C. 7411); and the national emission
standards for hazardous air pollutants under section 112 (42 U.S.C.
7412).
    As described in a recent EPA report, The Particle Pollution Report:
Current Understanding of Air Quality and Emissions through 2003 (EPA,
2004b), State and Federal programs have made substantial progress in
reducing ambient concentrations of PM10 and
PM2.5. For example, PM10 concentrations have
decreased 31 percent nationally since 1988. Regionally, PM10
concentrations decreased most in areas with historically higher
concentrations--the Northwest (39 percent decline), the Southwest (33
percent decline), and southern California (35 percent decline). Direct
emissions of PM10 have decreased approximately 25 percent
nationally since 1988.
    Programs aimed at reducing direct emissions of particles have
played an important role in reducing PM10 concentrations,
particularly in western areas. Some examples of PM10
controls include paving unpaved roads and using best management
practices for agricultural sources of resuspended soil. Additionally,
EPA's Acid Rain Program has substantially reduced sulfur dioxide
(SO2) emissions from power plants since 1995 in the eastern
United States, contributing to lower PM concentrations. Of the 87 areas
that were designated nonattainment for PM10 in the early
1990s, 64 now meet those standards. In cities that have not attained
the PM10 standards, the number of days above the standards
is down significantly.
    Nationally, PM2.5 concentrations have declined by 10
percent from 1999 to 2003. Generally, PM2.5 concentrations
have also declined the most in regions with the highest
concentrations--the Southeast (20 percent decline), southern California
(16 percent decline), and the Industrial Midwest (9 percent decline).
With the exception of the Northeast, the remaining regions posted
modest declines in PM2.5 concentrations from 1999 to 2003.
Direct emissions of PM2.5 have decreased by 5 percent
nationally over the past 5 years.
    National programs that affect regional emissions have contributed
to lower sulfate concentrations and, consequently, to lower
PM2.5 concentrations, particularly in the Industrial Midwest
and Southeast. National ozone-reduction programs designed to reduce
emissions of volatile organic compounds (VOCs) and nitrogen oxides
(NOX) also have helped reduce carbon and nitrates, both of
which are components of PM2.5. Nationally, SO2
emissions have declined 9 percent, NOX emissions have
declined 9 percent, and VOC emissions have declined by 12 percent from
1999 to 2003. In eastern States affected by the Acid Rain Program,
sulfates decreased 7 percent over the same period.
    Over the next 10 to 20 years, national and regional regulations
will make major reductions in ambient PM2.5 levels. The
Clean Air Interstate Rule (CAIR) and the NOX SIP Call will
reduce SO2 and NOX emissions from electric
generating units and industrial boilers across the eastern half of the
U.S., regulations to implement the current ambient air quality
standards for PM2.5 will require direct PM2.5 and
PM2.5 precursor controls in nonattainment areas, and new
national mobile source regulations affecting heavy-duty diesel engines,
highway vehicles, and other mobile sources will reduce emissions of
NOX, direct PM2.5, SO2, and VOCs. The
EPA estimates that these regulations for stationary and mobile sources
will cut SO2 emissions by 6 million tons annually in 2015
from 2001 levels. Emissions of NOX will be cut by 9 million
tons annually in 2015 from 2001 levels. Emissions of VOCs will drop by
3 million tons, and direct PM2.5 emissions will be cut by
200,000 tons in 2015, compared to 2001 levels.
    Modeling done by EPA indicates that by 2010, 18 of the 39 areas
currently not attaining the PM2.5 standards will come into
attainment just based on regulatory programs already in place,
including CAIR, the Clean Diesel Rules, and other Federal measures.
Four more PM2.5 areas are projected to attain the standards
by 2015 based on the implementation of these programs. All areas in the
eastern U.S. will have lower PM2.5 concentrations in 2015
relative to present-day conditions. In most cases,

the predicted improvement in PM2.5 ranges from 10 percent to
20 percent.

D. Overview of Current PM NAAQS Review

    This action presents the Administrator's proposed decisions on the
review of the current primary and secondary PM2.5 and
PM10 standards. Primary standards for fine particles and for
thoracic coarse particles are addressed separately below in sections II
and III, respectively, consistent with the decision made by EPA in the
last review and with the conclusions in the Criteria Document and Staff
Paper that fine and thoracic coarse particles should continue to be
considered as separate subclasses of PM pollution. Thus, the principal
focus of this current review of the air quality criteria and primary
standards for PM is on evidence of health effects and risks related to
exposures to fine particles and to thoracic coarse particles. Secondary
standards for fine and coarse-fraction particles are addressed below in
section IV.
    Past and current decisions to address fine particles and thoracic
coarse particles separately are based in part on long-established
information on differences in sources, properties, and atmospheric
behavior between fine and coarse particles (EPA, 2005a, section 2.2).
Fine particles are produced chiefly by combustion processes and by
atmospheric reactions of various gaseous pollutants, whereas thoracic
coarse particles are generally emitted directly as particles as a
result of mechanical processes that crush or grind larger particles or
the resuspension of dusts. Sources of fine particles include, for
example, motor vehicles, power generation, combustion sources at
industrial facilities, and residential fuel burning. Sources of
thoracic coarse particles include, for example, resuspension of
traffic-related emissions such as tire and brake lining materials,
direct emissions from industrial operations, construction and
demolition activities, and agricultural and mining operations. Fine
particles can remain suspended in the atmosphere for days to weeks and
can be transported thousands of kilometers, whereas thoracic coarse
particles generally deposit rapidly on the ground or other surfaces and
are not readily transported across urban or broader areas. The approach
in this review to continue to address fine and thoracic coarse
particles separately is reinforced by new information that advances our
understanding of differences in human exposure relationships and
dosimetric patterns characteristic of these two subclasses of PM
pollution, as well as the apparent independence of health effects that
have been associated with them in epidemiologic studies (EPA, 2004,
section 3.2.3). See also American Trucking Associations v. EPA, 175 F.
3d at 1053-54, 1055-56 (EPA justified in establishing separate
standards for fine and thoracic coarse particles).
    Today's proposed decisions separately addressing fine and coarse
particles are based on a thorough review in the Criteria Document of
the latest scientific information on known and potential human health
and welfare effects associated with exposure to these subclasses of PM
at levels typically found in the ambient air. These proposed decisions
also take into account: (1) Staff assessments in the Staff Paper of the
most policy-relevant information in the Criteria Document and as well
as a quantitative risk assessment; (2) CASAC advice and
recommendations, as reflected in the CASAC's letters to the
Administrator, discussions of drafts of the Criteria Document and Staff
Paper at public meetings, and separate written comments prepared by
individual members of the CASAC PM Review Panel \5\ (henceforth,
``CASAC Panel''), and (3) public comments received during the
development of these documents, either in connection with CASAC
meetings or separately.
---------------------------------------------------------------------------

    \5\ The CASAC PM Review Panel is comprised of the seven members
of the chartered CASAC, supplemented by fifteen subject-matter
experts appointed by the Administrator to provide the types of
scientific expertise relevant to this review of the PM NAAQS.
---------------------------------------------------------------------------

    The EPA is aware that a number of new scientific studies on the
health effects of PM have been published since the 2002 cutoff date for
inclusion in the Criteria Document. As in the last PM NAAQS review, EPA
intends to conduct a review and assessment of any significant new
studies published since the close of the Criteria Document, including
studies submitted during the public comment period in order to ensure
that, before making a final decision, the Administrator is fully aware
of the new science that has developed since 2002. In this assessment,
EPA will examine these new studies in light of the literature evaluated
in the Criteria Document. This assessment and a summary of the key
conclusions will be placed in the rulemaking docket. A preliminary list
of potentially significant new studies identified to date has been
compiled and placed in the rulemaking docket for this proposal, and EPA
solicits comment on other relevant studies that may be added to this
list. This list includes a wide array of different types of studies
that are potentially relevant to various issues discussed in the
following sections, including issues related to the elements of the
standards under review.
    Throughout this preamble a number of conclusions, findings, and
determinations by the Administrator are noted. It should be understood
that these are all provisional and proposed in nature. While they
identify the reasoning that supports this proposal, they are not
intended to be final or conclusive in nature. The EPA invites comments
on all issues involved with this proposal, including all such proposed
judgments, conclusions, findings, and determinations.

II. Rationale for Proposed Decisions on Primary PM2.5 Standards

    As discussed more fully below, the rationale for the proposed
revisions of the primary PM2.5 NAAQS includes consideration
of: (1) Evidence of health effects related to short- and long-term
exposures to fine particles; (2) insights gained from a quantitative
risk assessment; and (3) specific conclusions regarding the need for
revisions to the current standards and the elements of PM2.5
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 drawn upon an integrative
synthesis of the entire body of evidence of associations between
exposure to ambient fine particles and a broad range of health
endpoints (EPA, 2004, Chapter 9), focusing on those health endpoints
for which the Criteria Document concludes that the associations are
likely to be causal. This body of evidence includes hundreds of studies
conducted in many countries around the world, using various indicators
of fine particles. In its assessment of the evidence judged to be most
relevant to making decisions on elements of the primary
PM2.5 standards, EPA has placed greater weight on U.S. and
Canadian studies using PM2.5 measurements, since studies
conducted in other countries may well reflect different demographic and
air pollution characteristics.
    As with virtually any policy-relevant scientific research, there is
uncertainty in the characterization of health effects attributable to
exposure to ambient fine particles. As discussed below, however, an
unprecedented amount of new research has been conducted since the last
review, with important new information coming from epidemiologic,
toxicologic, controlled human exposure,

and dosimetric studies. Moreover, the newly available research studies
evaluated in the Criteria Document 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 regulatory decision making 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 fine
particles and health effects.

A. Heath Effects Related to Exposure to Fine Particles

    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 fine particles and their
major constituents. The information highlighted here summarizes: (1)
New information available on potential mechanisms for health effects
associated with exposure to fine particles and constituents; (2) the
nature of the effects that have been associated with ambient fine
particles or fine particle constituents; (3) an integrative assessment
of the evidence on fine particle-related health effects; (4)
subpopulations that appear to be sensitive to effects of exposure to
fine particles; and (5) the public health impact of exposure to ambient
fine particles.
    As was true in the last review, evidence from epidemiologic studies
plays a key role in the Criteria Document's evaluation of the
scientific evidence. Some highlights of the new epidemiologic evidence
include:
    (1) New multi-city studies that use uniform methodologies to
investigate the effects of various indicators of PM on health with data
from multiple locations with varying climate and air pollution mixes,
contributing to increased understanding of the role of various
potential confounders, including gaseous co-pollutants, on observed
associations with fine particles. These studies provide more precise
estimates of the magnitude of an effect of exposure to PM, including
fine particles, than most smaller-scale individual city studies.
    (2) More studies of various health endpoints evaluating
associations between effects and fine particles and thoracic coarse
particles (discussed below in section III), as well as ultrafine
particles or specific components (e.g., sulfates, nitrates, metals,
organic compounds, and elemental carbon) of fine particles.
    (3) Numerous new studies of cardiovascular endpoints, with
particular emphasis on assessment of cardiovascular risk factors or
physiological changes.
    (4) Studies relating population exposure to fine particles and
other pollutants measured at centrally located monitors to estimates of
exposure to ambient pollutants at the individual level. Such studies
have led to a better understanding of the relationship between ambient
fine particles levels and personal exposures to fine particles of
ambient origin.
    (5) New analyses and approaches to addressing issues related to
potential confounding by gaseous co-pollutants, possible thresholds for
effects, and measurement error and exposure misclassification.\6\
---------------------------------------------------------------------------

    \6\ ``Confounding'' occurs when a health effect that is caused
by one risk factor is attributed to another variable that is
correlated with the causal risk factor; epidemiologic analyses
attempt to adjust or control for potential confounders (EPA, 2004,
section <IP_ADDRESS>; EPA, 2005a, section 3.6.4). A ``threshold'' is a
concentration below which it is expected that effects are not
observed (EPA, 2004, section 8.4.7; EPA, 2005a, section 3.6.6).
``Gaseous co-pollutants'' generally refer to other commonly-occuring
air pollutants, specifically O3, CO, SO2 and
NO2. ``Measurement error'' refers to uncertainty in the
air quality measurements, while ``exposure misclassification''
includes uncertainty in the use of ambient pollutant measurements in
characterizing population exposures to PM (EPA, 2004, section 8.4.5;
EPA, 2005a, section 3.6.2)
---------------------------------------------------------------------------

    (6) Preliminary attempts to evaluate the effects of fine particles
from different sources (e.g., motor vehicles, coal combustion,
vegetative burning, crustal \7\ ), using factor analysis or source
apportionment methods with fine particle speciation data.
---------------------------------------------------------------------------

    \7\ ``Crustal'' is used here to describe particles of geologic
origin, which can be found in both fine- and coarse-fraction PM.
---------------------------------------------------------------------------

    (7) Several new ``intervention studies'' providing evidence for
improvements in respiratory or cardiovascular health with reductions in
ambient concentrations of particles and gaseous co-pollutants.
    In addition, the body of evidence on PM-related effects has greatly
expanded with findings from studies on potential mechanisms or pathways
by which particles may result in the effects identified in the
epidemiologic studies. These studies include important new dosimetry,
toxicologic and controlled human exposure studies, as highlighted
below:
    (8) Animal and controlled human exposure studies using concentrated
ambient particles (CAPs), new indicators of response (e.g., C-reactive
protein and cytokine levels, heart rate variability), and animal models
simulating sensitive human subpopulations. The results of these studies
are relevant to evaluation of plausibility of the epidemiologic
evidence and provide insights into potential mechanisms for PM-related
effects.
    (9) Dosimetry studies using new modeling methods that provide
increased understanding of the dosimetry of different particle size
classes and in members of potentially sensitive subpopulations, such as
people with chronic respiratory disease.
1. Mechanisms
    In the last review, EPA considered the lack of demonstrated
biologic mechanisms for the varying effects observed in epidemiologic
studies to be an important caution in its integrated assessment of the
health evidence. Much new evidence is now available on potential
mechanisms or pathways for PM-related effects, ranging from effects on
the respiratory system to indicators of cardiovascular response; these
new findings are discussed in depth in Chapter 7 of the Criteria
Document. While questions remain, the new findings have advanced our
understanding of the complex and different patterns of particle
deposition and clearance in the respiratory tract and provide insights
into potential mechanisms for PM-related effects and support the
plausibility of the findings of epidemiologic studies.
    Although there are differences among the size fractions of
particles, fine particles, including accumulation mode and ultrafine
particles, and thoracic coarse particles can all penetrate into and be
deposited in the tracheobronchial and alveolar regions of the
respiratory tract (i.e., the ``thoracic'' regions).\8\ Penetration into
the tracheobronchial and alveolar regions is greater for accumulation
mode particles than for coarse or ultrafine particles, since coarse and
ultrafine particles are more efficiently removed from the air in the
extrathoracic region than are accumulation-mode fine particles; the
evidence from dosimetric studies is

reviewed in detail in Chapter 6 of the Criteria Document.
---------------------------------------------------------------------------

    \8\ Particles are often classified in modes based on their
distribution by characteristics such as mass, surface area, and
particle number. ``Coarse mode'' particles are those with diameters
mostly greater than the minimum in the particle mass distribution,
which generally occurs between about 1 and 3 [mu]m. ``Accumulation
mode'' particles are those with diameters from about 0.1 [mu]m to
between about 1 and 3 [mu]m. Ultrafine particles are generally those
with diameters below about 0.1 [mu]m (EPA, 2004, pages 2-14).
---------------------------------------------------------------------------

    Fine particles have varying physical or chemical characteristics
that may influence health responses. Physical characteristics that may
be of importance are solubility or physical state of the particles
(e.g., solid, liquid). Fine particle components include metals, acids,
organic compounds, biogenic constituents, sulfate and nitrate salts,
elemental carbon, and reactive components such as peroxides; size and
surface area of the particles can also influence health responses. By
way of illustration, Mauderly et al. (1998) discussed particle
components or characteristics hypothesized to contribute to health,
producing an illustrative list of 11 components or characteristics of
interest for which some evidence existed. The list included: (1)
Particle mass concentration, (2) particle size/surface area, (3)
ultrafine particles, (4) metals, (5) acids, (6) organic compounds, (7)
biogenic particles, (8) sulfate and nitrate salts, (9) peroxides, (10)
soot, and (11) co-factors, including effects modification or
confounding by co-occurring gases and meteorology. The authors stressed
that this list is neither definitive nor exhaustive, and note that ``it
is generally accepted as most likely that multiple toxic species act by
several mechanistic pathways to cause the range of health effects that
have been observed'' (Mauderly et al., 1998). The range of health
outcomes linked with fine particle exposures is also broad, including
effects on the cardiovascular and respiratory systems, and potential
links with developmental effects in children (e.g., low birth weight)
and death from lung cancer. It appears unlikely that the complex mixes
of particles that are present in ambient air would act alone through
any single pathway of response. Accordingly, it is plausible that
several physiological responses might occur in concert to produce
reported health endpoints.
    As discussed in section 7.10 of the Criteria Document, the
potential pathways for direct effects on the respiratory system include
lung injury and inflammation, increased airway reactivity and asthma
exacerbation, and increased susceptibility to respiratory infections.
New toxicologic or controlled human exposure studies have reported some
evidence of inflammatory responses in animals, as well as increased
susceptibility to infections. Toxicologic studies also report evidence
of lung injury, inflammation, or altered host defenses with exposure to
ambient particles or particle constituents. Some toxicologic evidence,
particularly from results of studies using diesel exhaust particle
exposures, also indicates that PM can aggravate asthmatic symptoms or
increase airway reactivity.
    Potential pathways for fine particle-related effects also include
systemic effects that are secondary to effects in the respiratory
system. These include impairment of lung function leading to cardiac
effects, pulmonary inflammation and cytokine production leading to
systemic hemodynamic effects, lung inflammation leading to increased
blood coagulability, and lung inflammation leading to hematopoiesis
effects. While more limited than for direct pulmonary effects, some new
toxicologic studies suggest that injury or inflammation in the
respiratory system can lead to changes in heart rhythm, reduced
oxygenation of the blood, changes in blood cell counts, and changes in
the blood that can increase the risk of blood clot formation, a risk
factor for heart attacks and strokes. In addition, health studies have
suggested potential pathways for effects on the heart that include
effects related to uptake of particles or particle constituents in the
blood, and effects on the autonomic control of the heart and
circulatory system. In the last review, little or no evidence was
available from toxicologic studies on potential cardiovascular effects.
More recent studies have provided some initial evidence that particles
can have direct cardiovascular effects. Particle deposition in the
respiratory system also could lead to cardiovascular effects, such as
fine particle-induced pulmonary reflexes resulting in changes in the
autonomic nervous system that then could affect heart rhythm. Also,
inhaled fine particles could affect the heart or other organs if
particles or particle constituents are released into the circulatory
system from the lungs; some new evidence indicates that the smaller
ultrafine particles or their soluble constituents can move directly
from the lungs into systemic circulation.
    The potential mechanisms and/or general pathways for effects
discussed above are primarily effects related to short-term rather than
long-term exposure to fine particles; for the most part, air pollution
toxicologic studies are not designed to assess long-term exposure
effects. While repeated occurrences of some short-term insults, such as
inflammation, might contribute to long-term effects, it is likely that
wholly different mechanisms are involved in the development of chronic
health responses. Some mechanistic evidence is available, however, for
potential carcinogenic or genotoxic effects of ambient fine particles
and combustion products of coal, wood, diesel, and gasoline (discussed
in section 7.8 of the Criteria Document).
    Overall, the findings indicate that different health responses are
linked with different particle characteristics and that both individual
components and complex particle mixtures appear to be responsible for
many biologic responses relevant to fine particle exposures. In
evaluating the new body of evidence, the Criteria Document states:
``Thus, there appear to be multiple biologic mechanisms that may be
responsible for observed morbidity/mortality due to exposure to ambient
PM. It also appears that many biologic responses are produced by PM
whether it is composed of a single component or a complex mixture''
(EPA, 2004, p. 7-206).
2. Nature of Effects
    In the last review, evidence from health studies indicated that
exposure to PM (using various indicators) was associated with premature
mortality and indices of morbidity including respiratory hospital
admissions and emergency room visits, school absences, work loss days,
restricted activity days, effects on lung function and symptoms,
morphological changes, and altered host defense mechanisms.\9\ As
reviewed in Chapter 8 of the Criteria Document, recent epidemiologic
studies have continued to report associations between short-term
exposure to fine particles or fine particle indicators, and effects
such as premature mortality, hospital admissions or emergency
department visits for respiratory disease, and effects on lung function
and symptoms. In addition, recent epidemiologic studies have provided
some new evidence linking short-term fine particle exposures to effects
on the cardivascular system, including cardiovascular hospital
admissions and more subtle indicators of cardiovascular health. Long-
term exposure to PM2.5 and sulfates has also been associated
with mortality from cardiopulmonary diseases and lung cancer, and
effects on the respiratory system such as decreased lung function or
the development of chronic respiratory disease. The

evidence for such effects is summarized below.

    \9\ Historical reports of dramatic pollution episodes,
considered in the 1987 review of the PM NAAQS, provided clear
evidence of mortality associated with high levels of PM and other
pollutants, such as the air pollution episode that occurred in
London in 1952 (EPA, 1996a, pp. 12-28 to 12-31).
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a. Effects Associated With Short-Term Exposure to Fine Particles

    Numerous epidemiologic studies have demonstrated statistical
associations between short-term exposure to fine particles and health
outcomes ranging from total mortality to respiratory symptoms, as
discussed below. Figure 1 summarizes results from both multi-city and
single-city epidemiologic studies using short-term exposures to
PM2.5, including all U.S. and Canadian studies that used
direct measurements of PM2.5 and for which effect estimates
and confidence intervals were reported.\10\ 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. In
the discussions that follow, an individual study result is considered
to be statistically significant if the 95 percent confidence interval
does not include zero. Positive effect estimates indicate increases in
the health outcome with PM2.5 exposure. In considering these
results as a whole, it is important to consider not only whether
statistical significance at the 95 percent confidence level is reported
in individual studies, but also the general pattern of results,
focusing in particular on studies with greater statistical power that
report relatively more precise results.
---------------------------------------------------------------------------

    \10\ In the following discussion of specific studies, results
from single-pollutant models are referred to, as shown in Figure 1,
unless otherwise noted.
---------------------------------------------------------------------------

i. Mortality
    Since the last review, a large number of new time-series studies of
the relationship between short-term exposure to PM, including
PM2.5, and mortality have been published, including several
multi-city studies that are responsive to the recommendations from the
last review. As discussed in section 8.2 of the Criteria Document,
these include studies that have been conducted in single cities or
locations in the U.S. or Canada, as well as Mexico City and locations
in Europe, South America, Asia, and Australia.
    Several recent multi-city studies have been published since the
last review that are of particular relevance for this review. The
results of multi-city studies on associations between PM10
and mortality across 90 U.S. cities (Dominici, 2003) and across ten
U.S. cities (Schwartz, 2003b), while not specifically on fine
particles, have provided important new information to help address
uncertainties regarding a number of issues, including model
specification, potential confounding by co-pollutants and the form of
concentration-response functions (EPA, 2004, section <IP_ADDRESS>). Two
multi-city studies have included measurements of PM2.5; one
was conducted in six U.S. cities (Schwartz et al., 2003a; Klemm and
Mason, 2003) and the other in eight Canadian cities (Burnett and
Goldberg, 2003). In the last review, results from one multi-city study
(the Six Cities study) were available, in which the authors reported
significant associations for total mortality with PM2.5 and
PM10, but not with PM10-2.5. Reanalyses of Six
Cities data have reported results consistent with the findings of the
original study, with statistically significant increases for total
mortality with short-term exposure to PM2.5 (Schwartz,
2003a; Klemm and Mason, 2003). In a study using data from the eight
largest Canadian cities, positive associations were reported for
PM2.5, PM10, and PM10-2.5 with
mortality, and the association with PM2.5 was statistically
significant (Burnett and Goldberg, 2003).
    Single-city studies of mortality associations with short-term
exposures to fine particles have also been conducted in areas across
U.S. and Canada as well as in Europe, Australia and Mexico (some using
fine particle indicators such as British Smoke). In general, it can be
seen in Figure 1 that the effect estimates for associations between
mortality and short-term exposure to PM2.5 are positive and
a number are statistically significant, particularly when focusing on
the results of studies with greater precision. For total nonaccidental
mortality, the effect estimates from the multi-city and single-city
studies with greater precision generally fall in a range of 2 to 6
percent increases per 25 [mu]g/m3 PM2.5.\11\
Somewhat larger effect estimates have been reported for associations
with cardiovascular or respiratory mortality than with total
nonaccidental mortality although the confidence intervals may also be
larger, especially for respiratory mortality since respiratory deaths
comprise only a small proportion of total deaths (EPA, 2005a, p. 3-15).
Some studies evaluated seasonal variation in effects, and there is no
consistent pattern in results. The Criteria Document concludes that the
results of recent epidemiologic studies are generally consistent with
findings available in the previous review (EPA, 2004, p. 8-305).
---------------------------------------------------------------------------

    \11\ In general, the results of studies conducted over shorter
time periods and/or smaller areas have a broader range or effect
estimates with larger standard errors, as shown in Figure 1.
---------------------------------------------------------------------------

    In addition, associations have been reported between mortality and
short-term exposure to a number of fine particle components, including
sulfates, nitrates, metals, organic compounds and elemental carbon
(EPA, 2004, Section <IP_ADDRESS>.2), as well as gaseous precursors such as
SO2 and NO2 and other gaseous pollutants such as
CO. Further, three recent studies have used PM2.5 speciation
data to evaluate the effects of air pollutant combinations or mixtures
using factor analysis or source apportionment methods to evaluate
potential associations between mortality and PM2.5 from
different source categories. These studies reported that short-term
exposures to fine particles from combustion sources, including motor
vehicle emissions, coal combustion, oil burning and vegetative burning,
were associated with increased mortality (EPA, 2004, Section
<IP_ADDRESS>.3). However, different patterns of associations between various
components or source categories of fine particles and total or
cardiovascular mortality are seen in different studies (EPA, 2004, p.
8-70, Tables 8-3, 8-4).
ii. Respiratory Morbidity
    As discussed in Section <IP_ADDRESS> of the Criteria Document, recent
epidemiologic studies have provided further evidence for fine particle
effects on morbidity, including effects such as hospital admissions or
emergency department for respiratory diseases, respiratory symptoms and
lung function changes.

(a) Hospital Admissions or Emergency Department Visits for Respiratory
Diseases

    In the last review, results were available from one study that
reported associations between PM2.5 and hospitalization for
respiratory diseases; these findings were also supported by a number of
studies using other fine particle indicators. Numerous studies had also
reported statistically significant associations between hospital
admissions or emergency department visits for respiratory diseases
short-term exposures with various indicators ambient PM, especially
PM10, in areas where fine particles are the predominant
fraction of PM10, such as locations in the Eastern U.S. and
in Ontario, Canada (EPA, 1996a, p. 13-39).
    The body of evidence has been expanded with numerous new studies in
the U.S. and other countries that have reported associations between
PM2.5 and hospitalization or emergency department visits
(discussed more fully in Section 8.3.2 of the Criteria Document). As
shown in Figure 1, all U.S. and Canadian studies report

associations between PM2.5 and hospitalization for all
respiratory causes that are positive and statistically significant. A
number of studies have also reported findings for hospital admissions
for individual disease categories (COPD, pneumonia, and asthma) that
are positive, but not always statistically significant, perhaps due to
smaller sample sizes for the specific respiratory diseases. The effect
estimates for respiratory hospital admissions tend to fall in the range
of 5 to 15 percent per 25 [mu]g/m3 PM2.5.\12\ In
addition, several studies have reported positive, statistically
significant associations between exposure to PM2.5 and
emergency department visits for respiratory diseases. The effect
estimates for these associations range up to about 25 percent per 25
[mu]g/m3 PM2.5 (EPA, 2005a, pp. 3-20, 3-21).
---------------------------------------------------------------------------

    \12\ Some studies have evaluated seasonal variation in effects,
and no consistent pattern is apparent in the results. For example,
stronger associations were reported between PM2.5 and
asthma hospitalization in the warmer season in Seattle (Sheppard et
al., 2003) but in the cooler season in Los Angeles (Nauenberg and
Basu, 1999).
---------------------------------------------------------------------------

(b) Respiratory Symptoms and Lung Function Changes

    Associations between short-term exposure to PM2.5 and
symptoms in U.S. and Canadian studies are presented in Figure 1. As
discussed in Section 8.3.3 of the Criteria Document, a number of new
studies have reported significant associations between short-term
exposure to PM and increased respiratory symptoms (e.g., cough, wheeze,
shortness of breath) and decreased lung function in people with asthma.
In studies of nonasthmatic subjects, there were generally positive
associations between short-term PM2.5 exposures and
respiratory symptoms that often were not statistically significant and
the results for changes in lung function were somewhat inconsistent.
The Criteria Document concludes that the findings of these studies
suggest associations with fine PM in reduced lung function and
increased respiratory symptoms. For example, significant associations
were reported between ambient PM2.5 and lower respiratory
symptoms in children in a number of U.S. cities (Schwartz and Neas,
2000), and significant associations were found with reduced lung
function in Philadelphia (Neas et al., 1999). These findings are
supported by results from numerous studies conducted in Europe and
Central and South America. The Criteria Document finds that the recent
epidemiologic findings are consistent with those of the previous review
in showing associations with both respiratory symptom incidence and
decreased lung function (EPA, 2004, Section <IP_ADDRESS>).
iii. Cardiovascular Morbidity
    In the last review, none of the available studies had evaluated
associations between exposure to PM and cardiovascular morbidity,
though some studies had reported associations with cardiopulmonary
morbidity. In this area, the evidence on PM-related effects has been
greatly expanded. Numerous recent studies, including multi-city
analyses, have reported significant associations between short-term
exposures to PM and health endpoints related to cardiovascular
morbidity, including hospitalization or emergency department visits for
cardiovascular diseases, incidence of myocardial infarction, cardiac
arrhythmia, changes in heart rate or heart rate variability and changes
in cardiac health indicators such as fibrinogen or C-reactive protein
(EPA, 2004, section <IP_ADDRESS>.1).

(a) Hospital Admissions and Emergency Department Visits for
Cardiovascular Diseases

    Several recent studies, including multi-city analyses, have
reported significant associations between short-term exposures to
various PM indicators and hospital admissions or emergency department
visits for cardiovascular diseases. Among the studies using
PM2.5 measurements are a number of single-city analyses of
hospitalization or emergency department visits for cardiovascular
diseases. As shown in Figure 1, studies conducted in Los Angeles,
Toronto and Detroit have reported associations with hospital admissions
or emergency department visits for all cardiovascular diseases that are
positive and statistically significant or nearly so (Burnett et al.,
1997; Ito, 2003; Moolgavkar, 2003). As was true for respiratory
diseases, the results for specific diseases (ischemic heart disease,
dysrhythmia, congestive heart disease or heart failure, and stroke) are
positive but often not statistically significant. The effect estimates
reported for associations with hospitalization for cardiovascular
diseases range from about 1 to 10 percent per 25 [mu]g/m3
PM2.5 (EPA, 2004, p. 8-310); effect estimates reported for
associations with emergency department visits are generally somewhat
larger.

(b) Cardiovascular Health Indicators

    In addition to the greatly expanded body of evidence on
hospitalization or emergency department visits for cardiovascular
diseases, new epidemiologic studies have also reported associations
with more subtle physiological changes in the cardiovascular system
with short-term exposures to PM, particularly PM10 and
PM2.5 (EPA, 2004, p. 9-67). Associations between short-term
exposures to ambient PM (often using PM10) have been
reported with measures of changes in cardiac function such as
arrhythmia, alterations in electrocardiogram (ECG) patterns, heart rate
or heart rate variability changes, although the Criteria Document urges
caution in drawing conclusions regarding the effects of PM on heart
rhythm, recognizing the need for further research to more firmly
establish and understand links between particles and these more subtle
endpoints. Recent studies have also reported increases in blood
components or biomarkers such as increased levels of C-reactive protein
and fibrinogen. Several of these studies report significant
associations between various cardiovascular endpoints and short-term
PM2.5 exposures, including one in which statistically
significant associations were reported between onset of myocardial
infarction and short-term PM2.5 exposures averaged over 2
and 24 hours (EPA, 2004, p. 8-165; Peters et al., 2001). In this study,
the effect estimates for the two averaging periods are quite similar in
magnitude suggesting that for certain health outcomes very short-term
fine particle concentration fluctuations are important (EPA, 2004, p.
9-42; Peters et al., 2001). These new epidemiologic findings provide
important insight into potential biologic mechanisms that could
underlie associations between short-term PM exposure and cardiovascular
mortality and hospitalization that have been reported previously.

b. Effects Associated With Long-Term Exposure to Fine Particles

    In the last review, results were available from several cohort
studies that suggested associations between long-term exposure to PM
(using various indicators) and both mortality and respiratory
morbidity. Two studies of adult populations (the Six Cities and ACS
studies) reported associations between increases in mortality and long-
term exposure to PM2.5, and results of a 24-city study
indicated that long-term exposure to fine particles was associated with
increased respiratory illness in children.
    As discussed below, the new evidence available in the current
review includes an extensive reanalysis of data from the Six Cities and
ACS studies, new analyses using updated data from the ACS and
California Seventh Day

Adventist (AHSMOG) studies, and a new analysis using data from a cohort
of veterans. In addition, new studies have been published on the
association between long-term exposure to fine particles and
respiratory morbidity using data from a cohort of schoolchildren in
Southern California. In general, the newly available evidence has
supported earlier findings, and the results of reanalyses have
increased confidence in the associations reported in previous
prospective cohort studies.
i. Mortality
    In the 1996 Criteria Document, statistically significant
associations between long-term exposure to both PM2.5 and
sulfates and mortality were reported in studies from the Six Cities and
ACS cohorts (Dockery et al., 1993; Pope et al., 1995). These studies
reported effect estimates of 6.6 percent (95 percent CI: 3.5, 9.8)
increases in total mortality per 10 [mu]g/m3
PM2.5 in the ACS study and 13 percent (95 percent CI: 4.2,
23) increases in total mortality per 10 [mu]g/m3
PM2.5 in the Six Cities study, with somewhat larger effect
estimates reported for cardiopulmonary mortality (EPA, 2004, p. 8-117).
A number of reviewers raised questions about the adequacy of
adjustments for potential confounders and other issues (61 FR 65642,
December 13, 1996). Subsequently, as discussed in more detail in
Section 8.2.3 of the Criteria Document, the Health Effects Institute
conducted a major reanalysis of the data from the Six Cities and ACS
studies by a group of independent investigators to address questions
and uncertainties raised about these prospective cohort studies. The
reanalysis included two major components, a replication and validation
study and a sensitivity analysis. In the first part of the reanalysis,
the investigators validated the data used by the original investigators
in both studies, and they were able to replicate the original results.
The results confirmed the original investigators' findings of
associations with both total and cardiorespiratory mortality, and the
authors reported that the results were not dependent on the computer
programs used in the original analyses (EPA, 2004, p. 8-91; Krewski et
al., 2000, p. 91).
    The second component of the reanalysis project evaluated an array
of different models and variables to determine whether the original
results would remain robust to different analytic assumptions. This
included controlling for other individual level variables, such as
cigarette smoking, alcohol consumption, obesity and occupational
exposures to dusts or other pollutants, and evaluation of the
sensitivity of results to the addition of a range of additional city-
level variables such as population change, income, education levels,
and access to health care. The sensitivity analysis included assessment
of effects in different subgroups of the population. The investigators
also evaluated the sensitivity of the results to the inclusion of
gaseous co-pollutants, and tested the effects of different statistical
modeling approaches, including methods to adjust for spatial patterns,
such as the correlation in pollutant levels between cities.
    The authors found that adjustment for individual-level variables
did not alter the results for the association between long-term
PM2.5 or sulfate exposure and mortality (Krewski et al.,
2000, p. 218). In addition, in most (but not all) cases the
associations between mortality and long-term exposure to
PM2.5 and sulfates were unchanged when additional city-level
variables were added to the models (Krewski et al., 2000, p. 233).
Analyses to assess the potential modification of effects in different
subgroups of the population found, for the most part, little difference
in effects for different subgroups. However, education level was found
to modify the estimated effect of fine particles, in that associations
were statistically significant for those subgroups with lower education
levels, whereas the effect estimates from associations for the subgroup
with better than high school education were appreciably smaller and
were statistically insignificant. The authors suggest that educational
attainment may be a marker for lower socioeconomic status and thus
greater vulnerability to fine particle-related effects (EPA, 2004, p.
8-94; Krewski et al., 2000, p. 232).\13\
---------------------------------------------------------------------------

    \13\ In multivariate models, the association found between
mortality and long-term PM2.5 exposure was little changed
with addition of education level to the model (Krewski et al., 2000,
p. 184). This indicates that education level was not a confounder in
the relationship between fine particles and mortality, but the
relationship between fine particles and mortality is larger in the
population subsets with lower education in this study and not
statistically significant in the population subset with the highest
education (EPA, 2004, p. 8-100).
---------------------------------------------------------------------------

    In single-pollutant models, none of the gaseous co-pollutants was
significantly associated with mortality except SO2. Further
reanalysis included multi-pollutant models with the gaseous pollutants,
and the associations between mortality and both fine particles and
sulfates were unchanged in these models, except when SO2 was
included, which decreased the size of the effect estimates for
PM2.5 to one-sixth of its original value and for sulfates to
less than one-third of its original value (EPA, 2004, p. 8-136; Krewski
et al., 2000, pp. 183-184).\14\ However, the regional association of
SO2 and PM2.5 was relatively high, such that the
effects of the separate pollutants could not be distinguished. The
authors conclude that these findings support the notion that increased
mortality may be attributable to more than one component of ambient air
pollution, and that throughout the reanalyses, fine particles,
sulfates, and SO2 demonstrated positive associations with
mortality (Krewski et al., 2000, p. 233-234). As discussed more
generally in the Criteria Document, this result may be reflecting the
relatively high correlation between PM2.5 levels and
SO2 levels that would be expected in cities across the
industrial Midwest and northeastern states, the role that
SO2 has as a precursor to sulfate components in the mix of
PM2.5, and/or the likelihood that SO2 is part of
the causal pathway linking exposure to PM2.5 to adverse
health outcomes (EPA, 2004, section <IP_ADDRESS>).
---------------------------------------------------------------------------

    \14\ For a 24.5 [mu]g/m3 change in PM2.5,
the relative risk for the association between mortality and
PM2.5 alone was 1.20 (95 percent CI: 1.11-1.29), and
after adjustment for SO2 it was 1.03 (95 percent CI:
0.95-1.13). The relative risk for SO2 alone was 1.49 (95
percent CI: 1.36-1.64) and after adjustment for PM2.5 was
1.46 (95 percent CI: 1.32-1.63) (Krewski et al., 2000, p. 184). The
relative risk for sulfates alone was 1.28 (95 percent CI: 1.18-1.40)
and after adjustment for SO2 it was 1.14 (95 percent CI:
1.04-1.25) (Krewski et al., 2000, p. 184). These relative risks for
PM2.5 are equivalent to effect estimates of 7.5 percent
and 1.2 percent increases in mortality per 10 [mu]g/m3,
in single-pollutant and two-pollutant models, respectively.
---------------------------------------------------------------------------

    Finally, Krewski and colleagues used several methods to address
spatial patterns in the data; for example, concentrations of air
pollutants may be correlated between cities within a region. These
analyses were primarily based on sulfate concentrations, since more
cities had data for sulfates than for fine particles. Addressing
spatial patterns in the data generally reduced the size of the
association between sulfates and mortality, but the models all
continued to show associations between mortality risk and long-term
sulfate exposures, although not all were statistically significant
(Krewski et al., 2000, p. 228). Overall, considering the results of the
extensive set of replication and sensitivity analyses, the authors
report that the reanalysis confirmed the association between mortality
and fine particle and sulfate exposures (EPA, 2004, p. 8-95; Krewski et
al., 2000).
    In addition, extended analyses were conducted for the ACS cohort
study that included follow-up health data and air quality data from the
new fine particle

monitoring network for 1999-2000. In this study of the expanded ACS
cohort, significant associations were reported between long-term
exposure to fine particles (using various averaging periods for air
quality concentrations) and premature mortality from all causes,
cardiopulmonary diseases, and lung cancer (Pope et al., 2002; EPA,
2004, 8-102). This extended analysis included the use of more recent
data on fine particle concentrations, as well as data on gaseous co-
pollutant concentrations, though no multi-pollutant model results are
presented. Further evaluation of the influence of other covariates
(e.g., dietary intake data, occupational exposure) used methods similar
to those in the reanalysis described above, and new statistical
approaches were used for modeling the PM-mortality relationship as well
as adjusting for spatial correlation (EPA, 2004, section <IP_ADDRESS>.2).
The investigators reported that the associations found with fine
particle and sulfate concentrations were not markedly affected by
adjustment for numerous socioeconomic variables, demographic factors,
environmental variables, indicators of access to health services or
personal health variables (e.g., dietary factors, alcohol consumption,
body mass index). Similar to the results of Krewski et al. (2000),
education level was found to be a modifier in the relationship between
fine particles and mortality, in that associations were statistically
significant for those subgroups with lower education levels, whereas
effect estimates from associations for those with better than a high
school education were close to zero and were statistically
insignificant.
    There are also new analyses using updated data from the AHSMOG
cohort. These include estimated PM2.5 concentrations from
visibility data, along with new health information from continued
follow-up of the Seventh Day Adventist cohort. Positive associations
were reported for mortality with PM2.5 in males, but the
estimates were generally not statistically significant (Abbey et al.,
1999; McDonnell et al., 2000; EPA, 2004, pp. 8-110 and 8-117). In
addition, one new set of analyses was done using subsets of PM exposure
and mortality time periods and data from a Veterans Administration (VA)
cohort of hypertensive men. The investigators report inconsistent and
largely nonsignificant associations between PM exposure (including,
depending on availability, TSP, PM10, PM2.5,
PM15 and PM15-2.5) and mortality (EPA, 2004, pp.
8-110 to 8-111; Lipfert et al., 2000b).
    The Criteria Document and Staff Paper place greatest weight on the
findings of the Six Cities and ACS studies (including reanalyses and
extended analyses) that include measured fine particle data (in
contrast with AHSMOG effect estimates based on TSP or visibility
measurements), have study populations more similar to the general
population than the VA study cohort, and have been replicated and
examined through exhaustive reanalysis (EPA, 2005a, at 5-22; see also
EPA, 2004, at <IP_ADDRESS>.5.). In these studies, effect estimates for
deaths from all causes fall in a range of 6 to 13 percent increased
risk per 10 [mu]g/m3 PM2.5, while effect
estimates for deaths from cardiopulmonary causes fall in a range of 6
to 19 percent per 10 [mu]g/m3 PM2.5. For lung
cancer mortality, the effect estimate was a 13 percent increase per 10
[mu]g/m3 PM2.5 in the results of the extended
analysis from the ACS cohort (Pope et al., 2002; CD, Table 8-12).
    The prospective cohort studies have used air quality measurements
averaged over long periods of time, such as several years, to
characterize the long-term ambient levels in the community. The
exposure comparisons are basically cross-sectional in nature, and do
not provide evidence concerning any temporal relationship between
exposure and effect (EPA, 2004, p. 9-42). As discussed in the Criteria
Document, it is not easy to differentiate the role of historic
exposures from more recent exposures, leading to potential exposure
measurement error that is increased if average PM concentrations change
over time differentially between areas (EPA, 2004, p. 5-118). Several
new studies have used different air quality periods for estimating
long-term exposure and tested associations with mortality for the
different exposure periods. As discussed in section <IP_ADDRESS> of the
Staff Paper, these analyses indicate that averaging PM concentrations
over a longer time period results in stronger associations, and that
the longer series of data is likely a better indicator of cumulative
exposure. Thus, in evaluating these findings, EPA has focused on the
results of analyses using fine particle or sulfate measurements for the
longer exposure periods in the studies.
ii. Respiratory Morbidity
    In the last review, several studies had reported that long-term PM
exposure was linked with increased respiratory disease and decreased
lung function. One study, using data from 24 U.S. and Canadian cities
(``24 Cities'' study), reported associations with these effects and
long-term exposure to fine particles or acidic particles, but not with
PM10 exposure (Dockery et al., 1996; Raizenne et al., 1996).
More specifically, statistically significant associations were reported
between long-term exposure to fine particles and decreases in several
measures of lung function evaluated at a single point in time (Raizenne
et al., 1996). In addition, positive but not statistically significant
associations were reported between long-term exposure to fine particles
and prevalence of a range of respiratory conditions (e.g., asthma,
bronchitis, chronic cough) (Dockery et al., 1996).
    In the current review, new studies conducted in the U.S. have been
based on data from cohorts of schoolchildren in 12 Southern California
Communities and an adult cohort of Seventh Day Adventists (AHSMOG)
(EPA, 2004, section <IP_ADDRESS>). Information specifically on associations
with long-term PM2.5 exposures are available from the
Southern California children's cohort study. Early findings from cross-
sectional analyses done at the beginning of the study suggested
associations between long-term PM2.5 exposures and
respiratory morbidity, but the findings were generally not
statistically significant.\15\ Later publications from this cohort have
reported associations with lung function growth in children over four-
year follow-up periods. In a study of a cohort of children followed
from 4th to 7th grade, some measures of decreases in lung function
growth were statistically significantly associated with increasing
exposure to PM2.5, whereas in a second cohort of 4th
graders, the associations generally did not reach statistical
significance (Gauderman et al., 2002). Decreases in measures of lung
function growth were also reported for cohorts of older children, but
the associations did not reach statistical significance (Gauderman et
al., 2000). The Criteria Document finds that these studies ``provide
the best evidence'' on effects of long-term fine particle exposure
(EPA, 2004, p. 8-314). However, this is the only cohort study to have
evaluated associations with decreases in lung function growth in
children over time. Considered together, the Criteria Document finds
that the evidence from these studies indicates that long-term
PM2.5 exposures may

result in chronic respiratory effects (EPA, 2004, p. 8-314).
---------------------------------------------------------------------------

    \15\ In an initial report on the prevalence of respiratory
illnesses reported at the beginning of the study, positive
associations, though not statistically significant, were reported
between long-term PM2.5 exposure and risk of bronchitis
and cough only in the subset of children with asthma (McConnell et
al., 1999), and no significant associations with long-term
PM2.5 exposure were reported for the full cohort (Peters
et al., 1999a). In addition, long-term PM2.5 exposure was
associated with decreases in some lung function measurements made at
that time, but the associations were only statistically significant
for females (Peters et al., 1999b).
---------------------------------------------------------------------------

3. Integration and Interpretation of the Health Evidence
    In evaluating the evidence from epidemiologic studies, the Criteria
Document and Staff Paper focused on well-recognized criteria, 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; the nature
of concentration-response relationships; and information from so-called
natural experiments or intervention studies. These evaluations
addressed key methodological issues that are relevant to interpretation
of evidence from epidemiologic studies. Further, findings from
epidemiologic studies were integrated with experimental (e.g.,
dosimetric and toxicologic) studies, in considering the extent of
coherence and biological plausibility of effects observed in
epidemiologic studies. This integrative assessment provided the basis
for the judgments made in the Criteria Document and Staff Paper about
the extent to which causal inferences can be made about observed
associations between health endpoints and PM2.5 (as well as
other indicators or constituents of ambient PM), acting alone and/or in
combination with other pollutants. Key elements of these evaluations
are briefly summarized below.
    (1) For short-term exposures to fine particles, in considering the
magnitude and statistical strength of the associations, there is a
pattern of positive and often statistically significant associations
for cardiovascular and respiratory health outcomes with short-term
exposure to PM10 and PM2.5. Of particular note
are several multi-city studies that have yielded relative risk
estimates for associations between short-term exposure to various
indices of PM and mortality or morbidity. Although small in size, the
effect estimates from multi-city studies have great precision due to
the statistical power of the studies. New analyses of pre-existing
cohorts with studies of long-term exposure to fine particles are
available that confirm and strengthen conclusions from the previous
review, although the effect estimates are sensitive to education level,
co-pollutant effects of SO2, and spatial correlation, as
discussed above.
    (2) The Criteria Document and Staff Paper have evaluated the
robustness of epidemiologic associations in part by considering the
effect of differences in statistical model specification, potential
confounding by co-pollutants and exposure error on PM-health
associations (EPA, 2004, section <IP_ADDRESS>; EPA, 2005a, sections 3.4.2
and 3.6).
    As discussed in section 8.4.2 of the Criteria Document and section
3.6.3 of the Staff Paper, the influence of alternative modeling
strategies on epidemiologic study results was assessed, with a
particular focus on the recent set of analyses to address statistical
modeling questions in epidemiologic studies for short-term PM
exposures. Numerous recent studies used a certain type of statistical
method (i.e., generalized additive methods (GAM)) in widely used
statistical software (Splus), and it was discovered that the default
program settings could potentially result in biased effect estimates
for associations between pollutants and health outcomes. Results from a
number of epidemiologic studies were reanalyzed to address this
problem. These reanalyses also more broadly included the use of
alternative statistical models and alternative methods of control for
time-varying effects, such as weather or season (HEI, 2003). In
general, the results of the reanalyses to address the use of default
program settings in the Splus software 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). For example, in comparing results for
numerous studies of mortality associations with PM10, the
Criteria Document found that the extent of reduction in effect
estimates resulting from reanalysis was smaller than the variation in
effect estimate size across studies (EPA, 2004, p. 8-229 and Figure 8-
15). A review panel commentary on the set of reanalysis studies (using
various PM indicators) notes that most studies were considered to show
``little or no change'' in results with initial reanalyses to address
questions about the use of modeling specifications in the statistical
software package (HEI, 2003, pp. 258-259).
    In addition, the reanalyses also refocused attention in general on
the control for relationships between health effects and weather
variables in time-series epidemiologic studies; such issues had been
also discussed at length in the 1996 Criteria Document (EPA, 2004,
section <IP_ADDRESS>). The reanalysis results showed greater sensitivity to
the modeling approach used to account for temporal effects and weather
variables than to correcting the initial problem with default settings
in the use of GAM in Splus software (EPA, 2004, p. 8-236). For example,
in the review panel commentary, sixteen of the reanalyzed studies were
considered to have ``little or no change'' in results of initial
reanalyses, while only two studies showed ``substantial'' changes
(Goldberg and Burnett, 2003; some results in Ito, 2003; HEI, 2003, pp.
258-259). In contrast, four of the eight studies that were reanalyzed
with additional methods to adjust for time-related variables were
considered to show ``substantial'' changes in effect estimate size
(HEI, 2003, p. 262).
    The recent time-series epidemiologic studies evaluated in the
Criteria Document have included some degree of control for variations
in weather and seasonal variables. As summarized in the HEI review
panel commentary, selecting a level of control to adjust for time-
varying factors, such as temperature, in time-series epidemiologic
studies involves a trade-off. For example, if the model does not
sufficiently adjust for the relationship between the health outcome and
temperature, some effects of temperature could be falsely ascribed to
the pollution variable. Conversely, if an overly aggressive approach is
used to control for temperature, the result would possibly
underestimate the pollution-related effect and compromise the ability
to detect a small but true pollution effect (EPA, 2004, p. 8-236; HEI,
2003, p. 266). The selection of approaches to address such variables
depends in part on prior knowledge and judgments made by the
investigators, for example, about weather patterns in the study area
and expected relationships between weather and other time-varying
factors and health outcomes considered in the study. While recognizing
the need for further exploration of alternative modeling approaches for
time-series analyses, the Criteria Document found that the studies
included in this part of the reanalysis in general continued to
demonstrate associations between PM and mortality and morbidity beyond
those attributable to weather variables alone (EPA, 2004, pp. 8-340, 8-
341). Further, considering the full set of reanalyses, 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, again recognizing that further
evaluation of alternative modeling strategies was warranted (EPA, 2004,
p. 9-48).

    For long-term exposure to fine particles, the reanalysis and
extended analyses of data from prospective cohort studies, discussed
above in section II.A.2, have shown that reported associations between
mortality and long-term exposure to fine particles are robust to
alternative modeling strategies (Krewski et al., 2000). As stated in
the reanalysis report, ``The risk estimates reported by the Original
Investigators were remarkably robust to alternative specifications of
the underlying risk models, thereby strengthening confidence in the
original findings'' (Krewski et al., 2000, p. 232). In extended
analysis, Krewski et al. (2000) identified model sensitivities related
to education level and spatial correlation, as well as to co-pollutant
effects of SO2, as discussed below.
    The Criteria Document also included extensive evaluation of the
sensitivity of PM-health responses to confounding by gaseous co-
pollutants (EPA, 2004, section 8.4.3, Figures 8-16 to 8-19). Results of
new multi-city short-term exposure studies, that combine data from
locations with different mixes of pollutants, provide important new
results. Using PM10, the NMMAPS results indicated that
associations with mortality were not confounded by co-pollutant
concentrations across 90 U.S. cities (Dominici, 2003),\16\ and a
similar lack of confounding was observed in a mortality study across 10
U.S. cities (Schwartz, 2003b) (EPA, 2004, Figure 8-16). That is, in
these studies, the size of the effect estimates are little changed and
the associations remain statistically significant in multi-pollutant
models including one or more of the gaseous co-pollutants. Similar
results are seen in some single-city studies using PM2.5 for
some health outcomes in which the single-pollutant model association
was statistically significant (EPA, 2004, Figures 8-16 to 8-18),
including the association with mortality in Santa Clara County, CA
(Fairley, 2003); associations with hospital admissions in Detroit (for
heart failure and pneumonia in Ito, 2003) and Seattle (for asthma in
Sheppard et al., 2003); and associations with cardiovascular-related
biomarkers in Boston (Gold et al., 2000). The size of the effect
estimates were little changed in other studies as well in which the
single-pollutant model associations were not statistically significant
(e.g., for some health outcomes in Ito, 2003; for mortality in Chock et
al., 2000). In yet other studies, however, for some combinations of
pollutants in some areas, substantial reductions in the size of the
effect estimates for PM2.5 were observed; notably,
Moolgavkar (2003) reports substantial reductions in effect estimates
when CO is included in models for mortality and hospitalization in Los
Angeles, and Thurston et al. (1994) and Delfino et al. (1998) report
substantial reductions when O3 is included in models for
hospital admissions in Toronto and emergency department visits in
Montreal, respectively.\17\ It is recognized that collinearity between
co-pollutants can make interpretation of such multi-pollutant model
results difficult (EPA, 2004, p. 8-253). Further, associations between
long-term exposure to PM2.5 and mortality were not generally
sensitive to inclusion of co-pollutants, with the notable exception of
the inclusion of SO2 in multipollutant models used in the
reanalysis of the ACS study, as discussed above in section II.A.2 (EPA,
2004, p. 8-136). Overall, the Criteria Document concluded that these
studies indicate that effect estimates for associations between
mortality and morbidity and various PM indices are generally robust to
confounding by co-pollutants, while recognizing that disentangling the
effects attributable to various pollutants within an air pollution
mixture is challenging (EPA, 2004, p. 9-37).
---------------------------------------------------------------------------

    \16\ In the HEI Review Panel commentary on the results of the
NMMAPS multi-city analyses, the Panel stated that the results did
not show a confounding effect of other pollutants, observing that
the PM10 effects on mortality were not changed by
addition of either O3, SO2, NO2 or
CO to the models (HEI, 2000, p. 77).
    \17\ The correlation coefficients between concentrations of
PM2.5 and the noted co-pollutants in these studies were
high; the coefficient with CO in Los Angeles was 0.58, and the
coefficients with O3 were 0.58 and 0.72 in Montreal and
Toronto, respectively.
---------------------------------------------------------------------------

    Finally, as discussed in section 3.6.2, a number of recent studies
have evaluated the influence of exposure error on PM-health
associations. This includes both consideration of error in measurements
of PM and other co-pollutants, and the degree to which measurements
from an individual monitor reflect exposures to the surrounding
community. As further discussed in section 3.6.2, 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). In comparing fine and
thoracic coarse particles, the Criteria Document observes that 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 less likely to penetrate into buildings (EPA, 2004, p.
9-38). Therefore, while the Criteria Document concludes that
associations reported with PM10, PM2.5 and
PM10-2.5 are generally robust, it recognizes that factors
related to exposure error may result in reduced precision for
epidemiologic associations with PM10-2.5 (EPA, 2004, p. 9-
46).
    (3) Consistency refers to the persistent finding of an association
between exposure and outcome in multiple studies of adequate power in
different persons, places, circumstances and times (CDC, 2004). The
1996 Criteria Document reported associations between short-term PM
exposure and mortality or morbidity from studies conducted in locations
across the U.S. as well as in other countries, and concluded that the
epidemiologic data base had ``general internal consistency'' (EPA,
1996a, p. 13-30). New multi-city studies have allowed evaluation of
consistency in effect estimates across geographic locations, using
uniform statistical modeling approaches; the results suggest that
effect estimates differ from one location to another, but the extent of
variation is not clear. For example, the Canadian 8-city study reported
no evidence of heterogeneity in city-specific results in the initial
study findings; however, in the reanalysis to address model
specification issues, the findings suggested more evidence of
heterogeneity in associations between mortality and short-term
PM2.5 exposure (Burnett and Goldberg, 2003; EPA, 2004, p. 9-
39). The Criteria Document discussed a number of factors that would be
likely to cause variation in PM-health outcomes in different
populations and geographic areas in section <IP_ADDRESS>, including
indicators of exposure to traffic-related pollution, population
characteristics that affect susceptibility or exposure differences,
distribution of PM sources, or geographic features that would affect
the spatial distribution of PM (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 concluded that ``[f]ocusing on the studies with the most
precision, it can be concluded that there is much consistency in
epidemiologic evidence regarding associations between short-term and
long-term exposures to fine

particles and cardiopulmonary mortality and morbidity.'' (EPA, 2004, p.
9-47).
    (4) The form of concentration-response relationships (e.g., linear,
sigmoid) and the potential existence of thresholds was one of the
important research questions remaining in the previous review. The
Criteria Document recognized that it is reasonable to expect that there
likely are biologic thresholds for different health effects in
individuals or groups of individuals with similar innate
characteristics and health status (EPA, 2004, Section <IP_ADDRESS>).
Individual thresholds would presumably vary substantially from person
to person due to individual differences in genetic-level susceptibility
and pre-existing disease conditions (and could even vary from one time
to another for a given person). Thus, it would be difficult to detect a
distinct threshold at the population level, below which no individual
would experience a given effect, especially if some members of a
population are unusually sensitive even down to very low
concentrations. The person-to-person difference in the relationship
between personal exposure to PM of ambient origin and the concentration
observed at a monitor may also add to the variability in observed
concentration-response relationships, further obscuring potential
population thresholds within the range of observed concentrations (CD,
p. 9-43, 9-44).
    Several new epidemiologic studies have used different modeling
methods to address this question, and most have been unable to detect
threshold levels in the relationship between short-term PM exposure
(generally using PM10) and mortality; in fact, one single-
city analysis suggests that statistical methods would allow detection
of a threshold in the epidemiologic data if a clear threshold existed.
However, a few analyses in individual cities have provided suggestions
of some potential threshold levels, generally at fairly low ambient
concentrations. One single-city study used PM2.5 and
PM10-2.5 measurements in Phoenix and reported that there was
suggestive evidence of a threshold for the association between
mortality and short-term exposure to PM2.5 in the range of
20-25 [mu]g/m3 (Smith et al., 2000; EPA, 2004, p. 8-322).
    The shape of the concentration-response function for long-term
exposure to PM2.5 with mortality was evaluated using data
from the ACS cohort. In the ACS reanalysis, the authors report that the
concentration-response functions for PM2.5 and all-cause and
cardiopulmonary mortality demonstrate near-linear increasing trends
through the range of particle levels observed in the fine particle
cohort (Krewski, p. 160). However, the HEI Review Committee concluded
that these results show no clear evidence either for or against overall
linearity (Krewski, p. 265). In the extended ACS study, the authors
reported that the associations for all-cause, cardiovascular and lung
cancer mortality ``were not significantly different from linear
associations'' (Pope, et al., 2002).
    Thus, evaluation of the health effects data summarized in the
Criteria Document provides no evidence to support selecting any
particular population threshold for PM2.5. The Staff Paper
also recognized, however, that it is reasonable to expect that, for
individuals, there may be thresholds for specific health responses and
that it is possible that such thresholds exist toward the lower end of
these ranges (or below these ranges) 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) Few studies are available that assess the extent to which
reductions in ambient PM actually lead to reductions in health effects
attributable to PM. As discussed in sections <IP_ADDRESS> and <IP_ADDRESS> of the
Criteria Document, several epidemiologic studies were done in the Utah
Valley area over a time period when a major source of PM was closed,
resulting in markedly decreased PM10 concentrations. An
epidemiologic study reported that respiratory hospital admissions
decreased during the plant closure time period (EPA, 2004, p. 8-131;
Pope et al., 1989). Newly available controlled human exposure and
animal toxicology studies, using particles extracted from stored
PM10 sampling filters from the Utah Valley, have shown
inflammatory responses that are greater with extracts of particles
collected during the time period of source operation than when the
source was closed, suggesting that the PM from the steel mill was more
harmful than other ambient PM on an equal mass basis (EPA, 2004, p. 9-
73). Epidemiologic studies in Dublin, Ireland and Hong Kong also
provides evidence for reduced relative risks for mortality when PM
(measured as BS or PM10) and SO2 were reduced as
the result of interventions aimed at reducing air pollution. The
Criteria Document concluded that this small group of studies add
further support to the results of the hundreds of other epidemiologic
studies linking ambient PM exposure to an array of health effects, and
provide strong evidence that reducing emissions of PM and gaseous
pollutants has beneficial public health impacts (EPA, 2004, p. 9-45 to
9-46).
    (6) Several issues related to fine particle exposure time periods
were assessed in the Criteria Document, as summarized in section 3.6.5
of the Staff Paper. As discussed above in this section, these include
the exposure time periods used in long-term exposure studies as well as
health outcome associations with very short time periods (e.g., 2-hour
average). An additional issue is the time period (``lag'') between fine
particle exposure and health outcome that is reported in short-term
exposure study results. In these epidemiologic studies, associations
are often tested for a range of lag periods, for example, with PM
concentrations from the same day as the effect, and one or more days
preceding the effect. In evaluating these results, it is important to
consider the pattern of results that is seen across the series of lag
periods. If there is an apparent pattern of results across the
different lags, with positive associations reported for a series of
consecutive lag periods, then selecting the single-day lag with the
largest effect from a series of positive associations is likely to
underestimate the overall effect size, since single-day lag effect
estimates do not fully capture the risk that may be distributed over
adjacent or other days (EPA, 2004, sections 8.4.4 and <IP_ADDRESS>). For
many epidemiologic studies, the authors have reported just such a
pattern of associations across several consecutive lag periods (EPA,
2004, p. 8-279). However, if there is no apparent pattern or reported
effects vary across lag days, any result for a single day may well be
biased (CD, p. 9-42).
    Some new studies have used a ``distributed lag'' model approach,
that captures an effect of PM over a series of days following
exposure.\18\ Where effects are found for a series of lag periods, a
distributed lag model will more accurately characterize the effect
estimate size. 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. Effect estimates from distributed lag models are thus
often, but not always, larger in size that those for single-day lag
periods (EPA, 2004, p. 8-281).
---------------------------------------------------------------------------

    \18\ The available studies have generally used PM10,
but not PM2.5 or PM10-2.5.

---------------------------------------------------------------------------

    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. For example, for a
health outcome such as a delayed asthma response, the lag period of a
day or several days might be expected between exposure and outcome;
however, some cardiovascular responses might be expected to occur
within a very short time period (e.g., an hour) after exposure (EPA,
2004, p. 8-279). As shown in Figures 8-24 to 8-28, the Criteria
Document notes a pattern of stronger associations between
PM10 and mortality or cardiovascular hospitalization with
shorter lag periods (e.g., same-day or 1-day lagged PM10).
For other effects, however, such as respiratory symptoms, asthma
emergency department visits or hospitalization, stronger effects were
reported with PM concentrations averaged over several days (EPA, 2004,
pp. 8-273 to 8-279). Thus, the Criteria Document concludes that one
would expect to see different best-fitting lags for different health
effects, based on potentially different biological mechanisms as well
as individual variability in responses (EPA, 2004, p. 8-342). For some
health outcomes, it is reasonable to expect associations to be observed
with PM exposures on the same day or with very short lag periods, but
not longer lag periods. In other cases, multi-day average exposure
periods or distributed lag models would more appropriately estimate
potential PM-related health risks.
    (7) Looking more broadly to integrate epidemiologic evidence with
that from exposure-related, dosimetric and toxicologic studies, EPA has
considered the coherence of the evidence and the extent to which the
new evidence provides insights into mechanisms by which PM, especially
fine particles, may be affecting human health. Progress made in gaining
insights into potential mechanisms lends support to the biologic
plausibility of results observed in epidemiologic studies. For
cardiovascular effects, the convergence of important new epidemiologic
and toxicologic evidence (especially from studies using concentrated
ambient particles) builds support for the plausibility of causal
associations, especially between fine particles and physiological
endpoints indicative of increased risk of cardiovascular disease and
changes in cardiac rhythm. This finding is supported by new
cardiovascular effects research focused on fine particles that has
notably advanced our understanding of potential mechanisms by which
PM2.5 exposure, especially in susceptible individuals, could
result in changes in cardiac function or blood parameters that are risk
factors for cardiovascular disease. For respiratory effects,
toxicologic studies have provided evidence that supports plausible
biologic pathways for fine particles, including inflammatory responses,
increased airway responsiveness, or altered responses to infectious
agents. Further, coherence across a broad range of cardiovascular and
respiratory health outcomes is supported by evidence from epidemiologic
and toxicologic studies done in the same location, for example, in the
series of studies conducted in or evaluating ambient PM from Boston and
the Utah Valley (EPA, 2004, 7-42 to 43, 7-46 to 47, and 9-45).
Toxicologic studies have suggested that some combustion-related
particles, including particles from wood burning and diesel engine
exhaust, but not others such as coal fly ash, may have carcinogenic
effects (EPA, 2004, Section 7.8.4). This evidence supports the
plausibility of the observed relationship between fine particles and
lung cancer mortality. Evidence for PM-related infant mortality and
developmental effects poses an emerging concern, but the current
information is still very limited in support of the plausibility of
potential ambient PM relationships. More generally, toxicologic animal
studies often test effects of exposures to individual chemical
components, and thus the physical and chemical characteristics may
differ from those of particles in ambient air to which humans are
exposed. These and other differences in toxicologic and epidemiologic
study designs complicate the assessment of coherence in results from
across disciplines (EPA, 2004, section <IP_ADDRESS>; Schlesinger and Cassee,
2003).
    Overall, the Criteria Document finds that much more evidence is now
available related to the coherence and plausibility of effects than in
the last review. For short-term exposures, integration of evidence from
epidemiologic and toxicologic studies indicates both coherence and
plausibility of effects on the cardiovascular and respiratory systems,
especially for fine particles (EPA, 2004, p. 9-79). There is evidence
supporting coherence and plausibility for the observed associations
between long-term exposures to fine particles and lung cancer mortality
(EPA, 2004, p. 9-78).
    (8) In summary, as discussed in the Staff Paper (section 3.5) and
the Criteria Document (section 9.2.2), the extensive body of
epidemiologic evidence now available continues to support likely causal
associations between PM2.5 and a broad range of mortality
and morbidity health outcomes based on an assessment of the strength of
the evidence, including the strength and robustness of reported
associations and the consistency of the results. While the limitations
and uncertainties in the available evidence suggest caution in
interpreting the epidemiologic studies at the lower levels of air
quality observed in the studies, the evidence now available provides
strong support that both short-term and long-term exposures to fine
particles are plausibly associated with a broad range of effects on the
respiratory and cardiovascular systems. The Criteria Document
concludes: ``the epidemiological evidence continues to support likely
causal associations between PM2.5 and PM10 and
both mortality and morbidity from cardiovascular and respiratory
diseases, based on an assessment of strength, robustness, and
consistency in results.'' (EPA, 2004, p. 9-48). In its integrative
assessment, the Criteria Document finds that health evidence from
various disciplines provides a strong and coherent basis for concluding
that both short-term and long-term exposure to fine particles is
associated with health effects ranging from subtle changes in lung
function to premature mortality.
4. Sensitive Subgroups for PM2.5-Related Effects
    As described in the PM Criteria Document, the term susceptibility
refers to innate (e.g., genetic or developmental) or acquired (e.g.,
personal risk factors, age) factors that make individuals more likely
to experience effects with exposure to pollutants. A number of
population subgroups have been identified as potentially susceptible to
health effects as a result of PM exposure, including people with
existing heart and lung diseases, including diabetes, and older adults
and children. In addition, new attention has been paid to the concept
of some population groups having increased vulnerability to pollution-
related effects due to factors such as socioeconomic status or factors
that result in particularly elevated exposure levels, such as residence
near sources such as roadways (EPA, 2004, p. 9-81).
    A good deal of evidence indicates that people with existing heart
or lung diseases are more susceptible to PM-related effects. In
addition, new studies have suggested that people with diabetes, who are
at risk for cardiovascular disease, may have

increased susceptibility to PM exposures. As discussed in Section
<IP_ADDRESS> of the Criteria Document, this body of evidence includes
findings from epidemiologic studies that associations with mortality or
morbidity are greater in those with preexisting conditions, as well as
evidence from toxicologic studies using animal models of
cardiopulmonary disease. In addition, dosimetric evidence indicates
that deposition of particles is increased, and can be focused in ``hot
spots'' in the respiratory tract, in people with chronic respiratory
diseases.
    Two age groups, older adults and the very young, are also
potentially at greater risk for PM-related effects. Epidemiologic
studies have generally not shown striking differences between adult age
groups. However, some epidemiologic studies have suggested that serious
health effects, such as premature mortality, are greater among older
populations (EPA, 2005a, p. 8-328). In addition, preexisting
respiratory or cardiovascular conditions are more prevalent in older
adults than younger age groups; thus there is some overlap between
potentially susceptible groups of older adults and people with heart or
lung diseases.
    Epidemiologic evidence has reported associations with emergency
hospital admissions for respiratory illness and asthma-related symptoms
in children. Several factors may make children susceptible to PM-
related effects, including the greater ventilation rate per kilogram
body weight in children, greater prevalence of chronic asthma, and the
fact that children are more likely to be active outdoors and thus have
greater exposures. In addition, there is a more limited body of new
evidence from epidemiologic studies for potential PM-related health