Review of the National Ambient Air Quality Standards
for Participate Matter:
Policy Assessment of
Scientific and Technical Information
OAQPS Staff Paper
Office of Air Quality Planning and Standards
U.S. Environmental Protection Agency
EXTERNAL REVIEW DRAFT
November 1995
DO NOT QUOTE OR CITE
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DISCLAIMER
This draft Office of Air Quality Planning and Standards (OAQPS) Staff Paper
contains the assessments, judgments, and conclusions of the staff of OAQPS and does not
necessarily represent those of the U.S. Environmental Protection Agency (U.S. EPA). This
draft report is being circulated for peer review and public comment. Comments should be
addressed to Ms. Trish Koman, U.S. EPA, Office of Air Quality Planning and Standards,
MD-15, Research Triangle Park, North Carolina 27711.
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ACKNOWLEDGEMENTS
This Staff Paper is the product of the Office of Air Quality Planning and Standards
(OAQPS). For the primary standards, the principal authors include Dr. Jane C. Caldwell,
Patricia D. Koman, Eric G. Smith of OAQPS, and Dr. Tracey J. Woodruff of the Office of
Policy Planning and Evaluation (OPPE). For the secondary standards, principal authors
include Rich Damberg, Chebryll Edwards, and Bruce Polkowsky of OAQPS. The authors
would like to acknowledge the substantial contributions of Dr. Karen Martin, John D.
Bachmann, and John Haines for their guidance of the overall efforts, Terence Fitz-Simons,
David Mintz, and Miki Wayland for providing analytical support, and Tricia Crabtree for
providing substantial wordprocessing and general support for the Staff Paper. The Staff
Paper includes comments from OAQPS, the Office of Research and Development, OPPE,
Regional Offices, and the Office of General Counsel within EPA.
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TABLE OF CONTENTS
List of Tables
List of Figures
I. PURPOSE 1-1
H. BACKGROUND H-l
A. Legislative Requirements n-1
B. History of PM NAAQS Reviews H-3
1. Establishment of the NAAQS for Paniculate Matter H-3
2. First Review of NAAQS for Paniculate Matter H-3
3. Recent Litigation n-4
4. Current Review of the Paniculate Matter NAAQS n-4
m. APPROACH m-i
A. Bases for Initial Analytical Assessments , ni-1
1. Primary Standards ni-1
2. Secondary Standards m-2
B. Organization of Document IH-2
IV. AIR QUALITY CONSIDERATIONS IV-1
A. Multi-modal Size Distribution: Fine and Coarse Fractions of PM IV-2
B. Fine and Coarse Fractions' Distinct Properties IV-7
1. Chemical Composition, Solubility, and Acidity IV-7
2. Sources and Formation Processes IV-10
3. Atmospheric Lifetime, Transport, and Infiltration Indoors .... IV-11
4. Correlations Between PM2.5 and Coarse Fraction IV-15
C. Trends of U.S. PM Levels IV-15
D. Current U.S. PM Levels IV-19
E. Air Quality Comparisons of PM2.5 and PM10 IV-24
1. Mass Concentration Ratios of PM25 to PM10 IV-24
2. Correlations Between PM25 and PMIO IV-28
3. Ratio of Highest Daily Value to Annual Mean IV-36
F. Background PM Levels IV-40
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V. CRITICAL ELEMENTS IN THE REVIEW OF THE PRIMARY
STANDARDS V-1
A. Mechanisms *-l
1. Dosimetric Considerations V-l
a. Current Standard V-l
b Recent Dosimetry Considerations of Interest V-5
2. Possible Mechanisms of Action for Health Effects Associated
with Ambient Levels of Paniculate Matter Exposure V-6
a. Inflammation V-8
b. Aggravation of Underlying Condition V-10
c. Inflammation and Bronchoconstriction V-ll
d. Particle Accumulation V-12
e. Impaired Respiratory Defense V-13
B. Sensitive Subpopulations V-14
1. Individuals with Respiratory and Cardiovascular Disease V-15
2. Individuals with Infections V-17
3. The Elderly V-18
4. Children V-18
5. Smokers V-19
6. Mouth or Oronasal Breathers V-19
C. Nature of Effects V-19
1. Mortality V-22
a. Mortality from Short-term Exposures to PM V-22
i. Historical Findings from Community
Epidemiology V-22
ii. Recent Findings V-23
iii. Specific Causes of Mortality Associated with PM . V-24
iv. Experimental Animal Studies V-25
b. Mortality from Long-term Exposures to PM V-25
i. Recent Findings V-25
ii. Specific Causes of Mortality V-26
c. Extent of Mortality Displacement V-27
2. Aggravation of Existing Respiratory and Cardiovascular Disease . V-29
a. Hospital Admissions and Emergency Department Visits . . V-29
b. School Absences, Work Loss Days, and Restricted
Activity Days V-30
3. Respiratory Mechanics and Symptoms V-31
a. Acute Pulmonary Function Changes and Respiratory
Symptoms from Short-term Exposures V-31
i. Community Air Pollution V-31
ii. Controlled Exposures to Laboratory Aerosols .... V-32
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b. Long-term Exposure to PM V-34
i. Chronic Pulmonary Function Changes V-34
ii. Chronic Respiratory Disease V-34
iii. Lasting Physiological Effects V-35
4. Morphological Damage V-35
5. Altered Clearance and Other Host Defense Mechanisms V-36
6. Cancer V-38
D. Strength and Coherence of Epidemiological Evidence V-39
1. Consistency and Coherence V-40
2. Model Sensitivity V-41
3. Exposure Misclassification V-41
4. Confounding in Short-term Studies V-43
a. Weather V-44
b. Confounding by Other Pollutants V-45
i. Sulfur Dioxide V-46
ii. Ozone V-50
iii. Carbon Dioxide V-51
iv. Nitrogen Dioxide V-52
c. Summary of Short-term Confounders V-53
5. Confounding in Long-term Studies V-53
E. Concentration-Response Information V-55
1. Criteria for Assessment V-56
2. Concentration-Response Relationships from Short-term Studies . . V-58
a. PM,o/PM2.5 Studies V-58
b. Sulfate Studies V-62
c. TSP Studies V-62
3. Concentration-Response Relationships from Long-term Studies . . V-64
a. PM2.5 Studies V-65
b. Supporting Studies with Other Indicators V-68
VI. STAFF CONCLUSIONS AND RECOMMENDATIONS ON PRIMARY
NAAQS VI-1
A. Averaging Time and Form of the Standards VI-1
1. Short-Term Standards VI-2
a. Averaging Time VI-2
b. Form VI-3
2. Long-Term Standards VI-3
a. Averaging Time VI-3
b. Form VI-5
B. Particulate Matter Indicator VI-5
1. General Considerations VI-5
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2. Alternative Refinements for PM,0 Indicator VI-7
a. Indicators for the Fine and Coarse Fractions of PM10 . . . VI-8
i. Fine Particles VI-8
ii. Coarse Fraction of PM10 VI-14
b. Chemical Class Indicators - Sulfates and Acid Aerosols . VI-15
3. Staff Conclusions and Recommendations for a Particle Indicator VI-17
C. Level of the Standards VI-19
1. General Considerations and Approach VI-20
2. Specific Considerations and Conclusions for PM2 5 Standards . . VI-22
a. 24-Hour PM2.5 Standard VI-22
i. Levels of Interest from Short-term
Epidemiological Studies VI-22
ii. Margin of Safety Considerations for a 24-Hour
PM2.5 Standard VI-25
b. Annual PM25 Standard VI-27
i. Levels of Interest from Long-term
Epidemiological Studies VI-27
ii. Margin of Safety Considerations for an Annual
PM2.5 Standard VI-28
3. Staff Recommendations for PM25 Standards VI-30
a. 24-Hour PM2 5 Standard VI-30
b. Annual PM2 5 Standard VI-32
4. Staff Conclusions and Recommendations for PM10 Standards . . VI-33
D. Summary of Staff Recommendations VI-35
VH. CRITICAL ELEMENTS IN THE REVIEW OF THE SECONDARY
STANDARD FOR PARTICULATE MATTER VII-1
A. Introduction VEt-1
B. Effects of PM on Visibility VII-1
1. Types of Visibility Impairment VII-1
2. Social Valuation of Visibility VII-2
3. Visibility-Impairing Particles VII-3
4. Metrics for Expressing Visibility Impairment and Light
Extinction VH-4
5. Overview of Current Visibility Conditions VEI-5
6. Estimated Background Levels of Fine Particles and Associated
Light Extinction VII-6
7. Role of Humidity in Light Extinction VII-6
8. Rayleigh Scattering VU-7
9. Significance of Anthropogenic Sources of Fine Particles VH-8
10. Regional Differences in Anthropogenic Pollutant Levels VII-8
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11. Regional Variation in Urban Visibility VH-9
12. Staff Considerations Pertaining to the Effects of PM on
Visibility VH-9
C. Effects of PM on Materials Damage and Soiling VH-12
1. Materials Damage vn-12
a. Effects on Metals VH-13
b. Effects on Paint VH-14
c. Effects on Stone VH-15
d. Effects on Electronics VH-16
2. Staff Considerations Pertaining to the Effects of PM on
Materials Damage VI1-16
3. Soiling VH-16
4. Societal Costs VH-19
a. Soiling/Property Value VH-19
b. Soiling/Materials VII-20
5. Staff Considerations Pertaining to the Effects of PM on Soiling . VH-21
D. Summary of Staff Conclusions and Recommendations on Secondary
NAAQS VH-21
APPENDIX A Considerations in Selecting Particle Size Cutpoint for Fine
Particles A-l
APPENDK B Chemical Composition Data for Paniculate Matter B-l
APPENDIX C Summary of PM2.5 Air Quality Databases on Model for
Predicting PM2.5 C-l
APPENDIX D Strengths and Limitations of Experimental Human and Animal
Studies D-l
APPENDIX E Epidemiological Evidence of Short-term Mortality Effects E-l
APPENDIX F Miscellaneous Tables of Effects Information F-l
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LIST OF TABLES
Number
IV-1 Particle Size Fraction Terminology Used in this Staff Paper IV-6
IV-2 Comparison of Fine Versus Coarse Mode Particles IV-8
IV-3 Median of 24-Hour PM2 5/PMi0 Mass Concentration Ratios IV-27
IV-4 Correlations of Fine, Coarse Fraction and PM10 IV-30
IV-5 Correlations of PM2.1 with PM10 and Sulfates with PM10 in 24 North
American Cities IV-31
IV-6 Summary of Ratios of Highest Annual Day to Annual Mean for PM2.5
and PM10 IV-37
FV-7 Distribution of Highest 24-Hour Value to Annual Mean Ratios for
PM10 IV-38
IV-8 Distribution of Highest 24-Hour Value to Annual Mean Ratios for
PM2.5 IV-39
V-l Major Regions of the Respiratory Tract V-2a
V-2 Sensitive Population Subgroups V-14
V-3 Particulate Matter Effects of Concern V-20
V-4 Epidemiological Studies of Short-Term PM Exposure Mortality Studies:
Comparison of Relative Risk (RR) Estimates For Total Mortality From
50 /ig/m3 Change in PM10 V-23a
V-5 Recent Epidemiological Short-Term Fine Particle Exposure Mortality
Studies . . V-24a
V-6 Short-Term PM Exposure and Mortality Study in Combined Six-City
Analysis Relative Risk for a 25th to 75th Percentile Increase in
Alternative Measures of Paniculate Air Pollution From Schwartz 1995 . V-24b
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LIST OF TABLES (Cont'd.)
Number
V-7 Comparison of Total Mortality and Cause-Specific Mortality For
Short-Term Exposure Studies V-24c
V-8 Commonly-Based Cross-Sectional Mortality Studies (Since 1980) .... V-25a
V-9 Prospective Cohort Mortality Studies V-25c
V-10 Relative Risk Between the Cleanest and Dirtiest Cities for Total
Population and Former and Current Smokers in the Prospective Cohort
Studies V-26a
V-ll Epidemiological Studies of Hospital Admissions for Respiratory
Disease V-29a
V-12 Epidemiological Studies of Hospital Admissions for COPD V-29b
V-13 Epidemiological Studies of Hospital Admissions for Pneumonia V-29c
V-14 Epidemiological Studies of Hospital Admissions for Heart
Disease V-29d
V-15 Epidemiological Studies of Acute Pulmonary Function
Changes V-31a
V-16 Epidemiological Studies of Acute Respiratory Disease V-31d
V-17 Epidemiological Studies of Chronic Pulmonary Function Changes .... V-34a
V-18 Epidemiological Studies of Chronic Respiratory Disease V-34b
V-19 Concentration-Response Information From Selected Short-Term
Exposure Studies V-58a
V-20 Concentration-Response Information From Selected Long-Term
Exposure Studies V-64a
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Vlll
LIST OF TABLES (Cont'd.)
Number
VI-1
VI-2
VH-1
VH-2
vn-3
vn-4
VII-5
vn-6
vn-7
vn-8
B-l
11-2
5-2
Page
Estimated Levels of Minimum Clear Increased Risk in Terms of
Measured or Estimated PM2 5 (24-Hour Average) VI-22a
Estimated Levels of Minimum Clear Increased Risk in Terms of
Measured or Estimated PM2 5 (Annual Average) VI-27a
Comparison of Residential Visibility Valuation Study Results VH-2a
Average Natural Background Levels of Aerosols and Light Extinction . VU-6a
Dry Particle Light Extinction Efficiency Values Used in 1993 Analysis
of IMPROVE Data VII-6b
Comparison of Total Light Extinction to Estimated Natural Light
Extinction for Several Eastern and Western Locations
VH-Sa
Visibility Model Results: Anthropogenic Light Extinction Budgets . . . VII-8b
Percentage Contribution by Source Category to Fine Particle (and Precursor)
Emissions in the East, Southwest, and Northwest VII-9a
Annual Average and Second Highest Maximum Fine PM Levels for
Selected U.S. Cities VH-9b
Percentage Contributions of Particle Types to Annual Average Total
Light Extinction in the Washington, D.C. and Southern California
Areas VH-9c
Respiratory Diseases and Related Impairments Associated with
Occupational Exposure to Particles
Controlled Human Exposures to Acid Aerosols and Other Particles (CD)
Possible Responses to Particle Deposition in the Respiratory Tract
(1982 Staff Paper)
5-3
Sensitive Population Subgroups (1982 Staff Paper)
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LIST OF FIGURES
Number
IV-1 Idealized Fine and Coarse Mode Particle Mass IV-3
IV-2 Multi-Modal Distribution of Paniculate Matter IV-4
IV-3 Chemical Composition of PM2.5, Coarse Fraction, and PM10 by
Region IV-9
IV-4 Atmospheric Lifetime of Particles Based on Size IV-13
IV-5 Sources of PM2.5 and PM10 in Homes IV-14
IV-6 Scatter Plot of PM2.5 and Coarse Fraction Concentrations IV-16
IV-7 PM-10 Trend, 1988-1993 (Annual Arithmetic Mean) IV-17
IV-8 PM-10 Trend, 1988-1993 (90th Percentile) IV-18
IV-9 Areas Designated Nonattainment for Particulates (PM-10) as of
September 1994 IV-20
IV-10 PM2.5 AIRS Data Summary, 1983-1993 IV-21
IV-11 PM-10 Air Quality Concentrations Map, 1993 Highest Second 24-Hour
Average IV-22
IV-12 PM-10 Air Quality Concentrations, 1993 IV-23
IV-13 Predicted Fine Particle Concentrations, 1993 IV-25
IV-14 Predicted Fine Particle Concentrations, 1993 IV-26
IV-15 Scatter Plot of PM2.5 and PM10 Concentrations IV-29
IV-16 Time Series of PM2.5, Coarse Fraction, PM10 Daily Concentrations in
Philadelphia, PA, 1990 IV-33
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LIST OF FIGURES (Cont'd.)
Number
IV-17 Time Series of PM2.5, Coarse Fraction, PM10 Daily Concentrations
in St. Louis, MO, 1993 IV-34
V-l Relationship Between Relative Risk Per 50 /*g/m3 PM10 and Specific
Causes of Mortality and Morbidity in Adults and Children V-40a
V-2 Relationship Between Relative Risk of Mortality Associated with PM10
and Levels of SOj, CO, NO2, and Ozone V-46a
V-3 Relationship Between Relative Risk of Mortality and PM-10 in St.
Louis and Eastern Tennessee (Dockery et al., 1992) V-59a
V-4 Relationship Between Relative Risk of Death and PM-10 in the Utah
Valley (Pope et al., 1992) V-59a
V-5 Relationship Between Relative Risk of Death and PM-10 in
Birmingham (Schwartz, 1993a) V-60a
V-6 Relationship Between Relative Risk of Pneumonia Admission Among
the Elderly and PM-10 in Detroit (Schwartz, 1994d) V-60a
V-7 Relationship Between Relative Risk of COPD Admissions Among the
Elderly and PM-10 in Detroit (Schwartz, 1994d) V-60b
V-8 Relationship Between Relative Risk of Pneumonia Admissions Among
the Elderly and PM-10 in Birmingham (Schwartz, 1994e) V-60b
V-9 Relationship Between Ischemic Heart Disease Admissions Among the
Elderly and PM-10 (Schwartz and Morris, In Press) V-61a
V-10 Relationship Between the Odds of Cough Incidence Versus PM-10
Concentration from the Six City Study (Schwartz et al., 1994) V-61b
V-ll Relationship Between Percent of Children Reporting Symptoms and
PM-10 in Utah Valley (Pope and Dockery, 1992) V-61b
V-12 Relationship Between Respiratory Hospital Admissions and Sulfate
Concentrations in Ontario (Burnette et al., 1994) V-62a
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LIST OF FIGURES (Cont'd.)
Number
V-13 Relationship Between Relative Mortality and TSP or SO2 in
Philadelphia (Samet et al., 1995) V-62a
V-14 Relationship Between Mortality Risk Rate Ratios and PM-2.5 in the Six
City Study (Dockery et al., 1993) V-65a
V-15 Relationship Between Adjusted Mortality and PM-2.5 in the American
Cancer Society Study (Pope et al., 1995) V-65a
V-16 Relationship Between Bronchitis Prevalence and PM-15 in the Six
Cities Study (Dockery et al., 1993) V-69a
V-17 Relationship Between Relative Risk of Chronic Bronchitis and TSP for
NHANES I Survey Subjects (Schwartz, 1993b) V-69b
V-18 Relationship Between Relative Risk of Respiratory Illness and TSP for
NHANES I Survey Subjects (Schwartz, 1993b) V-69b
VII-1 Visual Range and Extinction Coefficient as a Function of Haziness
Expressed in Deciview VII-5a
VII-2 Average Reconstructed Light Extinction Coefficient Calculated From
the Aerosol Concentrations Measured During the First Three Years of
IMPROVE VH-5b
VII-3 Comparison of Sulfur Emission Trends and Extinction Coefficient for
the Southeastern U.S. Region During the Summer Months VH-5c
VQ-4 Spatial Variation in Average Relative Humidity and the Sulfate RH
Correction Factor VE-7a
•
VII-5 Effects of Fine Particle Increments on Calculated Visual Range . . . vn-lOa
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REVIEW OF THE NATIONAL AMBIENT AIR QUALITY STANDARDS
FOR PARTICULATE MATTER:
POLICY ASSESSMENT OF SCIENTIFIC AND TECHNICAL INFORMATION
I. PURPOSE
The purpose of this Office of Air Quality Planning and Standards (OAQPS) Staff
Paper is to evaluate the policy implications of the key studies and scientific information
contained in the EPA document, "Air Quality Criteria for Paniculate Matter" (U.S. EPA,
April 1995 External Review Draft; henceforth referred to as the CD), and to identify the
critical elements that EPA staff believes should be considered in review of the national
ambient air quality standards (NAAQS) for paniculate matter (PM). This assessment is.
intended to help bridge the gap between the scientific review contained in the CD and the
judgments required of the Administrator in setting ambient standards for PM. Thus,
emphasis is placed on identifying those conclusions and uncertainties in the available
scientific literature that the staff believes should be considered in selecting paniculate
pollutant indicators, forms, averaging times, and levels for the primary (health) and
secondary (welfare) standards. These specifications must be considered collectively in
evaluating the health and welfare protection afforded by PM standards.
While this Staff Paper should be of use to all parties interested in the standards
review, it is written for those decision makers, scientists, and staff who have some
familiarity with the technical discussions contained in the CD. This Staff Paper presents
factors relevant to the evaluation of current primary and secondary NAAQS, as well as staff
conclusions and recommendations of suggested options for the Administrator to consider.
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H. BACKGROUND
A. Legislative Requirements
Two sections of the Clean Air Act govern the establishment and revision of NAAQS (42
U.S.C. 7401 to 7671q, as amended). Section 108 (42 U.S.C. 7408) directs the
Administrator to identify pollutants which "may reasonably be anticipated to endanger public
health and welfare" and to issue air quality criteria for them. These air quality criteria are
intended to "accurately reflect the latest scientific knowledge useful in indicating the kind and
extent of all identifiable effects on public health or welfare which may be expected from the
presence of [a] pollutant in the ambient air . . ."
Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate
"primary" and "secondary" NAAQS for pollutants identified under section 108. Section
109(b)(l) defines primary standards 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." 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,
manmade [sic] 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."
The U.S. Court of Appeals for the District of Columbia Circuit has held that the
requirement for an adequate margin of safety for primary standards 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
'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)).
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against hazards that research has not yet identified (Lead Industries Associations. EPA, 647
F.2d 1130, 1154 (D.C. Cir. 1980), cert, denied. 101 S. Ct. 621 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176,1177 (D.C. Cir. 1981), cert, denied. 102 S. Ct. 1737
(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, by selecting ^primary standards that provide 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 she finds may pose
an unacceptable risk of harm, even if the risk is not precisely identified as to nature or
degree. :
In selecting a margin of safety, the 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. Given that the "margin of
safety" requirement by definition only comes into play where no conclusive showing of
adverse effects exists, such factors which involve unknown or only partially quantified risks
have their inherent limits as guides to action. 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, supraj 647 F.2d at 1161-62).
Section 109(d)(l) of the Act 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 ... as may be appropriate ...." Section
109(d)(2) requires that an independent scientific review committee be appointed and provides
that the 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 ...
revisions of existing criteria and standards as may be appropriate ...."
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B. History of PM NAAOS Reviews
1. Establishment of the NAAQS for Paniculate Matter
National ambient air quality standards for PM were first established in 1971, based on
the original criteria document (DHEW, 1969). Paniculate 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 natural sources. Particles may be
emitted directly or formed in the atmosphere by transformations of gaseous emissions such as
sulfur oxides, nitrogen oxides, and volatile organic substances. 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 reference method specified for determining attainment of the original standards
was the high-volume sampler, which collects PM up to a nominal size of 25 to 45 /xm (so-
called total suspended paniculate or TSP). The primary standards (measured by the
indicator TSP) were 260 /*g/m3, 24-hour average, not to be exceeded more than once per
year, and 75 /xg/m3, annual geometric mean. The secondary standard (measured as TSP)
was 150 /xg/m3, 24-hour average not to be exceeded more than once per year.
2. First Review of NAAQS for Paniculate Matter
In October 1979 (44 FR 56731), EPA announced the first review of the criteria
document and NAAQS for PM and, after a lengthy and elaborate process, promulgated
significant revisions of the original standards in 1987 (52 FR 24854, July 1, 1987).2 In that
decision, EPA changed the indicator for particles from TSP to PM,0, the latter referring to
particles with a mean aerodynamic diameter less than or equal to 10 microns.3 EPA also
2The revised standards were based on a revised Criteria Document (U.S. EPA, 1982a), a corresponding
Staff Paper (U.S. EPA, 1982b), and subsequent addenda to those documents (U.S. EPA, 1986a; U.A. EPA, 1986b).
A detailed description of the process followed in reviewing and revising the original Criteria Document and NAAQS
appears in the notice of final rulemaking (52 FR at 24636-37).
3The more precise term is 50 percent cut point or 50 percent diameter (Dy,). This is the aerodynamic particle
diameter for which the efficiency of particle collection is 50 percent. Larger particles are not excluded altogether,
but are collected with substantially decreasing efficiency and smaller particles are collected with increasing (up to
100 percent) efficiency. Ambient samplers with this cut point provide a reliable estimate of the total mass of
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revised the level and form of the primary standards by 1) replacing the 24-hour TSP standard
with a 24-hour PM,0 standard of 150 /xg/m3 with no more than one expected exceedance per
year and 2) replacing the annual TSP standard with a PM,0 standard of 50 /ig/m3, expected
annual arithmetic mean. The secondary standard was revised by replacing it with 24-hour
and annual standards identical in all respects to the primary standards. The revisions also
included a new reference method for the measurement of PM10 in the ambient air and rules
for determining attainment of the new standards. On judicial review, the revised standards
were upheld in all respects (Natural Resources Defense Council v. Administrator. 902 F. 2d
962 (D.C. Cir. 1990), cert, denied. Ill S. Ct. 952 (1991)).
3. Recent Litigation
The American Lung Association filed suit on February 15, 1994, to compel EPA to
complete the present review of the PM NAAQS by December 1995. The U.S. District
Court for the District of Arizona subsequently ordered EPA to complete the review and any
revision of the PM NAAQS by January 31, 1997, with a proposed decision on the NAAQS
required by June 30, 1996 (American Lung Association v. Browner, CIV-93-643-TUC-ACM
(D. Ariz., October 6, 1994)).
4. Current Review of the Paniculate Matter NAAQS
In December 1994, EPA presented its plans for completing review of the criteria
document and NAAQS for PM under the court order to the CASAC. In addition, EPA's
OAQPS completed a PM NAAQS Development Project Plan in January 1995, which
incorporated CASAC comments, and identified key issues to be addressed in this Staff Paper
and the basis for the additional scientific and technical assessments needed to address the
policy issues.
EPA desires to incorporate as much peer review and public input into the review as is
possible under the court-ordered schedule. Accordingly, as part of the development of the
CD, EPA hosted a public PM-Mortality Workshop in November 1994, at which seminal new
studies on particles and health effects were presented and discussed. In January 1995, the
suspended participate matter of aerodynamic size less than or equal to 10 /xm.
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EPA's National Center for Environmental Assessment (NCEA) hosted three public peer-
review workshops on drafts of key chapters of a revised CD. The NCEA subsequently
released a complete draft of the revised CD for CASAC and public review, and CASAC
reviewed the draft at a public meeting held on August 3-4, 1995. The NCEA is currently
revising the draft CD in response to CASAC and public comments.
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m. APPROACH
This Staff Paper is based on the scientific evidence reviewed in the revised CD and
takes into account CASAC and public comments on that document to the extent possible.
The staff has also considered comparative air quality analyses and exposure-response
assessments in evaluating the appropriateness of revising the current primary NAAQS and in
assessing potential alternative NAAQS. Technical and economic analyses examining
visibility impairment, soiling and materials damage, and possible ecosystem effects have also
been considered in evaluating the appropriateness of revising the current secondary NAAQS
and in assessing potential alternative NAAQS.
The approach taken in this Staff Paper is to assess and integrate the above information
in the context of those critical elements that the staff believes should be considered in
reviewing the primary and secondary standards. Attention is drawn to judgments that must
be made based on careful interpretation of incomplete or uncertain evidence. In such
instances, the Staff Paper provides the staffs evaluation, sets forth alternatives the staff
believes should be considered, and recommends a course of action.
A. Bases for Initial Analytical Assessments
To facilitate meeting the court-ordered schedule, the staff identified several possible
policy alternatives to provide a basis for commencing initial analytical assessments of air
quality, human exposure, and health risks. In so doing, the staff recognized that additional
alternatives might need to be analyzed as the review process continued (e.g., as a result of
CASAC and public review of drafts of the CD and this Staff Paper).
1. Primary Standards
Many health scientists have expressed the opinion that observed epidemiological
associations between PM,0 and health effects may actually be primarily the result of
exposures to the fine particle fraction of PM10 (particles that are approximately an order of
magnitude smaller than 10 /xm in aerodynamic diameter and generated largely from
combustion processes). As in the 1987 review of the NAAQS, selecting the most appropriate
indicator for PM is a major issue for this review. Thus, the staff planned for initial analytic
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November 1995 III-2
assessments of the assumption that this PM NAAQS review might result in setting or
retaining one or more primary standards from the following possibilities:
• Short-term Standard: A 24-hour standard using a fine particle indicator, a
PM,0 indicator, or both; and
• Long-term Standard: An annual standard using a fine particle indicator, a
PMj0 indicator, or both.
The staff also recognized that other indicators of PM pollution (e.g., sulfates and acids) may
be important in relating effects to PM pollution.
2. Secondary Standards
In revising the secondary standards, the staff has focused primarily on two types of
effects: 1) visibility impairment and 2) soiling and materials damage. In the case of
visibility, this Staff Paper briefly assesses available scientific information in order to
determine an appropriate regulatory approach for addressing regional haze. A key
consideration in this assessment is that a number of factors that influence visibility
impairment vary significantly between the eastern and western parts of the U.S. Thus, this
Staff Paper examines the advisability of a uniformly implemented and attained secondary
NAAQS as contrasted to the establishment of a regional haze program under section 169A of
the Clean Air Act. This Staff Paper also examines the available literature on material
damage and soiling to ascertain whether such information provides a basis for establishing a
separate national secondary NAAQS to protect against such effects.
B. Organization of Document
The remainder of this Staff Paper is organized as outlined below. Chapter IV
provides a summary of differences among the various fractions of PMIO, relevant physical
and chemical properties, air quality status and trends for both PM10 and fine particles, and
characterizations of average "background" concentrations.
Chapter V discusses biological mechanisms of toxieity, sensitive subpopulations, the
nature of health effects associated with PM, evaluations of the evidence, and concentration-
response information. Chapter V also presents staff judgments concerning which effects are
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important for the Administrator to consider in selecting appropriate primary standards and
uncertainties surrounding the specific agents of concern.
Drawing on these factors and on information contained in the previous chapters,
Chapter VI presents staff conclusions and recommendations for the Administrator to consider
in reaching a decision on revision of the primary NAAQS. The chapter addresses alternative
averaging times, forms, pollutant indicators, and levels, with a summary section that presents
the staffs overall recommendations for a suite of primary standards.
With respect to review of the secondary standards, Chapter VII presents information
on visibility impairment and soiling and materials damage, discusses pertinent considerations,
and offers staff conclusions and recommendations for the Administrator to consider in
reaching a decision on revision of the secondary NAAQS.
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IV. AIR QUALITY CONSIDERATIONS
Particulate matter (PM) represents a broad class of chemically and physically diverse
substances. The principal common feature of PM is existence as discrete particles in the
condensed (liquid or solid) phase spanning several orders of magnitude in size, from
molecular clusters of 0.005 /*m in diameter to coarse particles on the order of 100 jim.1 In
addition to characterizations by size, particles can be described by their formation mechanism
or origin, chemical composition, physical properties, and in terms of what is measured by a
particular sampling technique.
In most locations, a variety of diverse activities contribute significantly to PM
concentrations, including fuel combustion (from vehicles, power generation, and industrial
facilities), residential fireplaces, agricultural burning, and atmospheric formation from
gaseous precursors (largely produced from fuel combustion). Other sources include
construction and demolition activities, wind blown dust, and road dust. From these diverse
sources come the mix of substances that comprise PM. The major chemical constituents of
PM10 are sulfates, nitrates, carbonaceous compounds (both elemental and organic carbon
compounds), acids, ammonium ions, metal compounds, water, and crustal materials. The
amounts of these components vary from place to place and over time.
Examining air quality information is important to understanding possible human
exposures and potential impacts on health and welfare. This chapter briefly discusses the
chemical and physical properties of PM in the atmosphere and presents historical and current
PM10 and PM2.5 levels.
lln this staff paper, particle size or diameter refers to aerodynamic diameter. Aerodynamic diameter is
defined as the diameter of a spherical particle with equal settling velocity but a material density of 1 g/cm3.
This normalizes particles of different shapes and densities.
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A. Multi-modal Size Distribution: Fine and Coarse Fractions of PM
The health and environmental effects of PM and the fate of the components are
strongly related to the size of the particles. The aerodynamic size of particles plays a major
role in determining the extent to which they are able to penetrate into the respiratory tract
and how they behave once inside (e.g., how far the particles are able to penetrate, the extent
to which the body's clearance mechanisms are effective in removing the particles, and where
they are deposited as discussed in Chapter V). Furthermore, size is one of the most
important parameters in determining atmospheric lifetime and visibility impact of particles.
Atmospheric lifetime is also important to health effects because of its relationship to
exposure. Differences in surface area, number of particles, chemical composition, water
solubility, formation process, and emission sources also vary with particle size. Thus, size is
an important parameter in characterizing PM, and particle diameter has been used to define
the present standard.
The multi-modal distribution of particles based on diameter has long been recognized
(Whitby, Husar, and Liu, 1972; Whitby et al., 1975; Willeke and Whitby, 1975; National
Research Council, 1977; U.S. EPA, 1982a; U.S. EPA, 1982b; U.S. EPA, 1986b; CD
Chapter 3). Particles can be divided into fine and coarse modes based on particle size and
formation mechanism.
Although particles display a consistent multi-modal distribution over several physical
metrics such as surface area and mass, the specific distributions may vary over place,
conditions, and time because of different sources, atmospheric conditions, and topography.
Figure IV-1 illustrates an idealized mass distribution of the two distinct modes related to
particle size: fine and coarse particles. Fine particles can be further classified as nuclei,
ultrafine, and accumulation modes. The fine mode also accounts for most of the surface area
and number of particles, as shown in Figure IV-2.
The CD concludes that an appropriate cut point for distinguishing between the fine
and coarse modes lies in the range of 1.0 pirn to 3.0 urn where the minimum mass occurs
between the two modes (CD Chapter 3; Miller et al., 1979). However, the CD states that
the data do not provide a clear or obvious choice of cut point and that some overlap occurs
-------
70
60
50
40
30
20
10
0
0.1
Fine Particles
Coarse Particles
0.2
0.5 1.0 2 5 10 20
Aerodynamic Particle Diameter (Da), Mm
Total Suspended Particles (TSP)
PM 10
Fine Fraction (<2.5 pm)
Coarse
Fraction
(2.5-10 pm)
TSP
HiVol
RAC-
50 100
Figure IV-1. Idealized Fine and Coarse Mode Particle Mass
The dotted lines represent the mass captured by different monitors. For example, PM10
mass would be proportional to the portion of the coarse mode under the curve (the coarse
fraction) and all of the fine fraction.
ff
-------
IT)
'o
1—
X
•"a.
Q
ou
1.2r
1.0
9o 0.8
-a.
O
< 0.6
co
0.4
§
"§ 0.2
oo
I
I
c
r*
O*
CO
3.
s
0.01
0.1 1
Particle diameter
10
Figure rv-2. These normalized plots of number, surface and volume (mass)
distributions from Whitby (1975) show a bimodal mass distribution in a
smog aerosol. Historically, such particle size plots were described as
consisting of a coarse mode (2.5 to 15 /tm), a fine mode (0.1 to 2.5 |tm),
and a nuclei mode (< 0.05jim). The nuclei mode would currently fall
within the ultrafine particle range (0.005 to 0.1 jim).
I
o.
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November 1995 IV-5
between the modes. Appendix A outlines the policy considerations in choice of cut point for
measuring fine particles.
Table IV-1 introduces some of the size-related terminology used in this Staff Paper.
For the purposes of this document, PM2 5 is used to refer to gravimetric measurements with a
2.5 fj.m cut point while fine particles will be used more generally to refer to the fine mode.
Because of the possible overlap of fine and coarse modes in the intermodal region (i.e., 1 - 3
/xm), PM2 5 is only an approximation for fine particles. Moreover, monitor design,
measurement temperature, and inlet efficiency can also affect which particles are included in
the definitions of the various size fractions. Sampling method may also affect the amount of
semivolatile organics and nitrates and particle-bound water included in the measurement.
In addition to PM2.5 mass measurements, fine particles have been measured in the U.S. and
abroad using a variety of techniques resulting in a variety of indicators including British
Smoke (BS), Coefficient of Haze (COH), carbonaceous material (KM), and estimates from
visibility measurements. In the past, it was noted that visibly black plumes were emitted by
industrial sources; thus, light absorption was adopted as a measure of PM pollution (Chow,
1995). Measurements of the optical properties of particles may be related to gravimetric
mass measurements on a site- and time-specific basis with on-site calibrations.
BS preferentially measures carbonaceous particles found in the fine fraction. In
addition, the BS inlet design taken together with its other operating parameters restricts the
size of particles that are sampled. For example, it has been shown in wind tunnel tests that
the best estimate of the cut point is 4.5 /*m (Waller, 1980; McFarland, 1979). Most particles
larger than the cut point of 4.5 fim are either rejected at the inlet or lost in the inlet line
(U.S. EPA, 1982a). Furthermore, the BS reading varies more with darkness of particles
(i.e., carbon content) than with mass, thus making associations with mass highly case-
specific. In the U.S., elemental carbon is found predominantly in the fine mass ( < 1.0 pm
range) (NAS, 1980; U.S. EPA, 1982b).
Using a similar principle to BS, the principle of COH measurement is that visible
light is transmitted through (or reflected from as in the case of BS) a section of filter paper
before and after ambient air is drawn through it and the amount of light transmitted is
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IV-6
Table IV-1. Particle Size Fraction Terminology
Used in this Staff Paper
Fraction
Description
Fine particles
PM
2.5
Coarse particles, generally
Coarse fraction of PM
10
PM
10
Total Suspended Particles (TSP)
Fine mode particles which are generally formed
through chemical reaction, nucleation,
condensation of gases, and coagulation of smaller
particles; contains most numerous particles and
represents most surface
Particles with an upper 50 percent cut point of
aerodynamic diameters1 less than 2.5 /xm, a
measurable approximation for fine particles2
Coarse mode particles which are mostly
mechanically generated through crushing or
grinding
Particles with an upper 50 percent cut point of
aerodynamic diameters between 2.5 /im and 10
Particles with an upper 50 percent cut point of
aerodynamic diameters less than 10 /im, including
fine fractions and part of the general coarse mode
Particles with an upper 50 percent cut point of
aerodynamic diameters less than approximately 50
highly wind speed dependent
'Aerodynamic diameter is defined as the diameter of a spherical particle with equal settling velocity but a
material density of 1 g/cm3. This normalizes particles of different shapes and densities.
diameter will
„ indicates an upper cut point with a 50 percent cut point of X /tm diameter. Because samplers have a
collection efficiency that varies around the 50 percent cut point, not all particles less than X Mm diamp.^r ™;i
be collected and some particles greater than X /xm diameter will be collected.
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November 1995 IV-7
measured by a photocell (Chow, 1995; Fairley, 1990). In addition, this sampler uses a
funnel inlet and a small diameter transport tube nearly identical to the BS sampler. Although
the two samplers operate at different flow rates, the particles reaching the filter tape could be
expected to have a size range similar to that of the BS instrument (U.S. EPA, 1982a, see
Figure 3A-12).
Prior to the 1980s, PM was measured in California by optical reflectance of particles
collected on a sample tape (KM). Similar in principle to BS, KM has been shown to be
closely related to elemental carbon content in Los Angeles (Kinney and Ozkaynak, 1990).
Similar to BS, KM is also a fine particle measurement.
B. Fine and Coarse Fractions* Distinct Properties
In addition to being distinguishable based on size considerations, fine and coarse
particles have many other distinct properties, as summarized in Table IV-2. Fine and coarse
particles can be differentiated by their chemical composition, solubility, acidity, sources and
formation processes, atmospheric lifetime, infiltration indoors, and transport distances.
Furthermore, fine and coarse particle mass concentrations generally are poorly correlated
(Wilson et al., 1995; SAI, 1995).
1. Chemical Composition, Solubility, and Acidity
Figure IV-3 shows the synthesis of the available published data on the chemical
composition in U.S. cities broken down by region between PM25 and coarse fraction
particles which together comprise PM10 (CD, Chapter 6). Sulfates and organic carbon
dominate fine particles (together accounting for between 50 to over 90 percent of fine mass);
whereas, minerals dominate the coarse fraction of PMjo (ranging from over 50 percent to 70
percent of coarse fraction mass) (CD, Chapter 6). Differences across the country in sources
and atmospheric conditions contributes to this variability.
In general, fine and coarse particles have different solubility and acidity. With the
exception of carbon and some organic compounds, fine particles are largely soluble in water
and hygroscopic (i.e., they readily take up and retain water), although some are deliquescent
(i.e., they remain crystalline until a certain relative humidity is exceeded at which point they
become hygroscopic). The fine particle mode also contains most of the acid particles (CD,
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IV-8
Do Not Quote or Cite
TABLE IV-2. COMPARISON OF FINE VERSUS COARSE MODE PARTICLES
Fine Mode
Coarse Mode
Formed from:
Formed by:
Composed of:
Solubility:
Sources:
Lifetimes:
Travel
Distance:
Gases
Chemical reaction;
Nucleation,
Condensation,
Coagulation.
Evaporation of fog and cloud
droplets in which gases have
dissolved and reacted.
Sulfate, SO4=;
Nitrate, NO*
Ammonium, NH^:
Hydrogen ion, If;
Elemental carbon, C;
Organic compounds;
PNA;
Metals, Pb, Cd, V,
Ni, Cu, Zn;
Particle-bound water;
Biogenic organics.
Significant fraction soluble,
hygroscopic and deliquescent;
some portions insoluble.
Combustion of coal, oil,
gasoline, diesel, wood.
Atmospheric transformation
products of NOX, SO2, and
organics including biogenic
organics, e.g., terpenes.
High temperature processes,
smelters, steel mills, etc.
Days to weeks
100s to 1000s of kilometers
Large solids/droplets
Mechanical disruption
(crushing, grinding etc.),
Evaporation of sprays,
Suspension of dusts.
Resuspended dusts,
Soil dust, street dust.
Coal and oil fly ash.
Metal oxides of Si,
Al, Mg, Ti, Fe.
CaCO3, NaCl, sea salt,
Pollen, mold spores,
Plant parts.
Largely insoluble and non-
hygroscopic.
Resuspension of soil tracked
onto roads and streets.
Suspension from disturbed
soil, e.g., farming, mining.
Resuspension of industrial
dusts.
Construction, coal and oil
combustion, ocean spray.
Minutes to hours
1 to 10s of kilometers
Source: Wilson et al., 1995; CD Chapter 3
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IV-9
Figure IV-3. Chemical Composition of PM2 5, Coarse Fraction, and PM10 by Region
EASTERN U.S. URBAN AREAS
PM
2.5
WESTERN U.S. URBAN AREAS
PM2.5
•U (4 J%)
Unknown (23.0%)
EC (3.8%)
OCxl.4 (20.8%)-
Nitrit* (1.1%)-
Ntu«U b«««d on3 studwi.
Coarse Fraction
Unknown (•< 1.5%)
2S04 (46.0%)
(51.8%)
Unknown (1 J%)-|
EC (14.7*)
m.4(36.6%)
r«U (14.6%)
NH42SO4 (14.0%)
Ihral* (15.7%)
Coarse Fraction
NH42S04 (6.7%)-
lntuf(ici«nt Nrtftlo. OC. and EC d«ln •v«0abl«.
Unknown (27.0%)
NH42SO4 (3.1%)
^Min«r«U (70.0%)
Insufficient Nitr«U. OC. and EC d«U iv«)Ubl«.
PM
10
Unknown (28.2%)
EC P 4%)
OCX1.4 (85%)
OCx1.4 (28.6%)
Mirxrilt (35.6%)
NKr
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November 1995 IV-10
Chapter 3). By contrast, coarse particles are mostly insoluble, non-hygroscopic, and
generally basic (CD, Chapter 3).
Fine particles also display regional differences in chemical composition. For
example, fine particles in the Eastern U.S. are comprised of relatively more sulfate (47
percent) than the west (15 percent). Many western sites have a lower sulfate and a larger
nitrate contribution. Nitrates contribute 1 percent to the Eastern U.S. mass and 15 percent to
Western U.S. mass for fine particles; Western U.S. urban areas have twice the proportion
of organic carbon compounds as found in Eastern U.S. urban areas.
The proportions presented in this figure do not show relative concentrations; however,
the relative concentrations become apparent when the fine and coarse fractions are aggregated
into the PM10 figures. (Concentrations for selected cities and time periods studied for
chemical composition are also presented in Appendix B tables; national levels are presented
below.) Concentrations of coarse fraction particles are generally higher in the Western and
Southwestern U.S. than in the Eastern U.S. PMJO is a composite of fine and coarse particles
with sulfates dominating the eastern U.S. and minerals being more important in the Western
U.S. One of the primary reasons for the heterogeneity of PM10 composition is the
fundamental underlying differences between fine and coarse particles. As presented in the
CD, Appendix B portrays the available published data on chemical constituents of PMjo, fine
particles, and coarse particles, focusing on cities in which health studies were conducted.
Other than noting that mineral and soil compounds tend to dominate the coarse fraction, no
discernable patterns in chemical composition of the PM2.5 could be determined based on this
limited database that used several different analytical techniques.
2. Sources and Formation Processes
Fine and coarse particles generally have distinct sources and formation mechanisms
although tiiere may be some relatively small overlap. Fine particles are usually formed from
gases in two ways: (1) nucleation (i.e., formation of particles from low vapor pressure
substances, produced either from combustion or from chemical reaction of gases) and (2)
condensation of gases onto existing particles. Particles formed from nucleation also
coagulate to form relatively larger particles, although these particles normally do not grow
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November 1995 IV-11
above 1.0 jtm in aerodynamic diameter by these processes (CD, Chapter 3). Particles
formed as a result of chemical reaction of gases are termed secondary particles because the
direct emission from a source is a gas (e.g., SO2 or NO) that is subsequently converted to a
low vapor pressure substance in the atmosphere. Examples of fine particles include species
such as sulfates, organics, and ammonium. Transformation from gases to particles requires
substantial interaction in the atmosphere. Such transformation can take place locally, during
prolonged stagnations, or during transport over long distances. Moisture, sunlight,
temperature, and the presence or absence of fogs and clouds affect transformation. In
general, particles formed from these types of secondary processes will be more uniform in
space and time than those that result from primary emissions. Although primary particles are
also found in the fine fractions (the most common being particles less than 1.0 /tm in
aerodynamic diameter from combustion sources), secondary particles are predominately
found in the fine range, which is one of the reasons fine particles are more uniform in space
and time than coarse particles.
By contrast, most of the coarse fraction particles are emitted directly as particles
resulting from mechanical disruption such as crushing, grinding, evaporation of sprays,
suspensions of dust from construction and agricultural operations. Simply put, coarse
particles are formed by breaking up bigger particles into smaller ones. Some combustion-
generated particles such as fly ash and soot are also found in the coarse fraction.
3. Atmospheric Lifetime, Transport, and Infiltration Indoors
Larger particles deposit more rapidly than small particles, affecting transport,
infiltration of particles formed outdoors into homes and buildings where people spend most
of their time, and thus are exposed to PM. Measurements of indoor PM levels are especially
important because people on average spend 21 hours each day indoors and thus a large
amount of their exposure to PM may occur inside (CD, Chapter 7; Robinson and Nelson,
1995).
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Every particle attains an equilibrium between gravity and atmospheric resistance at its
terminal settling velocity.2 Compared to other sizes, fine particles with aerodynamic
diameters between 0.1 and 1.0 pm have the minimum terminal settling velocity of particles.
Figure IV-4 shows that fine particles will remain suspended for much longer times (on the
order of days to weeks for fine particles as opposed to minutes to hours for coarse particles)
and will travel much farther (i.e., hundreds to thousands of kilometers) than coarse fraction
\
particles (i.e., kilometers to tens of-kilometers) (CD Chapter 3; Watson, Rogers, and Chow,
1995). Therefore, fine particles have generally longer atmospheric lifetimes than coarse
particles. '
Fine particles originating outdoors infiltrate into homes and buildings to a greater
degree than coarse particles (CD, Chapter 7; Lioy et al., 1990). Figure IV-5 presents the
relative contribution of indoor particles by source category. Approximately two thirds of
indoors PMi0 concentrations originated outdoors. Even more of the fine particles
proportionately are of outdoor origin, about three quarters. Anuszewski et al. (1992) show
that light scattering particles measured by nephelometry have very high correlation between
indoor and outdoor concentrations (R2 = 0.9). Spengler et al. (1981) found that for the
Harvard Six City study, long-term mean infiltration of outdoor-origin PM3 5 was 70 percent
for homes without air conditioning and 30 percent in homes with air conditioning. (CD
Chapter 7). Koutrakis et al. (1992) using New York State data of homes without smoking or
fireplaces found that 60 percent of the PM2.5 mass was from outdoor sources (CD Chapter
\
7). Thus, ambient particles penetrate indoors and are available to be breathed into the
lungs.
Specific constituents of fine particles penetrate well indoors as well. Suh et al. (1994)
also provide evidence that ambient fine particles penetrate indoors in State College, PA. The
correlations between personal3 and outdoor sulfate measurements were high
settling velocity increases as the square of the particle diameter or when the particle density increases.
For small particles, vertical air movements caused by turbulence can counteract the gravitational settling velocity
and such particles can remain suspended for days (Willeke and Whitby 1975).
3Personal exposure monitoring is usually accomplished by the subject carrying a portable device as the
subject goes about routine daily activities.
-------
100%
10
100
1,000 10,000
Residence Time (seconds)
100.C
1,000,000
a
^ §s
u ^
4
s
'O
I
n'
r
i
o
a
2.'
63
M
O
V^J
I'
Figure IV-4. Aging times for homogeneously distributed particles of different aerodynamic ciameters in a 100 meter deep mixed layer.
Gravitational settling is assumed for bothe still and stirred chamber models (Watson, Rogers, and Chow 1995).
-------
Figure IV-5. Sources of PM2.5 and PM10 in Homes
Cooking II Other Indoor Sources
Smoking D Outdoor
5%
14%
4%
76°/c
PM2.5
N= 352 samples
Source: PTEAM Study, Riverside, CA
26%
66%
PM10
N= 350 samples
§ a.
Oi ^
b
•i
5% |
o.
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November 1995 IV-15
(R2 = 0.92) despite the negligible indoor sources of sulfur. The correlation between
personal and ambient acidity (H+) was lower (R2 = 0.38 and R2 = 0.63 when corrected for
personal ammonia), but still meaningful given that acidity is virtually all of outdoor origin.
4. Correlations between PM2.5 and Coarse Fraction
Daily monitored concentrations of PM2.5 correlate poorly with daily concentrations of
the coarse fraction as shown in the scatter plot in Figure IV-6a using over 11,000 data points
from locations across the U.S. The estimated R-squared statistic is close to zero (R2 =
0.08), indicating that almost no linear relationship exists between daily averages of PM2.5 and
the coarse fraction. For the annual average concentration shown in Figure IV-6b, where one
would expect to see a higher correlation because the averaging smooths some of the day-to-
day variability, there is still almost no correlation between annual PM2.5 and coarse fraction
as shown by the low R-squared statistic (R2 = 0.11). Note that in some specific instances,
fine and coarse fractions may be correlated (e.g., driving a vehicle down a dusty road would
produce fine particle emissions from the exhaust and coarse emissions from the road dust).
However, overall the fine and coarse fractions are poorly correlated.
In summary, the fine and coarse fractions of PM10 are distinct entities with differing
chemical composition, sources and formation processes, atmospheric lifetimes, infiltration
indoors, and transport distances. PM2 5 and coarse fraction mass concentrations are generally
poorly correlated.
C. Trends of U.S. PM Levels
States and local air pollution control agencies have been collecting PM10 data using
EPA-approved reference samplers and reporting these data to EPA's publicly available
Aerometric Information Retrieval System (AIRS) since mid-1987. Trends may readily be
examined for the 6-year period from 1988 to 1993 as illustrated in Figures FV-7 and IV-8.
The figures represent 799 trend sites, mostly from urban and suburban locations as well as a
few remote locations; monitoring sites with data in at least five of the six years are included.
The figures show the trend and site-to-site variability in the composite annual mean
and the ninetieth percentile of 24-hour PMj0 concentrations, respectively. The ninetieth
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IV-16
Figure IV-6. Scatter Plot of PM2 5 and Coarse Fraction Concentrations
6a. Daily PM7 s v. Coarse Fraction Concentrations
8
eg
8
OJ
t
8 -
N: 11304
1&B2
14.41
Stopa: 02S
150
200
250
DaBy Coarse Mass Concentration
6b. Annual Average PM2 5 v. Coarse Fraction Concentrations
o _
Si*
53-
o>
c
a.
K 107
MunCoana: 1657
MawRm: 20XO
Mafcept 1S.6S
Slope: 026
R-Squarwt 0.11
10
20
30
—]—
40
50
60
Annual Coarse Mass Concentration
(ug/m3)
-------
110
Figure iv-7. PM-10 TREND, 1988-1993
(90th PERCENTILE)
CONCENTRATION, UG/M3
100
90-j
80
70
60-
50-
40
30
20-
10-
0
799 SITES
1988
1989
1990
1991
1992
USEPA/OAQPS/EMAD/AQTAG
1993
i!
I
-------
70
60
50
40
30
20-^
10
Figure iv-s. PM-10 TREND, 1988-1993
(ANNUAL ARITHMETIC MEAN)
CONCENTRATION, UG/M3
799 SITES
NAAQS
1988
1989
1990
1991
1992
USEPA/OAQPS/EMAD/AQTAG
1993
\8
"-"
I
•3,
t—»
00
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External Review Draft Do Not Quote or Cite
November 1995 IV-19
percentile statistic is used because PM,0 sampling frequency varies among sites and may
change from one year to the next at some sites. This statistic is less sensitive to changes in
sampling frequency than are the maximum or second maximum peak values. The trend for
the composite annual mean shows a steady decline totaling 20 percent over the six-year
period from 1988 to 1993. The ninetieth percentile similarly decreases 19 percent over the
same period (U.S. EPA, 1993).
In 1990 EPA designated 70 areas nonattainment for PM10, and 13 additional areas
were added in 1994 for a total of 83 PM10 nonattainment areas. Based on air quality data for
1992 to 1994, 37 of these are eligible for redesignation to attainment. Figure IV-9 shows the
areas in nonattainment as of September 1994, also indicating the prevalent contributing
sources and size of population residing in nonattainment areas.
The data for PM25 concentrations are more limited than the PM10 data. Figure IV-10
illustrates that a total of 87 different sites reported PM2.5 data to AIRS from 1983 to 1993.
Over the 11 year period, less than 50 sites reported data to AIRS in any given year.
Additional special studies have also monitored PM2 5, but these data are not reported in
AIRS. Appendix C summarizes the databases which were assembled by EPA to support the
air quality analyses in this Staff Paper. Fine particle trends are not available because the
number of sites measuring PM2.5 is small compared to the PM10 database and the sampling
period is restricted to a few years. Furthermore, PM2 5 is measured using non-standard
sampling frequencies and non-standard sampling equipment. Thus, data are not sufficient to
produce fine particle trends.
D. Current U.S. PM Levels
Current U.S. PM,0 levels are illustrated in Figures IV-11 and IV-12. Figure IV-11
shows the annual mean PM10 concentration, and Figure FV-12 depicts the second highest 24-
hour PMj0 concentration in each county for which data were available and data completeness
criteria were met. Each figure shows a snapshot of measured air quality data from 1993 for
-------
AK
Figure IV-9.
Areas Designated Nonattainment for Particulates (PM-10)
O AREAS NONATTAINMENT DUE TO STATIONARY SOURCE EMISSIONS
• AREAS NONATTAINMENT DUE IN PART TO WOOD SMOKE EMISSIONS
O AREAS NONATTAINMENT DUE IN PART TO FUGITIVE DUST EMISSIONS
© AREAS NONATTAINMENT DUE TO MULTIPLE TYPES OF EMISSIONS
CIRCLE DIAMETER Q
INDICATES RELATIVE SIZE
OF AFFECTED POPULATION
Designated Nonattainment Areas as of September 1994
Note: Unclassified areas are not shown.
9-
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External Review Draft
November 1995
IV-21
Do Not Quote or Cite
Figure IV-10. PM2 5 AIRS Data Summary, 1983-1993
Figure IV-lOa. Geographic Distribution of Sites
AIRS Sites Reporting PM2.5 Data, 1983-93
SLAMS (14) ASPM(49) m UNKNOWN (24)
Figure IV-lOb. Number of Sites and Frequency of Sampling
Number of Sites Reporting, 1983-93
Days sampled
in one year
0-29
30-59
60-119
>120
Sampling Frequency, 1983-93
10 20 30
Number of Sites
40
50
50 100 150 200
Number of Sites
-------
Figure iv-n. PM-10 Air Quality Concentrations, 1993
Highest Annual Mean
§
; 80
150-
1 40
130-
120-
110 -
I 100-
s
c
c 90-
I SO-
Il.
§ 70-
60-
50 -
40 -
30-
20 -
10 -
i-' '
to
SJ
I
Concentration (uo/m3)
Z) <=20
21-30
31-40
>40
-------
Figure iv-i2. PM-10 Air Quality Concentrations, 1993
Highest Second Max 24-Hour Average
s
170 -
160-
150 -
140 -
130"
120 -
110 -
M
I 100-
c
e 90-
1. 80 -
0.
I 70-
60 '
50-
40 -
30 -
20 -
10 -
0
"X.
Concentration (ug/m3)
<
~
<55
55-104
105-154
>=155
I
!
8
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External Review Draft j)0 Not Quote or Cite
November 1995 IV-24
the 647 counties in the U.S. which have at least one monitor.4 Counties not represented
with a monitor are left blank.
Although PM2.5 levels are more difficult to illustrate than PM10, the large PM10 dataset
can be scaled to augment the monitored PM2 5 data. In the locations where both PMio and
PM2.5 were measured, it is possible to discern a relationship between the PM2.5 and PM10
values and other factors and then to apply that relationship to compose a morecomplete
picture of PM2 5 levels across the U.S. This approach was used to create Figures IV-13 and
IV-14, which depict annual mean and 24-hour values, respectively, of PM2.5 concentrations
predicted from PM10 values and other factors on a county basis. More detail of this
approach and the associated uncertainties are addressed in Appendix C.
E. Air Quality Comparisons of PM2 ? and PM10
In contrast to fine and coarse fractions which are distinct entities, fine particles are a
subset of PM10. PM2 5 and PM,0 may be related using mass ratios, correlations, and day-to-
day variation. Because of the limited PM2 5 monitoring compared to PMi0 monitoring, the
conclusions are dependent on the available data. Geographic differences from the Eastern
U.S. and the Western U.S. are discernable in the relationships between PM25 and PM10.
1. Mass Concentration Ratios of PM2 5 to PMj0
Ratios of daily PM2 5 to PM10 mass concentrations show what percentage of the PMi0
is attributable to fine particles. The national ratio of daily PM2 5 to PM10 is 0.58, indicating
that based on the available data, almost 60 percent of the PM10 mass is fine particles. The
percentage varies as much as by a factor of 2 depending on the region and season (SAI,
1995). The ratios also vary significantly by time period and site location because of changes
in sources over time.
Table FV-3 presents the medians of 24-hour PM2 5/PMIO mass concentration ratios by
region and season. The table shows significant variability by region.
4For counties with more than one monitor, the monitor with the highest concentration is used for plotting
purposes. In Figure IV-11, only annual means with at least seventy-five percent data completeness are used.
Note that tests for attainment and nonattainment of the PM10 standard are generally based on 3 years of data.
Since these figures represent only 1 year of data, no conclusion can be made concerning a county's attainment
or nonattainment status using these figures alone.
-------
Figure iv-13. Predicted Fine Particle Concentrations, 1993
Highest Annual Mean
170-
i BO
150-
140"
130-
120 -
110-
I 100-
3
c
c 90-
.a
&
a 80 -
o
0.
I 70~
fiO
SO'
40 -
30"
20 -
10 '
X,. .
Concentratiofi (u^m3) iZr~Z"i <= 15
16-20
21-25
>25
I
-------
Figure iv-14. Predicted Fine Particle Concentrations, 1993
Highest Second Max 24-Hour Average
ISO
150 H
140 -!
130 "I
120 -\
110-
S 100-j
s
i 7=75
I
Q
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External Review Draft
November 1995
Do Not Quote or Cite
IV-27
Table IV-3. Median of 24-hour PM2 5/PM10 Mass Concentration
Ratios '
Season
Region
CE
NE
SE
NW
sw
All regions
Spring
0.59
0.61
0.54
0.34
0.31
0.55
Summer
0.62
0.62
0.53
0.26
0.33
0.57
Fall
0.61
0.63
0.55
0.40
0.38
0.59
Winter
0.69
0.65
0.62
0.58
0.43
0.63
All
0.63
0.63
0.57
0.36
0.35
0.58
Source: SAI, 1995; using coincident monitored data from 1988-1993.
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External Review Draft rj0 jy0/ Quote or Cite
November 1995 IV-28
For example, the Eastern U.S. shows less variability in the ratio across season than the West
(especially the Northwest). The seasonal ratios range from 0.61 to 0.65 in the Northeast
while the ratios range from 0.26 to 0.58 in the Northwest. Moreover, the Eastern ratios for
all seasons combined (0.57-0.63) are almost twice that found in the West (0.35-0.36),
indicating that fine particles are a more dominant part of PM10 in the East due to the types of
sources.
One of the major reasons PM2 5 and PMi0 do not compare well in the Western U.S. is
the higher mass contribution of the coarse fraction in the arid Southwestern and Western
U.S. However, most of the health studies have been conducted in the Eastern U.S., where
PM2.5 and PMi0 correlate well and PM2 5 contributes well over half of the daily particle mass
or in Western urban locations, which are dominated by combustion sources, as discussed
further in Chapter V. The regional differences in the 24-hour mass concentration ratios also
reflect a difference in the correlation between daily PM2 5 and PM,0 values, driven primarily
by the regional differences in fine and coarse fractions.
2. Correlations Between PM2.5 and PM10
The PM2 5/PM10 mass concentration ratios presented above are averages over observed
concentration levels in a given region. Figure IV-15a displays the relative 24-hour
concentrations of PM2 5 and PMJO over increasing concentrations. Figure IV-15b presents a
similar comparison using annual mean concentrations. As presented in Table IV-4,
nationally PM25 correlates much better with PM10 than with the coarse fraction, as evinced
by the higher R-squared statistic for both daily and annual comparisons.
Table IV-5 presents annual and summertime correlations of daily measurements of
PM21 with PM,0 and daily measurements of sulfates with PM,0 in 24 North American Cities.
These measurements are all part of a single study so that the uncertainties about combining
sampling protocols are minimized. Daily PM21 is well correlated with PM,0 in most Eastern
U.S. cities (generally R2 statistic ranges from approximately 0.6 to 0.8 with one value near
0.3). Daily PM2 j is somewhat correlated with PM10 in the Canadian and California sites (R2
range 0.4 to 0.6). The Northern sites' correlations increase in the summer while the
California correlations decrease in the summer. California sites also show
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External Review Draft
November 1995
IV-29
Do Not Quote or Cite
Figure IV-15. Scatter Plot of PM2 5 and PM10 Concentrations
Figure IV-15a. Daily PM2 5 v. PM1Q Concentrations
8 -\
OJ
5i 8 -
a.
I §
S -
R 11304
3632
0.53
OSS
OJ6
Slop*: 021
R-Squirad: 0.60
100 150 200
Oafiy PM-10 Concentration
i
250
300
Figure IV-15b. Annual PM2 5 v.
S
Concentrations
o
CO
o _
Sf
o _
3
C
N.' 107
MaanPMIO: 37XW
UnnPMZJ: 20XXJ
MaMRatto: OJK
MwXanRcHo: 057
Slops: 022
R-Squ«r«t 038
I/."
£ *«{.'?••"
~r~
20
—T~
40
1
60
—I—
80
100
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External Review Draft
November 1995
IV-30
Do Not Quote or Cite
Table IV-4. Correlations of Fine, Coarse Fraction and PMi0
Daily Values
Annual Values
pM2ypM10
R-squared Statistic
0.60
0.58
PM2Ji/Coarse
Fraction
R-squared Statistic
0.08
0.11
Sample
Size, N
11,304
107
Source: SAI, 1995; Using monitored data from 1985 to 1993
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External Review Draft
November 1995
Do Not Quote or Cite
IV-31
Table IV-5. Correlations of PM2., with PM10 and Sulfates with PM10
in 24 North American Cities
Year Round Daily
Correlations
(SCyPM10)
Summer (May - Sept.)
Daily Correlations
(SOVPM10)
Eastern U.S. Sites
Oak Ridge, TN
Hendersonville,TN 0.34
Morehead, KY
Blacksburg, VA
Charlottesville, VA0.76
Zanesville, OH
Athens, OH
Parsons, WV
Uniontown, PA
Penn Hill, PA
State College, PA 0.81
West Coast Sites
Simi Valley, CA 0.56
Livermore, CA 0.52
Monterey, CA 0.42
Rural Sites
Springdale, AR
Aberdeen, SD
Yorkton, SK
Penticton, BC
Annual PM2.,
Mass Cone.
(i/g/m3)
0.72
0.34
0.64
0.67
0.76
0.59
0.81
0.62
0.76
0.62
0.81
0.40
0.34
0.61
0.61
0.62
0.76
0.62
0.29
0.38
0.69
0.77
0.79
0.48
0.61
0.72
0.83
0.55
0.92
0.85
0.81
0.62
0.90
0.36
0.42
0.59
0.71
0.67
0.77
0.66
0.64
0.34
0.67
0.88
17.1
16.4
20.0
N/A
16.0
16.9
N/A
17.0
21.0
19.3
N/A
Northern Sites
Dunnville, ON
Leamington, ON
Newtown, CT
Egbert, ON
Pembroke, ON
0.50
0.61
0.61
0.49
0.55
0.53
0.55
0.52
N/A
0.49
0.55
0.77
0.79
0.59
0.76
0.52
0.74
0.69
N/A
0.62
16.2
N/A
13.8
N/A
10.4
0.46
0.10
0.06
0.50
0.41
0.11
0.24
0.04
0.00
18.2
15.3
9.4
0.31
0.17
0.11
0.46
0.17
0.00
0.02
0.08
0.23
0.50
0.11
0.49
0.15
0.00
0.07
0.06
14.4
N/A
N/A
10.0
Source: Spengler (1995)
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External Review Draft Do Not Quote or Cite
November 1995 IV-32
a much lower correlation of sulfates with PM10, especially in the summer. Sulfate
correlations with PM10 are notably lower on the West Coast and in some of the rural sites
than in the northern or eastern sites. Rural sites also generally show poor correlations
between PM2, and PM10.
The PM2 5 component contributes more to the day-to-day variation in PM10 values.
Figure IV-16 presents a time series of the PM2 5, coarse fraction, and PM10 values in
Philadelphia, PA, in 1990. It can be seen that on some days, PM2J and the coarse fraction
increase and decrease together, and on other days they move in opposite directions.
However, in most periods, PM2 5 dominates the day-to-day variability in the PM10 mass, and
the coarse fraction acts almost as a constant. Wilson et al. (1995) present similar
conclusions for Philadelphia for 1992 and 1993, reporting a high correlation between daily
PM25 and PM,0 (R2 = 0.90); a moderate correlation between the coarse fraction and PM10
(R2 = 0.35); and a low correlation between fine and coarse faction (R2 = 0.11). To
understand how fine particles, PM10, and TSP compare an analysis of AIRS data in
Philadelphia in 1982 was conducted. The daily values of PM2 5 to PM10 are better correlated
(R2 = 0.90) than PM2.5 and TSP (R2 = 0.58). A moderate correlation was again observed
between the coarse fraction and PMJO (R2 = 0.44).
Figure IV-17 presents a similar time series plot of the PM2 5, coarse fraction, and
PMj0 values in St. Louis, MO, in 1993. This graph also suggests that much of the day-to-
day variability of PMJO mass is driven by the day-to-day variability of PM2 5. Wilson et al.
(1995) also examined St. Louis during the period 1988 to 1993 using PM,5 (which are
similar to PM10 measurements but would be expected to contain more coarse fraction mass)
and reported results similar to Philadelphia. A high correlation between daily PM2 5 and
PM15 was reported (R2 = 0.85); a moderate correlation between the coarse fraction and
PM10 (R2 = 0.55); and a low correlation between fine and coarse faction (R2 = 0.19).
Based on a wider examination of PM2 5 data available from the AIRS database, which
tends to contain urban and suburban locations, Wilson et al. (1995) reported that in most
cities where PM25 concentration exceeds the coarse fraction concentration, the variation in
daily PM]0 concentrations at any individual site characteristic of the community
-------
100
Figure IV-16. Philadelphia, PA, 1990
PM10, PM2.5, and Coarse Fraction
^ 80
co"
§ 60
1
i 4°
o
at
re
20
17 29 40 62. 66 78 90 101 11.3 125 137
Figure IV-16a. January through June Days when Monitoring Occurred
149
166
178
190
202
213 225 237 248 260 272 284 296 313 325
Figure IV-16b. July through December Days when Monitoring Occurred
337
349
361
Note: Sampling occurred on a one-in-six day schedule
Coarse Mass
PM-2.5
PM-10
9
-------
Figure IV-17. St. Louis, MO, 1993
PM10, PM2.5, and Coarse Fraction
CO
E
c
o
80
60 -
£ 40 -
c
0)
o
c
o
O
in
20 -
0 L
80 ,
13 25 36 48 62 74 86 97 109 121 133
Figure IV-17a. January through June Days when Monitoring Occurred
145
156
168
I
Q
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External Review Draft Do Not Quote or Cite
November 1995 IV-35
will be dominated by the variability in PM2.5. Wilson and colleagues also conclude 75
percent of the data sets in AIRS support the proposition that although epidemiological
correlations have been made with TSP and PM10, it is possible that the variability in the fine
particles, not the variability in PM,0 or the coarse fraction, produces a correlation with the
health endpoints.
In addition to the day-to-day variation in PM2 5, the day-to-day relationship between
PM concentrations monitored outdoors at a monitoring station to measurements of personal
exposure is important to interpreting the time series community health studies. Personal
exposure to outdoor pollutants can vary considerably from the concentrations measured at a
monitoring station. Typically, PM personal exposure measurements are higher than the
outdoor PM concentrations due to indoor sources of particles such as cooking, cleaning and
smoking. However, unless there is a day to day correlation between personal exposure and
other factors such as systematic measurement error or personal behaviors, individual personal
exposure will be higher on days when outdoor PM levels are high and lower on days when
outdoor PM levels are lower.
The CD reports a major new finding which differentiates between the low correlations
of PM personal exposure measurements with PM outdoor monitoring found in cross-sectional
exposure study designs versus time series designs (CD, Chapter 7). Janssen et al. (1995)
point out that the low correlations observed in most of the other studies reported in the
literature were cross-sectional (i.e., calculated on a group level), and were therefore mostly
•
determined by the variation between subjects. A more relevant model is the serial
correlation reported by Janssen et al. (1995) and noted by Lioy et al. (1990) for personal and
outdoor correlations.
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External Review Draft j)o Not Quote or Cite
November 1995 IV-36
These exposure studies report good serial correlations and poor cross-sectional
correlations that are consistent with the other cross-sectional results reported in the literature.
For instance, Janssen et al. (1995) report good serial correlations between personal exposure
measurements and stationary monitors for PMi0 (median R2 = 0.40, and as high as 0.96 for
children and median R2 = 0.25, and as high as 0.85 for adults). Excluding days with
exposure to environmental tobacco smoke raised the median R2 for PM,0 from 0.40 to 0.53
for children and from 0.25 to 0.50 for adults. Even better results were obtained for the
serial correlations of PM2 5 (median R2 = 0.74 for children). Thus, these results suggest that
a substantial amount of the day-to-day variation in personal exposure to fine particles can be
attributed to day-to-day variations in outdoor PM2 5 concentrations. The link to the health
database will be explored further in Chapters V and VI.
3. Ratio of Highest Daily Value to Annual Mean
Short-term variability in PM10 varies by region (CD Chapter 6). The highest daily
value (or peak) versus the mean value is seen in the northern and western continental US,
especially in the winter. The lowest variation prevails over the warm season in the
Southwest and Southeast. The CD concludes that the southern areas are more uniformly
covered by summertime PM10; whereas, the northern states experience more episodic high
concentrations of PM,0 (CD Chapter 6).
Staff further examined the ratios between the highest daily value in a year and the
annual mean and their dependence on year, region, and precipitation (relative to the long
term average precipitation for the given location). The results, summarized in Table IV-6,
indicate that for PM2 5 and PM,0, the average ratio of the highest daily value to annual
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External Review Draft Do Not Quote or Cite
November 1995 IV-37
TABLE IV-6. Summary of Ratios of Highest Annual Day to Annual Mean for PMi5 and PM10.
PM^j PM10
Summary Statistic
Highest-Annual-Day-to-Annual-Mean Ratio
Second-Highest-Annual-Day-to-Annual-Mean
Ratio
Second-Highest-3-Year-Value-to-Mean Ratio
Third-Highest-3-Year-Value-to-Mean Ratio
Fourth-Highest-3-Year-Value-to-Mean Ratio
Mean
3.08
2.52
3.27
2.98
2.80
Std.
Dev.
0.91
0.62
0.80
0.72
0.67
Mean
3.01
2.41
3.11
2.80
2.60
Std.
Dev.
1.53
0.78
1.50
1.25
0.81
The 3-year ratios were based on 1991-1993 data only, but the annual peak-to-mean ratios
used all available data.
mean is about 3, with standard deviations of about 0.9 and 1.5, respectively. No clear
patterns were discernable in the variation by year on the highest daily value-to-annual mean
ratios. The most noticeable effect of location was that Northwest sites tended to have higher
ratios compared to other regions, and based on analysis of annual precipitation, dry years
tended to have higher ratios than normal or wet years. Since the sites in the Northwest also
tended to be the sites with dry years, it is not clear whether location or precipitation is the
more important factor in determining the size of the ratio of highest daily value to annual
mean. In other words, the location and precipitation effects are highly correlated so it is
hard to separate out these two effects.
Table IV-7 presents more detailed distribution of the values for PMi0. Likewise,
Table IV-8 presents the same information for PM2.5. There is more certainty associated with
/
the PMjo analyses than the PM2 5 analyses because of the larger data base for PM10
(approximately 8,400 data points from across the country).
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External Review Draft
November 1995
IV-38
Do Not Quote or Cite
Table IV-7. Distribution of Highest 24-Hour-Value-to-Annual Mean Ratio for PM10
TABLE 7a. Distributions of highest-annual-peak-to-mean ratios,
compared by region: PM 10.
C emulative
Fraction
Minimum
1
5
10
20
30
40
50
60
70
80
90
95
99
Maximum
Mean
Std. Dev
Number
Northwest
1.29
1.62
1.97
2.17
2.43
2.66
2.86
3.09
3.38
3.76
4.30
5.51
7.36
13.98
43.87
3.72
2.62
1704.00
Central
1.40
1.73
1.91
2.03
2.21
2.37
2.49
2.63
2.80
3.04
3.36
3.94
4.57
7.06
16.54
2.89
1.05
1083.00
Northeast
1.32
1.63
1.91
2.04
2.19
2.33
2.46
2.58
2.72
2.90
3.12
3.58
4.12
5.83
16.09
2.75
0.86
3045.00
Southeast
Southwest
ALL
1.20
1.58
1.81
1.90
2.02
2.15
2.28
2.41
2.57
2.78
3.07
3.54
4.02
4.95
7.14
2.59
0.71
1160.00
1.35
1.60
1.81
1.96
2.17
2.35
2.57
2.78
3.02
3.37
3.73
4.67
5.58
8.16
15.12
3.13
1.40
1413.00
1.20
1.62
1.88
2.01
2.19
2.35
2.51
2.67
2.86
3.10
3.49
4.17
5.08
8.27
43.87
3.01
1.53
8405.00
TABLE 7b. Distributions of second highest-annual-peak-to-mean ratios,
compared by region: PM 10.
Cumulative
Fraction
Mini mum
1
5
10
20
30
40
50
60
70
80
90
95
99
Maximum
Mean
Std. Dev
Htmoer
Northwest
0.94
.30
.66
1.84
07
23
2.39
2.
2.
2,
3.
3.
4.
7.
55
74
98
31
89
70
36
26.88
80
22
Central
Northeast
Southeast
1704.00
1.08
1.37
1.70
1.80
1.94
2.04
2.12
2.21
2.32
2.46
2.67
2.97
3.35
4.19
5.65
2.33
0.54
1083.00
0.82
1.37
1.69
1.81
1.95
2.05
2.14
2.23
2.33
2.46
2.62
2.91
3.20
4.09
9.32
2.31
0.51
3045.00
1.05
1.35
1.60
1.70
1.81
1.88
1.95
2.03
2.13
2.23
2.39
2.62
2.89
3.52
6.21
2.12
0.43
1160.00
Southwest
1.15
1.36
1.65
1.76
1.90
2.02
2.12
2.25
2.41
2.62
2.91
3.35
3.94
5.16
7.33
2.45
0.76
1413.00
ALL
0.82
.35
.66
.78
.92
.03
.14
.24
2.37
2.54
2.76
19
67
06
26.88
2.41
0.78
8405.00
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Table IV-8. Distribution of Highest 24-Hour-VaIue-to-AnnuaI Mean Ratio for PM2<5
TABLE 8a. Distributions of highest-annual-peak-to-mean ratios,
compared by region: PM 2.5.
Cumulative
Fraction Northwest Central Northeast Southeast Southwest ALL
Minimum 1.55 1.57 1.53 1.67 1.55 1.53
1 1.96 1.57 1.66 1.67 1.62 1.62
5 2.18 2.16 1.90 1.76 1.85 1.91
10 2.37 2.49 2.08 2.01 1.97 2.07
20 2.71 2.61 2.30 2.17 2.15 2.30
30 2.95 2.72 2.47 2.29 2.31 2.54
40 3.20 2.89 2.63 2.50 2.54 2.73
50 3.43 2.99 2.79 2.77 2.72 2.91
60 3.72 3.09 2.94 2.91 2.95 3.11
70 3.84 3.34 3.11 3.15 3.26 3.39
80 4.28 3.78 3.34 3.39 3.70 3.78
90 4.96 4.18 3.85 4.64 4.13 4.32
95 5.20 4.50 4.33 5.19 4.51 4.86
99 6.44 4.64 5.00 5.66 5.89 5.81
Maximum 7.05 4.64 5.76 5.66 7.34 7.34
Mean 3.53 3.13 2.88 2.95 2.91 3.08
Std. Dev 0.96 0.68 0.72 0.99 0.92 0.91
Number 117.00 38.00 110.00 53.00 153.00 471.00
TABLE 8b. Distributions of second highest-annual-peak-to-mean ratios,
compared by region: PM 2.5.
Cumulative
Fraction Northwest Central Northeast Southeast Southwest ALL
Minimum 1.53 1.43 1.17 1.16 1.36 1.16
1 1.61 1.43 1.39 1.16 1.38 1.39
5 1.88 1.46 1.65 1.41 1.72 1.71
10 2.09 1.92 1.80 1.71 1.79 1.85
20 2.35 2.11 2.04 1.94 1.93 2.01
30 2.51 2.28 2.13 2.08 1.99 2.15
40 2.60 2.35 2.24 2.18 2.10 2.28
50 2.86 2.41 2.35 2.27 2.23 2.40
60 3.05 2.57 2.56 2.30 2.36 2.59
70 3.24 2.72 2.67 2.55 2.56 2.73
80 3.43 2.96 2.77 2.68 2.75 3.00
90 3.79 3.18 3.12 3.05 3.17 3.34
95 3.99 3.48 3.25 3.34 3.43 3.64
99 4.46 3.64 4.39 5.15 3.83 4.44
Maximum 4.54 3.64 4.84 5.15 4.03 5.15
Mean 2.90 2.50 2.43 2.36 2.35 2.52
Std. Dev 0.65 0.50 0.54 0.65 0.54 0.62
Wumber 117.00 ' 38.00 110.00 53.00 153.00 471.00
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F. Background PM Levels
Some PM is suspended in the atmosphere through mechanisms independent of the
activities of people. The range of concentrations can vary greatly over time and location.
The literature contains limited information on monitored or estimated values of background
average concentrations of PM for various averaging times (annual, seasonal, daily) or various
locations in the United States. In the literature there is also a large disparity in definitions of
"background" concentrations, and estimates of natural components of the PM are scarce.
There is no standardized terminology regarding the concept of PM background.5
Based on the CD's review of the limited literature, defining background levels of PM
and determining what part of PM is attributable to natural phenomena is a multi-dimensional
and complex concept. Background levels of PM vary by geographic location, altitude and
season. For the purposes of this document, background PM is defined as the range of PM
concentrations that would be observed in the U.S. in the absence of anthropogenic emissions
of PM and precursor emissions of VOC, NOX, and SOX in North America. An estimate of
background PM,0 annual average concentrations across the U.S. ranges between 4.5 and 6.3
fig/m3 including associated water (NAPAP, 1991). Similarly, an estimate of background fine
PM annual average concentrations across the U.S. ranges between 1.5 and 3.3 jwg/m3
including associated water (NAPAP, 1991). There is a definite geographic trend to these
levels with the lower value applicable to the Western and the higher value applicable to the
Eastern U.S. The Eastern U.S. is estimated to have more natural organic fine particles and
more water associated with hygroscopic fine particles than the West. Most of this
background estimate is believed to be due to natural sources.
The natural component of the background arises from physical processes of the
atmosphere that entrain fine particles of crustal material (i.e., soil) as well as emissions of
organic particles resulting from natural combustion sources such as wildfire. In addition
literature refers to many different terms for background including; "clean background", "average
background," "continental background," "clean continental background," and "background." None of these
studies defined a specific approach to determine whether anthropogenic sources were contributing to the
background.
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certain vegetation can emit fine organic aerosols as well as their precursors. The exact
magnitude of this natural part for a given geographic location can not be precisely
determined because the magnitude of the long-range transport of anthropogenic precursor
emissions is not well known. Only broad estimates for longer averaging times can be
developed at this time.
For the purposes of determining how background concentrations affect visibility, a
welfare consideration linked to fine particle concentrations, it is necessary to know the
contribution of each particle species to the estimated background concentrations because the
light extinction coeeficient varies by species. Estimates of background concentrations by
species have been developed using rural monitoring and consideration of anthropogenic
emissions, including precursors, to the species. Fine particle background also varies by
location and season, and these variations are important to assessing the relationship between
fine particle concentrations and visibility effects. These estimates and their importance to
developing a recommendation on the appropriateness of a national secondary standard to
address visibility effects can be found in Chapter VTI.
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V. CRITICAL ELEMENTS IN THE REVIEW OF THE PRIMARY STANDARDS
The health information most relevant to the review of the primary standards for PM is
presented in this chapter. It builds upon the integrative summary developed in the last
review (U.S. EPA, 1982b; 1986b), focusing on perspectives drawn from the significant new
body of information that has accumulated in the intervening years. The chapter begins with a
discussion of mechanisms of action, including the penetration, deposition, and clearance of
the major fractions of outdoor PM discussed in the previous chapter, as well as the possible
physiological and pathological responses to these particulate substances drawn from animal,
controlled human, and epidemiological studies. Past and recent evidence useful in
identifying potential sensitive populations is then discussed. Key findings from recent
evidence regarding the potential effects of PM are then outlined. Since a large proportion of
the evidence is from community epidemiological studies, the coherence and strength of the
epidemiological evidence is assessed. Finally, those studies most useful for developing
quantitative assessment of the potential health effects of PM are presented.
A. Mechanisms
In this section, possible mechanisms of constituents of PM which may produce
observed health effects, and the relevant information concerning such mechanisms will be
described. First, dosimetric considerations are discussed which helped to form the basis of
the current standard. Then a discussion of the most recent information concerning
dosimetry, as it pertains to the elucidation of the potential mechanisms of PM effect, is
presented. Finally, a discussion is provided concerning the possible mechanisms by which
PM may contribute to observed effects, recognizing that most of the controlled studies used
exposures to particulate substances much higher than found in contemporary atmospheres.
1. Dosimetric Considerations
a. Current Standard
This discussion describes dosimetric information and concepts upon which selection of
the indicator in the current standard is based. Such considerations formed the principle basis
of the approach used for selecting PMj0 as the indicator of the current standard (pp. 23-39,
U.S. EPA, 1982b).
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Exposure can be described, in the context of regulating PM, as the concentration of
particles available in the ambient air that a human or animal breathes. Dose is the amount of
this material that is inhaled and available for deposition at various target sites (e.g., regions
of respiratory tract) (CD, Chapter 10). The amount of particles deposited or retained in each
region of the respiratory tract is governed by exposure concentration, the particle diameter
and distribution, and physico-chemical properties of the inhaled particle (e.g., hygroscopy
and solubility), as well as species specific features of anatomy (airway geometry, ventilation
rate and physiology) (CD, Chapter 13). It is the dose that the target site or organ receives,
upon which manifestation of toxicity depends. In the previous review, based on dosimetric
considerations and on aerosol physico-chemical characteristics, the staff, with CASAC
concurrence, determined that the major risk of commonly occurring outdoor PM was
presented by those particles that penetrate to the tracheobronchial and alveolar regions of the
human respiratory tract (U.S. EPA, 1982b). Consequently, the determination of what is able
to be deposited in these areas, how long it stays there, and its toxicity are of great
importance in developing risk assessments for particle exposures and subsequent strategies
for the prevention of PM health effects.
As discussed in Chapter IV of this document, the mass and volume of typically
observed ambient particles tend to be distributed in two distinct size modes described as fine
mode and coarse mode particles (see Figure IV-1). While the fine mode contains most of the
surface area and numbers of particles, and about 1/3 to 1/2 of PM volume and mass, the
coarse mode, by comparison, contains much smaller numbers of particles and about 1/2 to
2/3 of paniculate volume and mass. (See Figure IV-2).
The human respiratory tract can be divided into three main regions: (1) extra-thoracic,
(2) tracheobronchial, and (3) alveolar regions as shown in Table V-l. They differ markedly
in structure, function, size, and sensitivity or reactivity to deposited particles (U.S. EPA,
1982b). In addition, there are differences in deposition and clearance of PM in the regions
of the lung. In humans, the principal mechanisms for deposition of particles of differing
diameter are inertial impaction (2 - 100 /xm diameter), sedimentation (0.5 - 2.0 /*m
diameter), and diffusion (< 0.5 fim diameter). A qualitative assessment of the deposition of
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TABLE V-l. MAJOR REGIONS OF THE RESPIRATORY TRACT
(Mort Lippmann, 1982 Staff Paper)
Region
Extrathoracic (ET)
Thoracic (TB+AL)
Tracheobronchial
(TB)
Alveolar (AL)
(Pulmonary)
Description
The head and pharynx, down
to and including the larynx.
Subdivisions:
Nose breathing
Anterior nares
Ciliated nasal passages
Nasopharynx
Mouth breathing
Mouth, oropharynx
Ciliated conducting airways
from the trachea! to the
terminal ciliated bronchioles.
(~ 16 generations).
Gas exchange region including
unciliated airways and alveoli.
Subdivisions: Respiratory
bronchioles, alveolar ducts,
alveolar sacs, atria, and
alveoli.
Principal Size
Range (s)
Deposited
~ 1 - > 100/xm"
hygroscopic
aerosols
> ~0.3/nn
-0.2 - 15/xmk
<20 (im*
Major Mechanisms
of Deposition
Impaction
Impaction
Sedimentation
Interception
(Fibers)
Diffusion(< 1 jan)
Sedimentation
Impaction (>2 /tm)
Major Mechanisms of
Clearance
Mucociliary action to
G.I. tract
Sneezing, blowing,
wiping to exterior
Dissolution to blood-
stream or mucous
Mucociliary action,
coughing to G.I. Tract
Dissolution to blood-
stream or mucous
Phagocytosis to TB
region, lymphatic system
Dissolution to blood-
stream, other fluids
Normal Clearance
Times for
Insoluble Particles
minutes
longer(nares)
hours
weeks-years
<
N>
'"Inspirability" Extrapolation by ISO, 1981.
•"Extrapolation of NYU data by Miller et al., 1979.
'Figures 11-8, 11-9 criteria document.
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typical ambient particles is summarized in the 1982 Staff Paper (U.S. EPA, 1982b). Based
on deposition for normal nasal breathing, over half of the total mass distribution of inhaled
PM would be deposited in the extra-thoracic region, most of this being coarse particles. Up
to half of the hygroscopic fine mass (e.g., sulfates that grow to 2-4 /tm diameter) is predicted
to also be deposited and dissolved in this same region. Smaller fractions (5-25 percent) of
hygroscopic and non-hygroscopic fine particles (mostly <. 1 /xm diameter) would be
deposited in the tracheobronchial and alveolar region respectively. A similar fraction of
coarse particles (2.5 - 8 /*m diameter) would be deposited in the same regions (U.S. EPA,
1982b).
In essence, regional deposition of ambient particles in the respiratory tract does not
occur at divisions that clearly correspond to the distribution of size of particles that occur in
the atmosphere. Nevertheless, little coarse particle mass of diameter larger than 15 /*m is
deposited in the tracheobronchial region and little mass greater than 10 /xm in diameter is
deposited in the alveolar region. Particles smaller than 10 /*m in diameter can be deposited
with varying efficiencies in both regions. A more complete discussion of possible responses
to particle deposition, potential mechanisms of those responses as well as regional deposition
is discussed in the 1982 Staff Paper (see Table 5-2 in Appendix F).
The above generalizations regarding typical particle deposition in normally breathing
adults are subject to great variability. Deposition into specific regions of the respiratory tract
and lung can be influenced by changes in respiratory flow rate, respiratory frequency, and
tidal volume. Consequently, the activity level of an individual may result in a change in the
mode of breathing (mouth versus nasal breathing) and can significantly alter regional as well
as total respiratory tract deposition of inhalable particles. Mouth breathing results in
decreased removal of particles by the upper respiratory tract allowing deeper penetration into
the lung. In addition, among normal adults subjects, baseline rates of deposition of particles
vary. Disease states have the potential for increased deposition of particles as constriction
and inflammation of airways or the increased buildup of mucous may in turn increase local
particle deposition. Asthmatics, patients with bronchitis, and cigarette smokers have been
shown to have increased deposition of particle in the tracheobronchial region. Furthermore,
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models of tracheobronchial deposition also suggests enhanced particle deposition of fine and
coarse fractions for children as compared to adults. (U.S. EPA, 1986b, CD, Chapter 10).
Deposition in the tracheobronchial region of coarse mode particles tend to be elevated
at the bifurcations where epithelial nerve endings are concentrated. Such nerve endings,
which connect to mechanical stimulation receptors, may cause reflex coughing and broncho-
constriction upon stimulation by particles. Consequently, individuals with increased
deposition rates (e.g., asthmatics) may experience even further increases in deposition of
particle due to broncho-constriction, altered clearance and buildup of fine and coarse fraction
particle at bifurcations.
Clearance is the removal of deposited particles from lung regions. The clearance
mechanisms of each region of the respiratory system are distinctly different as are the
expected residence times of any given inhaled particle. Alveolar macrophages engulf particles
deposited in lung parenchyma, and then either migrate to the terminal bronchioles where they
are transported via the mucocilliary escalator or migrate into the interstitium of the lungs to
the lymph nodes. Particle size has been reported to affect ingestion by macrophages.
Ultrafine particles of size 20 nm diameter are less effectively phagocytized by macrophage
than are larger particles of 200 nm diameter (Oberdorster, 1992). However, once ingested,
the clearance of particle-laden alveolar macrophages via the mucocilliary system may not be
affected by particle size if solubility and cytotoxicity of the particle are low (CD, Chapter
10).
Poorly soluble fine and coarse particles deposited in the alveolar region would be
expected to have clearance times on the order of weeks to months or longer. By
comparison, clearance of particles in the tracheobronchial region may take hours to days.
However, once deposited it is not certain whether transport rate and therefore clearance of
poorly soluble particles is independent of the nature of the particle (size, shape, and
composition) (CD, Chapter 13). While it is plausible that differential clearance may have a
role in specific susceptibility to PM effects and may be integral to mechanisms of PM
toxicity, there is insufficient information to support specific mechanisms (CD, Chapter 10).
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In conclusion, size divisions, according to the regional deposition of particles in the
human respiratory tract and the distribution of particles found in the atmosphere, form the
basis of the approach used for selecting the size fraction of the current standard, namely
PM,0. The risk of adverse health effects associated with extra-thoracic deposition of
commonly found particles larger than a nominal size of 10 /*m in diameter was judged to be
sufficiently low that they were excluded from the primary paniculate standard. Selection of
a size fraction for the standard based on a nominal 10 /xm indicator was supported by (1) the
overlap that occurs in deposition in tracheobronchial and alveolar regions of the lung of both
particle modes, (2) the overlap of size ranges in maximum efficiency for alveolar deposition
(2-4 jim in diameter), (3) chemical heterogeneity of the fine and coarse particle .modes, and
(4) the potential for coarse insoluble particles to cause broncho-constriction, altered
clearance, and alveolar tissue damage.
b. Recent Dosimetry Considerations of Interest
Knowledge of the effects of disease states on deposition and clearance may assist in
characterizing susceptible populations to PM and help elucidate possible mechanisms for
susceptibility. Variability of clearance may act as a contributing factor to susceptible
populations (age, sickness, smokers, etc.) of PM effects. Greater deposition of particles in
subjects with various lung conditions is verified in studies by Kim et al. (1988). Model
simulations of compromised lungs have been shown to have greater number of particles
deposited per alveolus (Miller et al., 1995). More recent studies also suggest that large
differences in clearance rates among different individuals to equivalent chronic exposures of
poorly soluble particles may result in large variations in respiratory tract burdens.
Consequently, deposition and clearance patterns of particles in the lung may influence the
type of response elicited. However, the contribution that differential deposition and
clearance of the components of PM might make to observed mortality has not been
elucidated or quantified.
Differences in what dose animals or humans receive from a particular concentration
of PM is important in attempts at extrapolation of observed effects between species. The
greater complexity of the nasal passages coupled with the obligate nasal breathing of rodents
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has been suggested to result in greater deposition in the upper respiratory tract of rodents
than in humans breathing orally or even nasally (Dahl, 1991), especially of coarse particles
(Miller et al., 1995). In regard to smaller diameter particles, model simulations suggest that
humans retain more alveolar particles than rats or mice (CD, Chapter 13). Anderson et al.
(1990) has shown increased deposition of ultrafme particles (0.02 - 0.24 pirn diameter) in
patients with chronic obstructive pulmonary disease (COPD). Thus, the differences in
deposition patterns of particles between species and between susceptible and nonsusceptible
subpopulations could be a contributing factor for the necessity of using relatively high
concentrations of larger diameter particles to elicit effects seen in experimental animal studies
(CD, Chapter 10). Consequently, dosimetry information adds support for the uncertainty in
extrapolation between human studies and experimental animal studies.
The ratio of number of particles to alveolar macrophages can be compared between
particles of differing size when dose as measured by mass is kept constant. Under such
conditions the larger number of smaller particles per unit mass have a higher probability of
interacting with alveolar macrophages. Accordingly, a compromised lung with greater
deposition has a greater probability of macrophage or alveolar surface area interaction.
Thus, there is support for a potential increased toxicity of smaller particles by increased
deposition in a subpopulation at risk and an increased probability of interaction with potential
targets of toxicity via increased numbers of particles and surface area.
2. Possible Mechanisms of Action for Health Effects Associated with Ambient Levels of
PM Exposure
This discussion focuses on more specific possible mechanisms by which airborne
particles may be exerting their effects. Upon deposition, substantial uncertainty still exists as
to how particles, alone or in combination with other atmospheric pollutants, produce
physiological and ultimately pathological effects. Because both the population affected and
PM are heterogenous, the mechanism(s) of action may also be diverse. Both fine and coarse
fraction particles have the potential for deposition in the tracheobronchial and alveolar
regions of the respiratory system and thus have access to potential respiratory targets. The
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previous staff assessment of the literature found evidence to support the following potential
mechanisms of toxicity for particles deposited in the thoracic region (U.S. EPA, 1982b):
• Chemical and mechanical irritation/stimulation resulting in bronchoconstriction by a
variety of fine and coarse particles;
• Enhanced sensitivity to subsequent bronchoconstrictive agents by sulfuric acid;
• Altered clearance rates, increased mucous production by deposited material, including
cigarette smoke, sulfuric acid, and dusts;
• Increased deposition and slowed clearance at bronchial bifurcations;
• Direct damage to tissues by acids;
• Decreased oxygen transport and probable increased resistance of blood flow through
pulmonary capillaries;
• Death of macrophages resulting in release of proteolytic enzymes that damage alveolar
tissues, by silica, other coarse dusts;
• Damage to macrophages, other host defense mechanisms by surface coating of toxic
materials;
• Combined effect of exposure and slowed clearance of particles; and,
• Enhancement of damage to lung function by childhood respiratory infections.
As noted in the original presentation, this summary of potential mechanisms is for qualitative
purposes only; many of the mechanistic studies supporting these suggestions involve
exposures significantly higher than those encountered under ambient conditions.
The increasing body of community epidemiological studies finding associations
between PM and mortality and morbidity in recent years have prompted a number of authors
to advance potential mechanisms of PM toxicity. One major area of interest is pulmonary
inflammation. Potential mechanisms for induction of an inflammatory response have been
described for: (1) aerosol acidity (Lippmann, 1989a), (2) presence of ultrafine particles
(Seaton et al., 1995), and (3) transition metal ions (Tepper et al., 1994). A second area of
renewed interest includes examination of the ways particles may affect individuals with
preexisting conditions. Frampton et al. (1995) list potential causes of PM induced mortality
as being: (1) premature death (i.e., hastening of death for individuals near death within
hours or days); (2) increased susceptibility to infectious disease; and (3) exacerbation of
chronic underlying cardiac or pulmonary disease. Also of significant interest are new
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approaches for controlled exposures to particles which are closest to those found under
ambient conditions than have been possible in past toxicologic studies (Sioutas et al., 1995).
Using this method, preliminary results suggest that it may be important in the development of
an appropriate experimental paradigm for elucidating mechanisms of PM mortality observed
in humans. Salient aspects of each of these areas is discussed briefly below.
a. Inflammation
The most serious effects associated with community studies of PM appear to be found
in individuals who have preexisting conditions. Even in the London episodes, the total
amount of inhaled PM by mass eliciting a response in humans was small. Therefore, it is
likely that the effect is amplified in conjunction with preexisting conditions that increase risk
for PM effects. Given that immunological responses can be quite rapid, consistent with the
period between increased PM exposure and an acute effect such as mortality, it is plausible
that inflammatory processes can amplify and spread the response from small amounts of PM.
Preexisting inflammation (e.g., from an ongoing infection) of the lung can amplify the
inflammatory response to residual fly ash in emphysemic rats (Costa et al., 1995). Indeed,
several of the risk factors for PM toxicity involve inflammatory response (e.g., asthma,
COPD, and infection). Lipfert (1994) in describing animal deaths as a result of the London
Fog of 1952 reports that the only documented animal deaths were among fat prize cattle
which had a tendency to suffer from "shipping fever" and that sheep and pigs were
unaffected both by shipping fever and the fog. A commonly offered explanation of the
susceptibility of the show cattle was that they were kept in cleaner stalls and thus had much
lower waste ammonia present that might serve to neutralize the high levels of acid aerosol
portions of the fog. The original report by the Ministry of Health (MOH, 1954), however,
not only confirmed the presence of the "fever" in the cows affected by the London fog but
also reported cattle death in previous fogs with ordinary stall maintenance and therefore high
ambient levels of ammonia that could neutralize acid particles.
Pathology from a limited sample of the affected cattle included capillary engorgement
with more limited alveolar wall thickening, swelling of alveolar epithelium and presence of
an exudate containing fine particles and neutrophils in some bronchioli. The MOH report
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also noted that twelve of the more serious cases from the London fog episode were of fat
young cattle in prime condition who after slaughter were shown to have emphysema,
commencing pneumonia, and slight enteritis. The report concludes that there may be some
anatomical or physiological peculiarity which renders fat cattle liable to develop pulmonary
emphysema. Thus, the cattle which shared susceptibility to the London fog with humans
may also share some of the same pre-existing conditions (e.g., COPD and inflammation).
Seaton et al., (1995) has proposed the hypothesis that the mechanism of PM involves
production of an inflammatory response by ultrafme particles (< 0.02 /*m diameter) in the
urban paniculate cloud. As a result, mediators are released capable of causing exacerbation
of lung disease in susceptible individuals and increased coagulability of the blood. Thus a
rationale is provided for the observed increase in cardiovascular deaths associated with urban
pollution episodes. Several hematological factors, including plasma viscosity, fibrinogen,
factor VII, and plasminogen activator inhibitor are not only known to be predictive of
cardiovascular disease (Lowe, 1993) but to also rise as a consequence of inflammatory
reactions. Low grade inflammation has been hypothesized to be particularly important in
altering the coagulability of blood as a result of activation of mononuclear cells in the lung
(MacNee and Selby, 1993). Activated white cells may initiate and promote coagulation
(Helin, 1986) via the final clotting pathway (Ottaway et al., 1984). Alveolar inflammation
may also cause the release of interleuken - 6 from macrophages and thus stimulate hepatocyte
to secrete fibrinogen (Akira and Kishimoto, 1992). Crapo et al., (1992) has suggested that
activation of lung macrophages in the absence of recruited neutrophils leads to acute damage
of capillary endothelial cells as well as alveolar lining cells, resulting in intracellular edema,
hemorrhage and fibrin deposition.
In support of Seaton's proposed mechanisms is the observation that ultrafme particles
cause greater inflammation (assayed by broncho-alveolar lavage) than larger particles of the
same substance (Chen et al., 1992); Oberdorster et al., 1992). Fine particles have been
shown to be taken up by lung epithelial cells (Stringer et al., 1995) and lung macrophages
(Godleski et al., 1995). They have also been shown to produce inflammation in vitro (Dye
et al., 1995) and in vivo (Kodavanti et al., 1995). As discussed below in section C, metals
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have been shown to increase the toxicity of particles. Installation of residual oil fly ash into
rats also produces an inflammatory response (Jaskot et al., 1995) with Dreher et al., (1995)
linking such inflammation to soluble vanadium, iron, and nickel compounds on the particles.
Ferric sulfate has been shown to alter pulmonary macrophage function (Skornik and Brain,
1983). In support of an inflammatory component to PM toxicity are several recent reports
involving diesel particles which have ascribed observed inflammatory/tumor promoting
effects to carbon cores rather than adsorbed organic (CD, Chapter 11). Thus, under this
proposed mechanism of PM effect, toxicity may involve a response to PM which involves
inflammation.
b. Aggravation of Underlying Condition
Aggravation of severity of underlying chronic lung disease has been hypothesized to
explain increases in daily mortality and longitudinal increases in mortality. Under such a
scenario individuals experience more frequent and severe symptoms of their preexisting
disease or a more rapid loss of function (CD, Chapter 13). Impaired respiratory function
may be a way in which PM exerts effects. As stated previously, acid aerosols have acute
effects on pulmonary function among some sensitive individuals. They may induce hyper-
reactive airways after 75 /xg/m3 H2SO4 for 3 hours (Fuwal and Schlesenger, 1994).
Therefore, the elderly with debilitating disease such as asthma may be stressed by the fine
acid aerosols. In an epidemiological study, Thurston et al., (1994b) have reported that
hospital admissions for asthma were more strongly associated with fine rather than coarse
fraction particles. Aggravation of asthma symptoms has also been reported for fine particles
(Ostro et al., 1991; Perry et al., 1983). In studies of cellular and immunological injury with
PM inhalation, Kleinman et al. (1995) reports that in eliciting responses 0.2 fim diameter
SO4"2 is greater than 0.6 /zm diameter NO3, which in turn is greater than 4/zm diameter
resuspended road dust. Measures of alveolar cord length and cross sectional area were most
reduced with the fine sulfate particles which could result in a decrease in compliance or
"stiffening" of the lung and smaller inflation volume.
A hastening of imminent death has also been proposed as one of the mechanisms of
PM induced mortality. While this is a plausible and reasonable suggestion, other evidence
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suggests that it may not explain the full effects of PM on mortality. For example, in
interviews with the family members of victims of the London pollution episode of 1952,
while some of those victims were reported to having chronic pre-existing conditions and
some having infections, several were reported to have no indication of a life threatening
disease process (Ministry of Health, 1954). Moreover, the CD points out that in prospective
cohort and time series studies, life shortening due to PM exposure is more than just a
hastening of imminent death (CD, Chapter 13). As shown in the time series studies,
increased mortality can be detected typically within a few days of increases in ambient PM
concentration (Samet et al., 1995). Therefore, the short time period between mortality and
elevations in PM is consistent with exacerbation of a preexisting condition rather than
initiation of life-threatening symptoms by PM alone.
c. Inflammation and Bronchoconstriction
Recently a methodology has been developed for concentration of ambient particles for
the purposes of exposing experimental animals to specific size fractions of the ambient PM
which may be associated with observed effects in humans (Sioutas et al., 1995). Such a
method is particularly valuable in studying the effects from and potential mechanism of
action for PM exposure as the issue of discrepancies between experimental doses and ambient
PM in terms of composition and magnitude of administered dose can be resolved.
Preliminary results have been reported to show that short-term exposure (6 hours) to
concentration of ambient particles (fine particles of 0.1-2.5 /xm diameter), which are 30 times
that of normal air (300 - 4 /*g/m3) , produce no effects on mortality or morbidity parameters
in healthy animals (Syrian Hamsters). Rats with monocrotyline-induced pulmonary
vascular/inflammation (Costa et al., 1994; White and Roth, 1989) or chronic bronchitis, as
well as their appropriate controls, also received similar exposure to concentrated ambient
particles for three days. Death was reported to occur during the exposure without visible
change in behavior and also overnight most significantly in animals with chronic bronchitis
exposed to the concentrated ambient particles. All animals were reported to exhibit
inflammation, however animals with chronic bronchitis exposed to the concentrated ambient
particles also exhibited significant broncho-constriction. Animals with bronchitis who died
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displayed the most pathological evidence of broncho-constriction followed by survivors with
bronchitis, and finally animals dying in the monocrotyline treatment group. In these studies,
highest mortality was reported to be correlated with inflammation plus broncho-constriction.
Thus, it has been hypothesized that airway responses together with preexisting inflammation
play a role in the observed mortality in humans after increases in PM exposure. This
hypothesis is consistent with the findings in the affected cattle in the London episode and the
profile of susceptibility described in the epidemiological literature describing acute mortality.
These findings also support the hypothesis that ambient particle share a different physico-
chemical composition than artificial particles used in human clinical and animal experimental
work. Therefore, it may be that multiple components of PM or other pollutants in the
ambient atmosphere must be present together in order for the full potential of PM toxicity to
be expressed.
d. Particle Accumulation
Another hypothesis for the mechanism of PM effects involves particle accumulation of
large lung burdens of poorly soluble particles. Large lung burdens of particles of even
relatively low inherent toxicity have been shown to cause lung cancer in rats (Mauderly et
al., 1994). While there is difficulty in elucidating how particle overload can induce acute
mortality, it may be a factor for former and current smokers among the elderly. It may also
be a factor for the elderly who have been chronically exposed to PM in the work place or
those who have resided in heavily industrialized cities before effective control of PM (CD,
Chapter 13). Populations with prior exposure to large particle concentrations such as
smokers, workers exposed to high particle levels, or those living in highly industrialized
cities with a history of numerous increases in ambient particle concentration have increased
risk for mortality from PM exposure (CD, Chapter 12). Therefore, while available evidence
does not support the mere accumulation of large burdens of PM in the lung as a mechanism
for reported PM effects, it is plausible that increased particle burdens from past exposure
could further augment the insult from recent increases in ambient particle concentration.
However, the mechanism by which prior exposure to particulate could predispose an
individual to acute PM effects is unknown.
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e. Impaired Respiratory Defense
Impaired respiratory defense has also been proposed as a contributing factor to PM
toxicity. Patients with pneumonia have increased risk of mortality and morbidity from PM
exposure. Cough, bronchitis, and lower respiratory illness have been reported to be
associated with increased ambient particle concentrations (CD, Chapter 12, see below).
Both mucocilliary transport and macrophage function are critical to host defense
against inhaled pathogens. Increased risk of infection has been associated with changes in
mucocilliary clearance (e.g., excessive mucus secretion into the airways can cause airway
blockage and reduced clearance). Alveolar macrophages are the primary defense cells of
lungs and impairment of their function would also be expected to increase risk of infection.
Clearance and macrophage function have been shown experimentally to be affected by
constituents of PM, notably fine acid aerosols.
H2SO4 and trace metals have been shown to have direct effects on alveolar
macrophages in animal experiments (CD, Chapter 11, see below). Kleinman et al. (1995)
also reported in their study of cellular and immunological injury by PM that antigen binding
to receptors in and respiratory burst activity by macrophages was depressed by exposure to
fine (0.2/tm diameter) SO4"2 particles. H2SO4 has also been shown to affect mucocilliary
transport and, in combination with ozone, resistance to bacterial infection. However, these
effects have been shown at concentrations which are much higher than those reported in the
recent epidemiological studies for which PM effects have been reported. Effects mediated
through clearance, in particular, would be expected to be manifested over an extended period
of exposure rather than a few days. While impaired host defense may not be plausible as a
mechanism for mortality associated with short-term fluctuations of PM level, it may
contribute to the long-term exposure mortality. In addition, the lag-time reported between
PM concentration elevations and general indicators of morbidity (e.g., missed school and
work loss days) is consistent with an increased susceptibility to infection which may
precipitate respiratory symptoms (see discussion below in section V.C).
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B. Sensitive Subpopulations
There are groups within the total population that consistently show susceptibility to
adverse health effects from PM exposure. These groups are the same as those which
succumbed to air pollution during "catastrophic" historical episodes and which are most
susceptible to effects during routine fluctuations in PM. They are described below in Table
V-2.
TABLE V-2: SENSITIVE POPULATION SUBGROUPS
Individuals with Chronic Obstructive Pulmonary Diseases (COPD):
Asthma
Bronchitis
Bronchiectasis
Emphysema
Individuals with Cardiovascular Disease
Individuals with Infections:
Influenza
Pneumonia
Elderly
Children
Smokers
Mouth or Oral-nasal Breathers
A discussion of sensitive subpopulations and their occurrence in the general
population is described in Table 5-3 of U.S. EPA (1982b). This discussion focuses on
characteristics of sensitive subpopulations identified above to be most at risk for adverse
health effects from PM exposure and how those characteristics support the plausibility of
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observed effects from epidemiologic studies. Such sub-populations may experience effects at
lower levels of PM than the general population and the subsequent magnitude of effect may
be greater. Enhanced susceptibility may be due to differences in dosimetry, tissue
sensitivity, or both.
1. Individuals with Respiratory and Cardiovascular Disease
Both the early London episode studies and the most recent community studies in
North America have found air pollution with elevated particle concentrations to be associated
with increased mortality, hospital admissions, and symptoms in individuals with respiratory
and cardiovascular disease.
COPD is the most common pulmonary cause of death (fourth leading cause of death
overall) and is a major cause of disability. COPD incidence increases with age of the
population (CD, Chapter 11). Patients with COPD have a larger relative risk of mortality
from PM exposure than the general population (CD, Chapter 12, see below). COPD is
characterized by airway obstruction in which there is increased resistance to airflow during
forced expiration. Airway obstruction is seen with such conditions as chronic bronchitis,
bronchiectasis (irreversible focal bronchial dilatation), emphysema, asthma, and bronchiolitis.
Two other forms of COPD, emphysema and chronic bronchitis, may result in chronic
inflammation of distal airways as well as destruction of the lung parenchyma (CD, Chapter
13). In addition, COPD causes a reduction of ventilatory reserves which may be expected to
predispose such patients to affecters of pulmonary function. COPD patients may also have
hyper-responsiveness to physical and chemical stimuli, altered distribution of PM resulting in
greater concentrations of PM in well ventilated areas, and impaired host defense mechanisms
as identified through increased rates of respiratory infection. Rates of regional clearance
appear to be reduced in humans with COPD (CD, Chapter 11).
Asthma is a particular form of COPD. There are approximately 13 million people in
the U.S. with asthma and that number is increasing (National Center for Health Statistics,
1994). In addition, mortality from asthma has been rising in recent years (Gergen and Weis,
1992) and air pollution has been implicated as a causative factor (CD, Chapter 11). Asthma
is a lung disease characterized by (1) airways obstruction that is reversible, but not so
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completely in some patients, either spontaneously or with treatment, (2) airways
inflammation, and (3) increased airway responsiveness to a variety of stimuli. The airways
of asthmatics may be hyper-responsive to a variety of stimuli including exercise, cigarette
smoke, odors, irritating fumes, changes in temperature, humidity, allergens, pollen, dust, as
well as viral infection (CD, Chapter 13). [A more complete discussion of the characteristics
of asthma may be found in the SO2 Staff Paper (U.S. EPA, 1994c)]. The heightened
responsiveness of the airways of asthmatics to such substances and conditions raises the
possibility of exacerbation of this pulmonary disease by PM. Asthmatics have been shown to
have increased deposition of PM after bronchoconstriction. A similar pattern is observed in
subjects with other forms of COPD. The sputum of asthmatics has a low pH indicative of a
potential loss of buffering of acidic particles (CD, Chapter 13).
Physical findings in COPD are highly variable especially in early stages (chest x-ray
findings, cough and sputum production, and wheezing all vary in character and intensity).
Small airway disease can also be extensive yet not appreciably affect spirometric pulmonary
function tests (FEV,). Therefore, the use of physical findings to accurately gage the effects
of changes of ambient air concentrations of PM is problematic. Accordingly, there may be
difficulty in detecting effects from particles through the use of pulmonary function tests, such
as the FEV!.
There appears to be increased risk from death and morbidity (increased hospital
admissions) due to cardiovascular causes associated with exposure to increased PM
concentration. Bates (1992) has postulated three ways in which pollutants could affect
cardiovascular mortality statistics: (1) acute airways disease misdiagnosed as pulmonary
edema, (2) increased lung permeability, leading to pulmonary edema in people with
underlying heart disease and increased left atrial pressure, and (3) acute bronchiolitis or
pneumonia induced by air pollutants precipitating congestive heart failure in those with pre-
existing heart disease (CD, Chapter 11). Patients with COPD, a subpopulation already
identified as being at increased risk from PM effects, have a tendency to have arrhythmias
(irregularity of the heart beat). In addition, enlarged airspaces have been hypothesized to
increase blood flow resistance through the pulmonary capillary network thereby increasing
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cardiac stress (U.S. EPA, 1982b). As with COPD, the preexisting condition of ischemic
heart disease occurs at high frequency in the general population and contributes significantly
to total mortality. The pathophysiology of many lung diseases is related to cardiac function.
Specifically, increased hospital admissions for ischemic heart disease and congestive heart
failure associated with PM may result from exacerbation of cardiovascular disease through
respiratory effects (Schwartz and Morris, in press). The inability to adequately perfuse
tissues is central to the pathophysiology of both myocardial infarction and congestive heart
failure. The diminished ability of lungs to oxygenate blood (e.g., through airway obstruction
and bronchoconstriction associated with COPD or with aging), as well as pulmonary edema
and increased left atrial pressure for those with pre-existing cardiovascular disease may
increase demands on the myocardium and thus precipitate ischemic cardiac events or
congestive heart failure in susceptible individuals. Results from animal studies suggest that
pulmonary hypertension or inflammation may increase susceptibility to effects of particles on
the lungs (Costa et al., 1994). In addition, terminal events in patients with end stage COPD
are often cardiac in nature and may be recorded as a cardiovascular death rather than as a
respiratory cause.
2. Individuals with Infections
Controlled exposures of individuals with influenza to high concentrations of
ammonium nitrate induced increased sensitivity of the respiratory epithelium as compared to
uninfected subjects (Utell et al., 1980). Respiratory infection is also a risk factor for
exacerbation of asthma and increased susceptibility of cardiopulmonary patients to stress
(Fishman, 1976). Increased infant mortality has been reported from pneumonia concurrent
with increased PM in Rio De Janeiro, Brazil (Penna and Duchiade, 1991). Frequently the
immediate cause of death in persons compromised by heart and lung diseases is pneumonia
or other respiratory infection (Samet et al., 1995). Consequently, because of the
interrelatedness of these diseases the specific causes of death may not always be readily
discernible (Samet et al., 1995).
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3. The Elderly
There is currently little information on how aging in the absence of pathology might
make the elderly more susceptible to the effects of ambient particles (Cooper et al., 1991).
There are, however, decreases in pulmonary functions associated with aging that may
decrease the capacity of the elderly to withstand respiratory insult. Older people already
have decreased oxygen exchange capacity. The PaO2 (partial pressure for arteriolar oxygen)
for a healthy 20-year old breathing room air is about 90 mmHG whereas the normal PaO2 at
age 70 is about 75 mmHg. This physiologic decrease with age is partly the result of a
decrease in lung elastic recoil (e.g., senile emphysema) leading to closure of small airways in
the tidal volume range. Increasing age is accompanied by decreases in lung volume, FEV,,
flow velocity/volume curves, resting cardiac output, and cardiac output reserve (Kenny,
1989). In addition, little is known about possible interactions between numerous medications
that the elderly typically take and exposure to ambient pollutants which may potentiate
adverse effects. In regard to animal studies, older animals as well as those with chronic
illness have been reported to have a more limited ability to adapt to stressors which may
include air pollution (CD, Chapter 11).
4. Children
Children have the potential to be inherently more susceptible to the effects of PM as
they show a greater incidence of asthma and decreased immunological protection (CD,
Chapter 13). For those who are under 20 years of age, asthma rates have increased
approximately 45 percent from 1980 to 1987 (50 per 1000 persons) (NIH, 1991). In
addition, children may spend more time outdoors at higher ventilation rates via increased
activity and have subsequent increased inhalation of outdoor pollutants. The changes in
dosimetry between children and adults are discussed below in section V.C. Infants in
particular have been hypothesized to be a susceptible subpopulation for PM effects as
exposure may increase the incidence or severity of acute respiratory infection including
bronchitis, bronchiolitis, and pneumonia (Samet et al., 1995). Recent studies in North
America have not found increased mortality or morbidity in infants, although they were
reportedly at increased risk of mortality in the London air pollution episode of 1952 and,
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more recently, to be at greater risk of mortality from pneumonia with elevated participate
pollution levels in Rio De Janeiro (Penna and Duchiade, 1991).
5. Smokers
As discussed in the CD, smoking has been identified as a key etiologic factor in
primary risk factors discussed above (e.g., COPD, increased risk for cardiovascular disease,
and respiratory infection) for PM effects. Environmental tobacco smoke (ETS) has been
shown to increase the risk to children of lower respiratory tract infections (bronchitis and
pneumonia) and increased frequency and severity of asthma exacerbations. These are also
risk factors of adverse heath effects from increased PM exposure.
6. Mouth or Oronasal Breathers
Although not necessarily a readily identifiable group distinct from those above,
dosimetric considerations indicate that individuals who, due to disease, increased activity, or
other reason habitually breathe through the mouth are at increased risk due to increased
penetration of both fine and coarse particles. Approximately 15 percent of the population
may fall into this category (Niinimaa et ah, 1980; U.S. EPA, 1994c).
C. Nature of Effects
The evidence for the kinds of health effects associated with exposures to PM comes
from a large body of literature dating back more than 40 years. This section updates and
expands upon findings presented in the previous Staff Paper (U.S. EPA, 1982b, 1986b). It
identifies and describes the principal health effects associated with PM, emphasizing the
substantial amount of recent information most pertinent to the review of the current PM
standards. Evidence for such associations drawn from epidemiological studies, controlled
human exposures, and animal toxicology is discussed and evaluated in the Criteria Document
(CD) and below. Based on the scientific information discussed and evaluated in the CD and
in this staff paper, the key health categories associated with PM are listed in Table V-3.
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V-20
Do Not Quote or Cite
TABLE V-3. PARTICULATE MATTER EFFECTS OF CONCERN
Increased Mortality
Aggravation of Existing Respiratory and Cardiovascular
Hospital Admissions and Emergency Department
School Absences
Work Loss Days
Restricted Activity Days
Disease
Visits
Respiratory Mechanics and Symptoms
Altered Clearance and Other Host Defense Mechanisms
Morphological Damage
Cancer
The majority of effects listed above have been consistently associated with PM
exposure from a large body of community epidemiological evidence. The strengths and
weakness of epidemiological studies in general are discussed in some detail in the CD, and
outlined briefly below. Particularly important issues concerning uncertainties in the recent
community studies of the health effects PM are presented in section V.D of this chapter.
Epidemiological studies identify site-, time-, and monitor-specific associations of incidence of
diseases or effects and risk factors; they do not demonstrate causality or provide clear
evidence of the mechanisms of such diseases or effects. Specifically, the community
epidemiological studies focus on showing whether associations exist, rather than on how they
might be explained at a pathogenic or mechanistic level. Experimental work in laboratory
animals and humans also helps to generate data from which to develop hypotheses concerning
mechanisms of PM effect which can in turn aid in the design of epidemiological studies. If
the exact pathogenic mechanisms are not known, however, as is the case of cardiovascular
disease and cigarette smoking, well-conducted, consistent, and coherent epidemiology studies
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may still provide strong evidence of effects. Nevertheless, because groups rather than
individuals are studied, uncertainties regarding cause and effect are increased. Consequently,
a variety of approaches and analyses are applied to assess whether chance could have
determined the findings. An advantage of such studies is that the population of concern
(humans) is examined under realistic exposure conditions. Additionally, large number of
subjects with a range of susceptibilities may be observed.
Qualitative support for some of these epidemiologic observations has been reported
for specific components of the ambient particle milieu in controlled clinical studies of humans
as well as studies in animals. For such studies, the biological responses occurring in the
respiratory tract following PM inhalation encompass a continuum of changes including:
respiratory symptoms such as wheeze and coughing, changes in pulmonary function, altered
mucocillary clearance, inflammation, changes in lung morphology and tumor formation (CD,
Chapter 11). In the vast majority of studies, however, results were observed only at
concentrations of specific substances or simple mixtures that are significantly higher than
those found in contemporary atmospheres.
Typically, experimental animal toxicology studies are designed to develop information
for understanding the mechanistic steps following particle deposition and health effects from
specific constituent(s) of the PM milieu. In the case of the study of the effects of PM, there
are several difficulties in using human clinical studies and experimental work in animals to
elucidate mechanisms of effects from PM exposure. These limitations hinder the
interpretation of this body of work with regard to determining either the risk of adverse
effects from particles in humans or in determining the mechanism of action of particles at
ambient levels. However, these studies do illustrate the potential for particles to cause
adverse effects and aid in development of proposed mechanisms for observed PM effects.
For example, this information shows that the site of respiratory tract deposition (and hence
particle size) clearly influences health outcome and that toxicity can vary greatly by chemical
species (e.g., cadmium toxicity differs from that of sulfuric acid).
A more complete discussion of the interpretation of such work can be found in
Appendix D and includes difficulties in reproducing the effects of PM in an appropriate
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animal model given the (a) numbers of individuals affected, (b) lack of distinct disease
pathology, (c) lack of appropriate equivalents to epidemiological endpoints, and (d) the
heterogeneity of the human population, physico-chemical composition of PM, and dosimetry
(within the human population and between humans and animals). In addition, studies using
particles generated in the laboratory are probably not an accurate reproduction of the
complex physico-chemical characteristics of particles found in the ambient air along with
varying amounts of pollutant gases (Sioutas et al., 1995). The lack of an effect of any one
of the chemical constituents of PM in experimental systems should always be interpreted with
caution given that responses to the differing components of mixtures may be synergistic,
additive, or antagonistic, and may vary with particle size and surface characteristics.
Key evidence illustrating each of the major effects categories listed in Table V-3 is
outlined below, with an emphasis on the more recent information.
1. Mortality
a. Mortality From Short-Term Exposures to PM
i. Historical Findings From Community Epidemiology
Reports of the effects of ambient PM on health date back to the dramatic pollution
episodes of Belgium's industrial Meuse Valley; Donora, Pennsylvania; and London, England.
In these cases, winter weather inversions led to very high particle concentrations (Firket,
1931; Ciocco and Thompson, 1961) which were associated with large increases in mortality
and morbidity, especially among individuals with preexisting cardio-pulmonary conditions.
Analyses of a series of episodes in London indicated excess mortality occurring with abrupt
increases in particles, including sulfuric acid, accompanied simultaneously by high levels of
S02 (U.S. EPA, 1969, p. 154). As noted above, livestock were also severely affected. In
studies of these episodes, indicators of PM such as British Smoke (BS) were used which
preferentially measures carbonaceous particles found in the fine fraction, as discussed in
Chapter IV.
During the review of the PM standards that culminated in 1987, this collection of
predominantly episode studies was augmented by several more extensive time-series analyses
examining the PM pollution/mortality relationship across 14 London winters. These studies
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differed from the original studies by examining the mortality/PM relationship using more
sophisticated statistical techniques to examine mortality during routine variations in PM and
sulfur dioxide levels. These analyses showed a continuum of response across PM levels and
suggested effects from exposure to PM occurred at levels more similar to those observed in
the U.S.. Some of these studies suggested, although not conclusively, that particles were
more likely to be responsible for the associations with air pollution than SO2 (Mazumdar and
Sussman, 1981).
ii. Recent Findings
Beginning in 1987, two important developments took place. Investigators started to
use more sophisticated statistical techniques, originally based on econometric techniques,
which allowed the evaluation of the association between short-term variations in PM and
mortality. Secondly, more information on PM levels became available in cities throughout
the U.S., through implementation of extensive monitoring networks, which allowed studies
of short-term PM levels and health effects. Since then numerous epidemiological studies
have reported an association between short-term exposures to PM and mortality. In these
studies, investigators have observed an association between daily or several day averages in
concentration of PM (as TSP, PM10, or PM25) and mortality in communities across the U.S.
and in several locations outside the U.S.. Of 29 studies published between 1988 and 1995,
25 have found a positive association between increases in ambient PM concentration and
mortality (Appendix E). These studies are consistent with the earlier analyses of the 14
London winters, but extend to lower concentrations and a large number of areas with
differing climate, particle composition, and varying amounts of SO2 and other gaseous
pollutants.
A summary of the studies using a variety of PM indicators which the CD concluded
were most appropriate for quantitative assessments are presented in Table V-4. These
•
studies have reported a consistent association between changes in PM levels and mortality,
finding a 1.5 percent to 19.0 percent increase in daily mortality associated with a 50 ng/m3
increase of PM concentrations (Table V-4). These studies have been conducted in a number
of different geographic locations in North America. Two in the west (Utah Valley and Los
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TABLE V-4. EPmEMIOLOGICAL STUDIES OF SHORT-TERM PM EXPOSURE MORTALITY STUDIES:
COMPARISON OF RELATIVE RISK (RR) ESTIMATES FOR TOTAL MORTALITY FROM
50 fiLg/m3 CHANGE IN PMIO
Study Location
Athens, Greece
Birmingham, AL
Chicago, IL
Chicago, IL
Kingston, TN
Los Angeles, CA
Santiago, Chile
St. Louis, MO
Toronto, ON Canada
Utah Valley, UT
Reference
Touloumi et al. (1994)
Schwartz (1993)
Ito et al. (1995)
Styer et al. (1995)
Dockery et al. (1992)
Kinney et al. (1995)
Ostro et al. (1995a)
Dockery et al. (1992)
Ozkaynak et al. (1994)
Pope et al. (1992)
Other Pollutants
PMIO Gig/m3) In Model
Mean Maximum
78 306 None
S02, CO
48 163 None
38 128 O3, CO
37 365 None
30 67 None
o,
58 177 None
03, CO
115 367 None
None
None, Poisson
SO2, Poisson
NO2, Poisson
O3, Poisson
28 97 None
°3
40 96 None
47 297 None
None, winter
None, summer
Max O3, summer
Avg O3, summer
Lag Times, d
1 d
1 d
^.3d
<.3d
3d
< 3d
<.3d
1 d
1 d
1 d
< 4d
1 d
1 d
1 d
1 d
<.3d
<. 3d
Od
<. 4d
^.4 d
<.4d
.< 4d
— 4d
RRper
50 /tg/m3
1.034
1.015
1.05
1.025
1.04
1.085
1.09
1.025
1.017
1.04
1.07
1.022'
1.026'
1.043'
1.026'
1.08
1.06
1.025
1.08
1.085
1.11
1.19
1.14
95 Percent
Confidence Interval
(1.025, 1.044)
(1.00, 1.03)
(1.01, 1.10)
(1.005, 1.05)
(1.00, 1.08)
(0.94, 1.25)
(0.94, 1.26)
(1.00, 1.055)
(0.99, 1.036)
(1.035, 1.06)
(1.04, 1.10)
(1.003, 1.042)
(1.005, 1.047)
(1.020, 1.066)
(1.005, 1.047)
(1.005, 1.15)
(0.98, 1.15)
(1.015, 1.034)
(1.05, 1.11)
(1.03, 1.35)
(0.92, 1.35)
(0.96, 1.47)
(0.92, 1.41)
u>
Relative risk calculated from parameter! given by author assuming a SO pg/m3 increase in PMIO or its equivalent.
•Calculated on basis of 50 itg/ms increase, from 50 to 100 figlm'.
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Angeles), two in the south (Kingston and Birmingham), one in the north (Toronto), and two
in the midwest (Chicago and St. Louis). Each of these locations differ in pollution patterns
and weather patterns. For example, Chicago and St. Louis have higher SO2 levels than Utah
Valley or Los Angeles. In addition, Birmingham has a more humid climate than Los
Angeles. Yet each study finds an association between increased mortality and PM that is
relatively consistent with other studies. It is of note that the coefficient of increased risk
implied by the 1952 episode in London (1.06) is consistent with those reported for the
current studies (Schwartz et. al., 1994).
Investigators have found a trend towards association between directly measured levels
of PM2.5 and short-term mortality in seven cities studied to date (Table V-5). The association
was statistically significant in four considered individually and in a group of six when
considered together (Table V-6). Associations between fine particles and mortality have been
found in four other areas using other surrogate indicators for fine particulates. Each of these
studies found a statistically significant positive association between surrogates for fine
particle mass and mortality.
The Schwartz et al. (in press) study evaluated the relative contribution of different
size fractions to risk of excess mortality from PM exposure within one study design. The
combined PM2 5 results of the Schwartz et al. (in press) study presented in Table V-5 are
compared to other particle indicators in Table V-6. In the analysis of all of the cities
combined, both PM,0 and PM2 5 were significantly associated with daily mortality, while the
coarse fraction mass coefficient was not statistically significant.
iii. Specific Causes of Mortality Associated with PM
Several studies have examined associations between PM level and mortality by cause
of death. In these studies, the investigators have reported stronger associations with
respiratory and cardiovascular causes of death, and deaths in the elderly (Styer et al., 1995;
Ostro, 1995a; Schwartz, 1994a; Pope et al., 1992). Results from these studies suggest that
the strongest association of increased risk of mortality from PM are for those individuals
with preexisting respiratory conditions. Table V-7 summarizes the relative risks for total
mortality and respiratory and cardiovascular causes of death, and mortality among the elderly
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TABLE V-5. RECENT EPEDEMIOLOGICAL SHORT-TERM FINE PARTICLE EXPOSURE MORTALITY STUDIES
Study
Dockery et al., 1992
St. Louis, MO
Dockery et al., 1992
Kingston, TN
Schwartz et al., in press
Boston, MA
Schwartz et al., in press
Knoxville, TN
Schwartz et al., in press
St. Louis, MO
Schwartz et al. , in press
Steubenville, OH
Schwartz et al., in press
Portage, WI
Schwartz et al., in press
Topeka, KS
Touloumi et al., 1994
Athens, Greece
Kinney and Ozkaynak, 1991
Los Angeles, CA
Fairley, 1990
Santa Clara County, CA
Ozkaynak etal., 1994
Toronto, Canada
Relative Risk
BS, KM, COM or SO4'
Per 25 /zg/m3 Converted to RR per 50
Fine Particle Indicator PM2J Increase Mg/m' PM)0
PM2.j 1.04
PMj.,, 1.04
PMj.5 1.06
PM2.j 1.04
PM2.j 1.03
PMj.5 1.03
PM2.j 1.03
PM2.3 1.03
BS 1.03
KM 1.02
CoH 1.02*
SO4- 1.025
95 % Confidence Interval
(1.00-
(0.97 -
(1.04-
(1.01 -
(1.01 -
(1.00-
(0.99 -
(0.95 -
(1.025-
(1.00-
(1.01 -
(1.015-
1.07)
1.12)
1.07)
1.07)
1.04)
1.06)
1.08)
1.11)
1.044)
1.055)
1.03)
1.034)
CD
*RR per 1200 CoH
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External Review Draft
November 1995
Do Not Quote or Cite
TABLE V-6. SHORT-TERM PM EXPOSURE AND MORTALITY STUDY IN COMBINED SIX-CITY ANALYSIS
RELATIVE RISK FOR A 25TH TO 75TH PERCENTILE INCREASE IN ALTERNATIVE MEASURES OF PARTICULATE AIR POLLUTION
FROM SCHWARTZ et al., in press.
Particle Measure
25th - 75th Percentile
Range
Estimated Increase in
Mortality
95% Confidence Interval
*CM = coarse fraction (PM,0 minus PM2.s)
T Statistic
PM,o
PM2.5
CM*
SO4
H+
22.1 fig/m3
13.7/ig/m3
10.6 /ig/m3
5.8 /tg/m3
18.9 nm/m3
1.9%
2.0%
0.5%
1.2%
0.2%
(1.2%, 2.5%)
(1.5%, 2.7%)
(-0.1%, 1.1%)
(0.7%, 1.8%)
(-0.6%, 0.9%)
5.73
7.13
1.68
4.87
0.45
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V-24c
External Review Draft
November 1995
Do Not Quote or Cite
TABLE V-7. COMPARISON OF TOTAL MORTALITY AND CAUSE-SPECIFIC
MORTALITY FOR SHORT-TERM EXPOSURE STUDIES
Study
Total Mortality,
Relative Risk per 50
3 PM10
Cause-specific
Mortality per 50
/ig/m3 PM10
Respiratory Related
Utah Valley, Pope et al. (1992)
Chicago, Styer et al. (1995)
Birmingham, Schwartz (1993)*
Santiago, Chile, Ostro et al. (1995a)
Elderly
Chicago, Styer et al. (1995)
Santiago, Chile, Ostro et al. (1995a)
Cardiovascular
Utah Valley, Pope et al. (1992)
Chicago, Styer et al. (1995)
Birmingham, Schwartz (1993)
Santiago, Chile, Ostro et al. (1995a)
1.08
(1.05- 1.11)
1.04
(1.00 - 1.08)
1.05
(1.01 - 1.10)
1.04
(1.035 1.06)
1.04
(1.00 1.08)
1.04
(1.035 - 1.06)
1.08
(1.05- 1.11)
1.04
(1.00 1.08)
1.05
(1.01 - 1.10)
1.04
(1.035 - 1.06)
1.20
(1.11 - 1.29)
1.12
(0.99 - 1.26)
1.08
(0.88 - 1.32)
1.06
(1.03 -1.10)
1.08
(1.03- 1.13)
1.05
(1.03 - 1.06)
1.09
(1.02- 1.17)
1.03
(0.98 - 1.09)
1.08
(1.02- 1.14)
1.04
(1.02 - 1.06)
The Schwartz (1993) study was of COPD.
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External Review Draft Do Not Quote or Cite
November 1995 V-25
for the studies evaluating PM. Respiratory related deaths generally describe presence of
acute respiratory illness (e.g., symptoms involving the upper respiratory tract and
pneumonia), as well as COPD and pneumoconioses. Studies presented in Table V-7 also
suggest that the elderly are at higher risk of mortality from PM exposure (Styer et al., 1995;
Ostroetal., 1995a).
iv. Experimental Animal Studies
Studies of short-term exposure to specific components of PM have been conducted in
an attempt to reproduce mortality from short-term exposure. The vast majority of such
studies have found mortality only at concentrations well above ambient levels, even in
sensitive species (e.g., guinea pig) and appear to be of little relevance to the effects observed
in humans. Lethality is used as an endpoint via a severe irritation response (e.g., laryngeal
or bronchial spasm) in healthy animals. Preliminary findings involving concentrated ambient
particles and mortality in animals at lower concentrations are discussed above in section V.B.
b. Mortality From Long-Term Exposures to PM
i. Recent Findings
In the last review, staff evaluated a large number of cross-sectional studies that found
associations between mortality and long-term exposures to various indicators of PM. These
as well as more recent cross sectional studies are summarized in Table V-8. Staff concluded
that such studies provided only suggestive evidence of long-term mortality. Less weight was
given to these studies because of a number of unaddressed potential confounders and
methodological problems inherent with such ecologic approaches. In the recent literature,
however, three prospective cohort studies have reported results that may lend additional
support to the earlier results. The results of these studies (Abbey et al., 1991; Dockery et
al., 1993; Pope et al., 1995) are presented in Table V-9 and are described briefly below.
Dockery et al., (1993) analyzed survival of 8,111 adults followed for 14 years in six
•
cities in the eastern U.S. (Harvard Six City Study). Extensive information was obtained
regarding individual level potential confounders such as smoking, social and economic status,
and occupation. After adjustment for these co-variates, the authors found several measures
of PM, (PM,0, PM2 5 and sulfates) were significantly associated with increases of mortality.
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TABLE V-8. COMMONLY-BASED CROSS-SECTIONAL MORTALITY STUDIES (SINCE 1980)
Source
Ozkayn/tk and
Thunton
(1989)
Table VI
Ozkaynak and
Thurston
(1987)
Table VO
Lipfert et al.
(1988)
Table 24
Lipfert et al.
(1988)
T«blt 24
I-ipffrt et at.
(1988)
Page 60
Lipfert (1993a)
Regr. 6.1,6.2
Time PM Sites Mean
Health Period/ PM Mean PM Range/ Per City Model1 PM Lag Other
Outcome No. Units Indicators Gig/m*) (Std. Dev.) City Pop. Type Structure Pollutants Other Factors
Total 1980 TSP
mortality 98 SMSA
SO4
Total 1980, PM,,
mortality 38 SMSA
PM,.,
Total 1980 Fe,
mortality 172-185
cities SO4
Total 1980 PM,,
mortality 68 cities
PM,,
Total 1980 TSP
mortality 122 cities SO.
Mortality 1980 TSP
from 149 SMSA
natural SO4
causes
78 (26)
11.1 (3.4)
38 (7-3)
20 (3.8)
1.2 (0.61)
9.5 (3.5)
38 (121)
18 (6)
88 (29)
9.0 (1.8)
68 (17)
9.3 (3.1)
1 NA OLS none none Pet. i Age 65,
sep. median age,
Pet. nonwhite, pop.
density,
Pet. poor, pet. w/ 4
yrs college.
1 NA OLS none none Same as above.
sep.
1 57,500 OLS none none Pet. & Age 65, birth
sep. rate;
Pet. Afr.-Amer. pop.
density, pet. poor,
Pet. pop. change, pet.
w/ 4 yrs. college;
Pet. Hispanic, adj.,
cig., sales; Pet. prior
res., hard water
1 57,500 OLS none none Same as above.
sep.
1 about OLS 10 years none Pet. i Age 65, birth
60,000 joint rate, pet. nonwhite,
pop. density, pet.
poor, adj. cig. sales,
pet. w/ 4 yn. college
10.6 928,000 OLS none none Pet. 2 Age 65, Pet.
(TSP) sep. Afr.-Amer., Pet.
Hispanic, Pet. other
nonwhite, pet. poor,
pet. pop. change, adj.
cig. sales, pet. w/ 4
yrs. college, hard
water, heating degr.
days pop. density
Relative Risk3 RR.
at TSP - 100, Confidence
SO4 - 15 Interval
1.012 TSP
1.17SO4
1.059PM,,
1.085 PMi.,
1.044Fe
1.13 SO4
1.036PM,,
1.082PM,,
about 1.0
1.072SO,
1.038 TSP
1.059 SO,
(0.96, 1.06)
(1.09, 1.24)
(0.95, 1.16)
(0.96, 1.21)
(1.02-1.07)
(1.06-1.20)
NSJ
NS'
NS'
(1.0,1.14)
(0.97, 1.10)
(0.99, 1.12)
Elasticity
0.01
0.086
0.045
0.068
0.041
0.071
0.027
0.059
NS
0.037
0.026
0.037
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November 1995
Do Not Quote or Cite
TABLE V-8 (cont'd). COMMONLY-BASED CROSS-SECTIONAL MORTALITY STUDIES (SINCE 1980)
Source
Lipfert (1993)
Regr. 13.1,
13.3
Lipfert (1993)
Regr. 9.1, 9.3
Lipfert (1993)
Regr. 13.5
Lipfert (1993)
R«gr. 12.1
Lipfert (1993)
Regr, 10.3,
10.4
Health
Outcome
Mortality
from
natural
causes
Mortality
from
natural
causes
Major
CVD
Major
CVD
COPD
Time
Period/
No. Units
1980
62 SMSA
1980
62 SMSA
1980
62 SMSA
1980
62 SMSA
1980
149 SMSA
PM
PM Mean
Indicators (/ig/m*)
PM,, 38
PM,., 18
TSP 68
S04 9.3
SO4 (IP) 4.3
SO4 (IP) 4.3
non-TSP 56.4
TSP 68.5
Sites Mean
PM Range/ Per City
(Std. Dev.) City Pop.
(29) 1 928,000
(4.5)
(17) 10.6 928,000
(3.1) (TSP)
(2.5) 1 928,000
(2.5) 1 928,000
(18) 10.6 928,000
(17)
Model
Type
OLS
sep.
Log-
linear
OLS
OLS
Log-
linear
PM Lag Other
Structure Pollutants Other Factors
none none Same as above
none none Same as above
without other
nonwhhe, heating
degr. days, pop.
density
none none Same as above with
other nofiwhite,
heating degree days,
pop. density
none none Pet. ^ Age 65,
median age, pet.
nonwhite, pop.
density, pet., poor
pet. w/ 4 yrs.
college
none none Pet. ^ Age 65, pet.
Afr.-Amer., Pet.
Hispanic, pop.
density, pet. poor,
adj. eig. sales
Relative Risk1
at TSP - 100,
S04 - 15
1.036 PM,,
l.OeOPMa.,
1.066 TSP
1.021S04
1.04SO4
1.19SO4
1.50 TSP
1.43 TSP
RR.
Confidence
Interval
(0.98,
(0.99,
1.10)
1.13)
(1.006, 1.13)
NS
NS
(1.03,
(1.22,
(1.20,
1.35)
1.83)
1.71)
Elasticity
0.027
0.043
0.044
0.012
0.011
0.054
0.23
0.25
'All regression models used PM indicator! one at a time (separate models) except as noted.
'At TSP = 100 ng/mj, SO4 " 15 fig/nf, corrected for migration.
'NS - not statistically significant, confidence limits not available.
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November 1995
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TABLE V-9. PROSPECTIVE COHORT MORTALITY STUDIES
Source
Abbey et
al. (1991)
Dockery et
al. (1993)
p. 1758
Pope et al.
(1995)
Table 2
Health
Outcome
Total
mortality
from
disease
Total
mortality
Total
mortality
Population
Calif. 7th
Day
Adventist
White
adult
volunteer!
In 6 U.S.
cities3
American
Cancer
Society,
adult
volunteers
in U.S.
Time PM
Period/ PM Mean
No. UniU Indicator! (jtg/m*)
1977-82 24 h TSP 102
Defined by > 200
air
monitoring
litei
1974-91 PM,j 29.9
PM5J 18
S64 7.6
1982-89 PM2J 18.2
PM, , 50
citiei
SO4 151 S04 11J
citiei
Sites
PM Range/ Per Total
(Std. Dev.) City Deaths Model Type
25-175 NA 845 Cox
(annual avg) proportional
hazards
18-47 1 1429 Cox
11-30 proportional
5-13 hazards
9-34 1 20,765 Cox
proportional
hazard
4-24 1 38,963
PM Lag Other
Structure Pollutant* Other Factor*
10 yn none age, §ex, race,
i mo king,
education,
airway disease
none none age, sex,
smoking,
education,
body mail,
occup.
exposure
hypertension4,
diabetes4
none none age, sex, race,
smoking,
education,
body mass,
occup.
exposure,
alcohol
consumption,
passive
smoking,
climate*
Relative
Risk1 at
SO, - 15,
PM,, - 50,
PMj.j-25
0.99 TSP1
1.42PM,,
1.31 PM,.,
1.46SO4
1.17PM,.,
1.10SO4
RR.
Confidence
Interval Elasticity
(0.87-1.13)' NSa
(1.16-2.01) 0.25
(1.11-1.68) 0.22
(1.16-2.16) 0.23
(1.09-1.26) 0.117
(1.06-1.16) 0.077
<
to
o
'For 1,000 h/yr >
JNS = non significant, confidence limits not ihown.
'Portage, WI; Topeka, KS; Watertown, MA; Harrisman-Kingrton, TN; Steubenville, OH.
'Used in other regression analyses not shown in this table.
JValue may be affected by filter artifacts.
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External Review Draft Do Not Quote or Cite
November 1995 V-26
The adjusted increases in risk (26 percent) between the cities with highest and lowest levels
of air pollution were nearly equal for PM10, PM2.5 and sulfates.
A similar study was conducted by Pope et al., 1995 which used 7-year survival data,
between 1982 and 1989, for over half a million adults in 151 U.S. cities (American Cancer
Society (ACS) Study). In this study, the association between multi-year concentrations of
sulfates and PM2J and mortality was evaluated. As in the Six City Study, individual level
information was used to adjust for important risk factors, such as age, sex, race, smoking,
passive smoking, and occupation. After adjustment for the other risk factors, PM2.5
concentrations were found to be associated with a 17 percent increase in mortality and those
of sulfate associated with a 15 percent increase in mortality between cities with the least and
most polluted air.
A third prospective cohort study was also conducted in California by Abbey et al.,
1991 (California Seventh Day Adventist Study), which did not find a significant association
between total mortality and TSP. However, this study has less statistical power than the
other two studies because the California Seventh Day Adventist study reports a smaller
number of deaths (60 percent of that reported in the Harvard Six City study and 4 percent in
the ACS study). In addition, TSP was used as the measure of exposure, which does not
spatially correlate as well as PM10 or fine particles.
ii. Specific Causes of Mortality
Both the Harvard Six City and the ACS studies evaluated specific causes of mortality
associated with PM as shown in Table V-10. As with the short-term studies, the increase in
risk of mortality associated with particle matter was mostly attributed to increases in
cardiopulmonary mortality. The Harvard Six City study reported a 37 percent increase in
cardiopulmonary mortality associated with PM2 5, after adjusting for covariates, between the
most polluted and least polluted city. Similarly, the ACS study reported a 31 percent
increase in cardiopulmonary mortality associated with PM2J, after adjusting for covariates,
between the most polluted and least polluted city.
However, unlike the short-term exposure studies, an association was also found
between lung cancer mortality and PM levels, though the results were not always statistically
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External Review Drqft
November 1995
Do Not Quote or Cite
™ raE M°ST FLUTED AND LEAST POLLUTED CITIES FOR FOR
POPULATION AND FORMER AND CURRENT SMOKERS IN THE PROSPECTIVE COHORT STUDIES
Endpomt
• — .
Total Mortality
Cardiopulmonary
Disease
Lung Cancer
— .- .
The results (and 95
29.6 jtg/m3) and th<
B) American
Endpoint
_
Total Mortality
Cardiopulmonary
Lung Cancer
• _
Total Population Relative Risk
Per 18.6 /xg/m3 Increase in
PM2.5
1.26
(1.08 - 1.47)
1.37
(1.11 - 1.68)
1.37
(0.81-2.31)
percent confidence intervals) were i
s lowest level of PM2.5 (Portage, W
Cancer Society Study, Pope et al.
Total Population Relative Rj.
24.5 jtg/m3 in PM2.5
^ — — —
1.17
(1.09 - 1.26)
1.31
(1.17-1.46)
1.03
(0.80-1.33)
Non-Smokers Relative Risk Former Smokers Relative Risk Current Smokers Relative
Per 18.6 /tg/m3 Increase in Per 18.6 /xg/m3 Increase in Risk Per 18.6 /tg/m3
PM2-5 PM2.5 Increase in PM2.5
1.19
(0.90- 1.57)
•
reported in the paper between the city with the
1, H.O^g/m3).
(1995)
sk Per Non-Smokers Relative Risk Per
24^5 /zg/m3 in PM2.5
1.22
(1.07-1.39)
1.43
(1.18- 1.72)
0.59
(0.23- 1.52)
1.35 1.32
(1.02-1.77) (1.04-1.68)
highest level of PM2.5 (Steubenville, OH, average
Current and Former Smokers Relative
Risk Per 24.5 fig/a? in PM2.5
1.15
(1.05 - 1.26)
1.24
(1.08-1.42)
1.07
(0.82 - 1.39)
1
w
intC™ls> Were reP°rted - ^ paper between the city with the highest and the lowest level of PM2.5 of the 47 cities
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External Review Draft Do Not Quote or Cite
November 1995 V-27
significant. The Harvard Six City Study reported a positive but nonsignificant increase in
mortality for lung cancer between the most polluted and least polluted cities as measure by
PM2J. The ACS study did not find an increase in lung cancer associated with PM2.5, but did
find a statistically significant 36 percent (95 percent confidence interval of 11 percent to 66
percent) increase in lung cancer mortality between the cities with the highest and lowest
levels of sulfates. Both the ACS study and the Harvard Six City study found no other
associations between PM levels and causes of mortality other than cardiopulmonary.
These two studies also evaluated the association between PM level and total and
cause-specific mortality by smoking status (Table V-10). The ACS study compared the risk
of mortality associated with PM separately for those who never smoked and those who have
at one time smoked. The Harvard Six City Study compared risk of mortality associated with
PM for the total population, former smokers, current smokers and nonsmokers. There was a
positive association between mortality and fine particles for all categories in the Harvard Six
City study, though the association was only statistically significant for the former smokers
and current smokers (Table V-lOa). In the ACS study, statistically significant positive
associations were reported for total and cardiopulmonary mortality for nonsmokers and the
population of people who were current or former smokers (Table V-lOb). Estimated
pollution-related mortality risk was as high for never-smokers as it was for current and
former smokers.
c. Extent of Mortality Displacement
Given the inevitability of death, an important consideration is the length of time for
which death has been advanced ("mortality displacement" or "prematurity of death") in these
studies. Findings of significant prematurity in PM-associated deaths would further heighten
concern about exposure to PM. From the description of the sensitive subpopulations for PM
exposure, it is reasonable to expect that some of the mortality associated with short-term
pollution is occurring in the weakest individuals who might have died within days even
without exposure to PM. Such a pattern is often seen for some other environmental insults,
such as high temperature (Kalkstein, 1991). Increased mortality has been reported in short-
term exposure studies primarily, but not exclusively, among the elderly (i.e., 65 years of age
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External Review Draft rj0 fj0t Quote or Cite
November 1995 V-28
or older) or individuals with preexisting respiratory disease. However, Schwartz (1994b);
Samet et al., (1995); and Bates (1992) also note that the sensitive subpopulations for PM
effects could be continually changing as people contract disease and recover. This
observation supports the hypothesis that death might be substantially premature if a person
becomes seriously ill and without the extra stress of PM would otherwise have recovered. It
is plausible that both of these types of life-shortening (i.e., a few days to much longer term
mortality displacement) may be observed in the studies because of the heterogeneity of the
population studied.
It is very difficult to determine the amount of time death is being advanced. Schwartz
(1994c) has reported an increase in sudden deaths for individuals who were not hospitalized
on days with high PM levels in Philadelphia. In this case, where it may be assumed that
patients with current life-threatening symptoms of disease would be more likely to be in a
hospital, it is difficult to be confident that only short-term displacement of mortality is
occurring.
Direct evidence from short-term exposure studies concerning the degree of mortality
displacement observed is limited. Spix et al., (1993) reported a statistical test for whether
PM mortality effects might be affecting those for whom death was imminent. They report
some evidence consistent with this hypothesis, but it was not statistically significant. The
authors speculate, on the other hand, that PM may also lead to the extra stress that causes the
death of a seriously ill person who may have otherwise recovered.
If the effect of PM is only to advance imminent death among particularly sensitive
individuals, the excess daily deaths during periods of high PM concentrations would be
canceled by subsequent mortality reductions. Thus, in this case, long-term differences in
mortality would not be expected to be observed. Pope et al. (1992) reported observable
long-term differences in mortality in the Utah Valley for a 44-month period in which particle
levels averaged 15 /zg/m3 higher than an intervening 13-month period of lower PM pollution.
The difference observed (3 percent higher mortality in the high PM period) was consistent
with that predicted from models of mortality associations with short-term PM exposures,
although the observed differences may have related both to short-term and long-term
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External Review Draft Do Not Quote or Cite
November 1995 V-29
exposure effects. Because this difference in mortality was observable across a 13-month
period, this observation suggests that the associations between PM and mortality in this
location are not restricted solely to mortality displacement on the order of a few days or
weeks, for which no systematic difference in observed mortality would be expected.
Quantification of the degree of life shortening observed in the long-term cohort
mortality studies (Dockery et al., 1993; Pope et al., 1995) is difficult and requires
assumptions about life expectancies. Lippmann and Thurston (in press) have suggested that
the mean life-shortening from PM exposure from these studies is on the order of two years.
Furthermore, they point out that the average life shortening implies that many individuals
have lives shortened by many years.
2. Aggravation of Existing Respiratory and Cardiovascular Disease
It is reasonable to anticipate that if associations between PM and mortality are
observed, that the same kinds of community based observational studies should find increased
morbidity with elevated levels of PM. This is indeed the case. Given the mortality results
as well as the earlier mechanistic and sensitive populations discussions, it is also not
surprising that the majority of such studies tend to find effects linked to populations with
respiratory or cardiovascular disease. Numerous studies have observed associations between
PM and responses ranging from severe effects such as increased hospitalization for
respiratory and cardiovascular conditions, to moderate exacerbation of respiratory conditions
and changes in pulmonary function. The key evidence for such effects is summarized below.
a. Hospital Admissions and Emergency Department Visits
A number of epidemiological studies report a positive association between short-term
exposures to PM and hospital admissions for respiratory-related and cardiac diseases.
Hospital admissions and emergency room visits for these diseases are an indication of their
incidence in the population. Table V-ll is a summary of the results for admissions for all
respiratory disease. Tables V-12 to V-14 show studies which investigated associations of PM
levels with specific respiratory or cardiovascular diseases such as COPD (emphysema,
chronic bronchitis, bronchiectasis, asthma etc,), pneumonia, and heart disease. As with the
mortality studies, associations between PM and hospital admissions have been observed in
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External Review Draft
November 1995
DoNotQfioteorCite
TABLE V-ll. EPIDEMIOLOGICAL STUDIES OF HOSPITAL ADMISSIONS FOR RESPIRATORY DISEASE
PM
Study Indicator
Burnett et al. (1994) sulfate
All ages in Ontario, Canada,
1983-1988
Thurston et al. (1994) PM^, sulfate,
All ages in Toronto, Ontario, PM,0, and TSP
Canada, July and August,
1986-1988
Thurston et al. (1992) sulfate, H +
All ages in Buffalo, Albany,
New York City, July and
August, 1988-1989
Schwartz (in press) PM10
Elderly in New Haven, CT,
1988-1990
Schwartz (in press) PMio
Elderly in Tacoma, WA,
1988-1990
Schwartz (in press) PM10
Spokane, WA
Pope (1989) All ages in Utah PMIO
Valley, UT
Other Pollutants
PM Mean & Range Measured
sulfate means Ozone
ranged from 3.1
to 8.2 jtg/m3
mean sulfate ranged Ozone, H + , SO2,
38 to 124 NO2
(nmole/m3), PM,0
30 to 39 ftg/m3, TSP
62 to 87 /ig/m5
mean sulfate ranged Ozone, H +
6.9 to 9.6 /*g/m3,
maximum 42 PM|0
mean = 41, Ozone, SO2
10% tile = 19,
90% tile = 67
mean = 37, Ozone, SO2
10% tile = 14,
90% tile = 67
mean = 46, Ozone
10% tile = 16, 90%
tile = 83
mean = 45.8, none
ranged from 1 1 to
365
Weather &
Other Factors
Temperature
Temperature
Temperature
Temperature
and dew point
adjusted for in
the moving
average
Temperature
and dew point
adjusted for in
the moving
average
Temperature
Pollutants in
model
ozone
none
ozone
none
SO2 (2 day
lag)
ozone (2 day
lag)
none
S02
03 (2 day
lag)
none
Result*
(Confidence Interval)
1.03**
(1.02, 1.04)
PM,o
1.09
(0.96, 1.22)
PM,o
1.01
(0.87, 1.15)
(not given for PM
measures)
1.06
(1.00, 1.13)
1.07
(1.01, 1.14)
1.09
(1.00 - 1.20)
1.10
(1.03, 1.17)
1.11
(1.02, 1.20)
1.12
(0.97 - 1.29)
1.085
(1.036- 1.136)
(statistically significant
results (RR) not given)
N)
VO
** Relative risk per 14 /ig/m3 sulfate.
rM,0 or 10O jtg/nr increase in TSP.
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November 1995
Do Not Quote or Cite
TABLE V-12. EPEDEMIOLOGICAL STUDIES OF HOSPITAL ADMISSIONS FOR COPD
PM
Study Indicator
Sunyer et al. (1993) ER black smoke
admissions 14 years and
older in Barcelona, 1985-
1989
Schwartz (1994f) PM,0
Elderly in Minneapolis,
MN, 1986-1989
Schwartz (1994e) PM,0
Elderly in Birmingham,
AL, 1986-1989
Schwartz (1994d) PMIO
Elderly in Detroit, MI
Other
pollutants
PM Mean & Range measured
winter 33% tile = SO2
49, 6795 tile = 77,
summer 33% tile =
36, 67% tile - 55
mean = 36, 10% Ozone
tile = 18, 90%
tile - 58
mean = 45, 10% Ozone
tile - 19, 90%
tile = 77
mean = 48, 10% Ozone
tile = 22, 90%
tile = 82
Weather & Pollutants
Other Factors in model
min temp, day none
of week and
year
SOj
8 categories of none
temp. & dew
pt., month,
year, lin. &
quad, time
trend
7 categories of
temp. & dew
pt., month,
year, lin. &
quad, time
trend
Temp., month, Ozone
lin. & quad.
time trend
Result*
(Confidence Interval)
winter: 1.15
(1.09, 1.21)
summer: 1.05
(0.98, 1.12)
winter: 1.05
(1.01, 1.09)
summer: 1.01
(0.97, 1.05)
1.25
(1.10, 1.44)
1.13(1.04- 1.22)
1.11 (1.04- 1.17)
Ni
vo
cr
* Relative risk calculated from parameters given by author assuming a 50 /tg/m3 increase in PMIO or 100 jig/m3 increase in TSP.
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TABLE V-13. EPEDEMIOLOGICAL STUDIES OF HOSPITAL ADMISSIONS FOR PNEUMONIA
PM
Study Indicator
Schwartz (1994f) PMIO
Elderly in Minneapolis, MN
1986-1989
Schwartz (1994e) PM10
Elderly in Birmingham, AL
1986-1989
Schwartz (1994d) PM10
Elderly in Detroit, MI
1986-1989
PM Mean Other pollutants
& Range measured
mean = 36, Ozone
10% tile = 18,
90% tile = 58
mean = 45, Ozone
10% tile = 19,
90% tile = 77
mean = 48, Ozone
10% tile = 22,
90% tile = 82
Weather &
Other Pollutants
Factors in model
8 categories of none
temp. & dew pt. ,
month, year, lin. &
quad, time trend
7 categories of none
temp. & dew pt.,
month, year, lin. &
quad, time trend
Temp, month, lin. ozone
& quad, time trend
Result*
(Confidence
Interval)
1.08
(1.01,
1.09
(1.03,
1.06
(1.02,
1.15)
1.15)
1.10)
0
* Relative risk calculated from parameters given by author assuming a 50 /xg/m' increase in PM10 or 100 fig/a? increase in TSP.
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TABLE V-14. EPIDEMIOLOGICAL STUDIES OF HOSPITAL ADMISSIONS FOR HEART DISEASE
PM
Study Indicator
Schwartz and Morris PM,0
(in press)
Elderly in Detroit, MI
1986-1989
Ischemic Heart Disease
Burnett et al. (1995) sulfate
All ages in Ontario,
Canada, 1983-1988
Cardiac disease admission
PM Mean Other pollutants
& Range measured
mean = 48, SO2, CO, ozone
10% tile = 22,
90% tile = 82
means ranged from Ozone
3.0 to 7.7 in the
summer and 2.0 and
4.7 in the winter
Weather &
Other
Factors
Temp, month, lin.
& quad, time trend
Temperature
included in separate
analyses by summer
and winter
Pollutants
in model
none
ozone, CO,
SO2
none
ozone
Result*
(Confidence
Interval)
1.06
(1.02, 1.10)
1.06
(1.02, 1.10)
1.04
(1.03, 1.06)
1.04
(1.03, 1.05)
Relative risk calculated from parameters given by author assuming a 50 /ig/m3 increase in PM,0 or 100 /ig/m3 increase in TSP.
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numerous communities throughout North America (Birmingham, Detroit, Spokane, Tacoma,
New Haven, Utah Valley, New York State, Ontario, Canada). Of the 12 studies, 11 of them
reported statistically significant, positive associations between PM level and increased risk of
admission to the hospital including evaluating cause-specific admissions for respiratory
diseases. The studies find a 3-24 percent increase in hospital admissions for respiratory
disease associated with a 50 /*g/m3 increase in PMi0. Specifically, studies reported 6-9
percent increase in admissions for pneumonia and an 11-25 percent increase for COPD for
the elderly associated with a 50 ftg/m3 increase in PM. A recent study of hospital admissions
for cardiovascular illness (Schwartz and Morris, in press) reported that PM was positively
and significantly associated with daily admissions for ischemic heart disease, with SO2, CO,
and ozone making no independent contribution to the effect. In the same study PM and CO
showed independent association for congestive heart failure admissions.
When viewed together, these studies demonstrate an association between hospital
admissions for respiratory and cardiac causes and PM. Evaluating the cause-specific
associations suggests a greater effect on admissions for COPD. These results are consistent
with those of the mortality studies, which also found a stronger association between
respiratory related mortality and PM than total causes of mortality.
b. School Absences. Work Loss Days and Restricted Activity Days
School absences, restricted activity days and work loss days can also be used as
indicators of acute respiratory conditions, though these are indirect measures compared to
actual diagnosis and measurement of respiratory conditions. It is not clear whether the
effects result from aggravation of chronic disease (e.g., COPD), acute infection, or non-
specific symptomatic effects. Nevertheless, the results of these studies show consistent
associations between such measures of morbidity and increasing levels of PM. Ransom and
Pope (1992) have reported a statistically significant positive association between PM levels
and school absences. Respiratory conditions are the most frequent cause of school absences
(CD, Chapter 12). In addition, three other studies report positive significant associations
between PM and work loss days and restricted activity days (Ostro, 1983; Ostro and
Rothschild, 1989; Ostro, 1987). A study by Ostro and Rothschild (1989) reported positive
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significant associations between PM and respiratory-related restricted activity days. All of
these studies report a two to four week lag time between elevations on PM levels and school
absences, work loss days and restricted activity days. This suggests that not only are there
immediate effects after elevations of PM exposure (e.g., mortality), but PM may elicit
effects which are exhibited at a later time. This result is also consistent with the hypothesis
of increased susceptibility to infection resulting from exposure to PM.
3. Respiratory Mechanics and Symptoms
Further exploration of the PM/health effect association shows PM is also associated
with effects on measures of lung function and respiratory symptoms. Effects on respiratory
mechanics can range from mild transient changes with little direct health consequence to
incapacitating impairment of breathing. Symptomatic effects also vary in severity, but at
minimum suggest a biological response that is often more sensitive than lung function
measurements.
a. Acute Pulmonary Function Changes and Respiratory Symptoms from Short-
term Exposures
i. Community Air Pollution Studies
In community epidemiological studies, associations between PM and acute pulmonary
function changes are also observed, consistent with respiratory-related effects observed in the
previously described mortality and morbidity studies. Table V-15 presents the results of the
studies. The functions studied include forced vital capacity (FVC), forced expiratory
capacity for one second (FEV,) and for three quarters of a second (FEV075), and peak
expiratory flow rate (PEFR).
Table V-16 provides a summary of studies reporting acute respiratory disease
symptoms associated with short-term PM exposures. These studies found associations
between short-term exposures of PM and upper respiratory symptoms (e.g., hoarseness, sore
throat), lower respiratory symptoms (chest pain, phlegm, and wheeze), fever, cough, and
acute respiratory illness. Eleven of these studies were conducted in children. Four of the
studies evaluated respiratory symptoms in all children (Schwartz et al., 1994; Hoek and
Brunekreef, 1993; Hoek and Brunkekreef,1995; Schwartz et al., 1991) and all but one found
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TABLE V-15. EPIDEMIOLOGICAL STUDIES OF ACUTE PULMONARY FUNCTION CHANGES
PM Indicator
Study
ADULTS
Pope and Kanner (1993) PM,0
Study of adults in the Utah
Valley from 1987 to 1989
CHILDREN
Koenig et al. (1993) Study of PM2.3
asthmatic and non-asthmatic
elementary school children in
Seattle, WA in 1989 and 1990
Dockery et al. (1982) TSP
School age children in
Steubenville, OH, measured
at three times between 1978
and 1980
Neas et al. (1995) Study of PM10, PM2.S
83 children in Uniontown,
PA, in the summer of 1990
PM Mean & Range
(^g/m3)
PM,0 daily mean was
55 and ranged from
1 to 181
PM2 j ranged from 5
to 45
up to 455
Mean PM,0 = 36,
max. = 83
Mean PM^ = 25,
max. = 88 /xg/m3
Other
Pollutants
Measured
Limited
monitoring of
SOj, NO2, and
ozone
none
SO2
O3, SO2, sulfate,
H+
Function Examined
FEV,
FVC
Asthmatics
FEV,
FVC
Non-asthmatics
FEV,
FVC
FVC
FEV0.73
PEFR per 25 fig/m3
PM2J
Decrease* (Confidence Interval)
29 ml (7,51)
15 ml (-15,45)
42 ml (12, 73)
45 ml (20, 70)
4 ml (7, 51)
15 ml (-15, 45)
8.1 ml
1.8ml
Note: decreases were statistically
significant
23.1 (-0.3,36.9)
*Decreases in lung function calculated from parameters given by author assuming a 50 jig/m3 increase in PM,0 or 100 fig/m3 increase in TSP.
FEV, Forced expiratory capacity for 1 second.
FVC Forced vital capacity.
PEFR Peak expiratory flow rate.
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TABLE V-15. EPIDEMIOLOGICAL STUDIES OF ACUTE PULMONARY FUNCTION CHANGES
Study
PM Indicator PM Mean & Range
Other
Pollutants
Measured
Function Examined Decrease* (Confidence Interval)
Quackenboss et al. (1991) PM2.5
Asthmatic children aged 6 to
15 years in Tucson, AZ,
measured in May and
November, 1988
Pope et al. (1991) Study of PMIO
asthmatic children in the Utah
Valley
Pope and Dockery (1992) PM10
Study of non-asthmatic
symptomatic and
asymptomatic children in the
Utah Valley
Hoek and Brunelcreef (1993) Black smoke,
Study of children aged 7 to PM,0
12 in Wageningen,
Netherlands
Roemer et al. (1993) Study of Black smoke,
children with chronic PM|0
respiratory symptoms in The
Netherlands
Not given
N02
PEFR
PM,0 ranged from 11 SO2, NO2, ozone PEFR
to 195
375 ml/s
Note: these are diurnal rather
than daily changes
55 ml/s (24, 86)
PM10 ranged from 11 SO2, NO2, ozone Symptomatic PEFR 30 ml/s (10, 50)
to 195
Asymptomatic 21 ml/s (4, 38)
PEFR
range of PM]0 was SO2> NO2
30 to 144
range of PM,0 was SO2, NO2
30 to 144
PEFR
PEFR
41 ml/s (-8, 90)
34 ml/s (9, 59)
oo
i—>
CT1
*Decreases in lung function calculated from parameters given by author assuming a 50 /ig/m3 increase in PM10 or 100 jig/m3 increase in TSP.
FEV, Forced expiratory capacity for 1 second.
FVC Forced vital capacity.
PEFR Peak expiratory flow rate.
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TABLE V-15. EPDDEMIOLOGICAL STUDIES OF ACUTE PULMONARY FUNCTION CHANGES
PM Indicator
Study
Dassen et al. (1986) School RSP (PM10),
age children in The TSP
Netherlands, measured in
November, 1984 and January,
1985
Other
PM Mean & Range Pollutants
(/ig/m3) Measured
TSP and RSP both SO2
exceeded 200
Function Examined
FVC
FEV,
PEFR
Decrease* (Confidence Interval)
slopes not given but FVC,
FEV,, and PEFR were
significantly reduced during
episodes
Studnicka et al. (1995) Study
of 133 children at a summer
camp in southern Austria in
1991
Hoek and Brunekreef (1994)
Study of children in 4 towns
in The Netherlands
Dusseldorf et al. (1994) Study
of 32 adults in a steel plant in
Wijkaan Zee, The
Netherlands
PM,
Means ranged from
6.6 to 10.7 /ig/m3
No. of sites not PM,0 mean was 45,
given 24-hr range was 14-126
/ig/m3
PM10 measured
PM,0 measured
at 3 sites
PM,0 mean was 54,
range was 4 - 137
/xg/m3
H+, S02,
ammonia
S02, N02,
sulfate, nitrate,
HONO
Iron, Mn,
sodium, silicon
FVC
FEV,
PEFR
FVC
FEV,
PEFR
PEFR evening
PEFR morning
17.5 ml/s (64,0, 99,0)
66.5 ml/s (-10,0, 143.0)
99 ml/s
-0.5 ml/s (-3.5, 2.5)
5.0 ml/s (-1.0, 11.0)
41.0 ml/s (12.5, 69.5)
45 ml/s (9, 81)
77 ml/s (34, 119)
<:
*Decreases in lung function calculated from parameters given by author assuming a 50 /tg/m3 increase in PMIO or 100 jig/m3 increase in TSP.
FEV, Forced expiratory capacity for 1 second.
FVC Forced vital capacity.
PEFR Peak expiratory flow rate.
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TABLE V-16. EPIDEMIOLOGICAL STUDIES OF ACUTE RESPIRATORY DISEASE
Study
PM,T fug/nrt
Other
PM Mean Minimum Maximum Other Pollutants Weather & Pollutants
Indicator Measured Other Factors in Model
RR per 50 jig/m3
increase*
(Confidence Interval)
CHILDREN
Schwartz et at. (1994)
300 elementary school
children in Six-Cities in
U.S., 1984-1988
Pope et al. (1991),
asthmatic school children
(4th, 5th grade) in the
Utah Valley, winter
1989-1990
PM
10
PM
2.3
30 13** 53***
18 ?** 37***
Ozone, NO2,
SO,
Temperature SO2, O3
PM1(
46 11
195
NO2, SO2, and
ozone. Values
were well below
the standard
Variables for none
temperature
and time trend
Cough+
1.51 (1.12,2.05)
Upper respiratory+
1.39 (0.97 - 2.01)
Lower respiratory+
2.03(1.36-3.04)
Upper respiratory+
1.20(1.03, 1.39)
Lower respiratory+
1.28 (1.06, 1.56)
u>
* Relative risk calculated from parameters given by author assuming a 50 /tg/m3 increase in PM,0 or 100 /ig/m3 increase in TSP.
** tOth percentile.
*** 90th percentile.
**** Odds ratio for increase is shortness of breath for a 56 /ig/m3 increase in PM10.
4- Statistically significant with 95 percent confidence interval.
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TABLE V-16. EPIDEMIOLOGICAL STUDIES OF ACUTE RESPIRATORY DISEASE
PM
Study Indicator
Pope and Dockery PM,0
(1992), symptomatic non-
asthmatic children in the
Utah Valley, winter
1990-1991
Pope and Dockery PM,0
(1992), asymptomatic
children in the Utah
Valley, winter 1990-1991
PMr fue/m3)
Other
Mean Minimum Maximum Other Pollutants Weather & Pollutants
Measured Other Factors in Model
76 7 251 None Variable for none
low
temperature
5-Day
Moving
Average
76 7 251 None Variable for none
low
temperature
5-Day
Moving
Average
RR per 50 /ig/m3
increase*
(Confidence Interval)
Upper respiratory +
1.20 (1.03, 1.39)
Lower respiratory +
1.27 (1.08, 1.49)
Cough +
1.29(1.12, 1.48)
Upper respiratory
1.30 (1.06, 1.58)
Lower respiratory
1.40(1.14, 1.70)
Cough
1.42(1.17, 1.73)
Upper respiratory
0.99 (0.78, 1.26)
Lower respiratory
1.13(0.91, 1.39)
Cough +
1.18 (1.00, 1.40)
Upper respiratory
1.04 (0.75, 1.43)
Lower respiratory
1.21 (0.92 - 1.59)
Cough
1.35 (1.07 - 1.72)
UJ
Relative risk calculated from parameters given by author assuming a 50 ^g/m3 increase in PM)0 or 100 fig/m3 increase in TSP.
*** 90th percentile.
**** Odds ratio for increase is shortness of breath for a 56 /ig/mj increase in PM10.
+ Statistically significant with 95 percent confidence interval.
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TABLE V-16. EPIDEMIOLOGICAL STUDIES OF ACUTE RESPIRATORY DISEASE
PM
Study Indicator
Ostro (1995b) Study of PM!0
83 African-American
Asthmatic Children in
Los Angeles, CA
Hoek and Brunekreef PM10
(1993), respiratory
disease in school children
aged 7 to 12 in
Wageningen,
Netherlands, winter
1990-1991
Schwartz et al. (1991) TSP
Study of acute respiratory
illness in children in 5
German communities,
1983-1985
Braun-Fahrlander et al. TSP
(1992) Study of preschool
children in four areas of
Switzerland
PM,. fug/m3)
Mean Minimum Maximum Other Pollutants
Measured
56 20 101 Ozone, NO2,
S02
N/A N/A 110 MaxS02 = 105
/ig/m3, max NO2
= 127 ng/m3
17-56 5-34** 41-118*** median SO2
levels ranged
from 9 to 48
ftg/m3, median
NO2 levels
ranged from 14
to 5 /ig/m3
(not given) SO2, NO2, and
ozone levels not
given
Weather &
Other Factors
Temperature,
humidity,
pollens, molds
Variable for
ambient
temperature
and day of
study
Most
significant
terms of day
of week, time
trend, and
weather
(terms not
listed)
city, risk
strata, season,
temperature
(not given)
Other
Pollutants
in Model
ozone
none
none (TSP
was not
significant
when NO2
added to
model)
none
RR per 50 /xg/m3
increase*
(Confidence Interval)
Shortness of breath
1.58 (1.05 -
2.30)****
No effect on cough
or wheeze
Upper respiratory +
1.14(1.00, 1.29)
Lower respiratory
1.06 (0.86, 1.32)
Cough
0.98(0.86, 1.11)
1.26(1.12, 1.42) +
Upper respiratory +
1.55(1.10,2.24)
* Relative risk calculated from parameters given by author assuming a 50 /ig/m3 increase in PMIO or 100 /tg/m' increase in TSP.
** 10th percentile.
*** 90th percentile.
**** Odds ratio for increase is shortness of breath for a 56 /tg/m3 increase in PM,0.
+ Statistically significant with 95 percent confidence interval.
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November 1995
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TABLE V-16. EPIDEMIOLOGICAL STUDIES OF ACUTE RESPIRATORY DISEASE
PM
Study Indicator
Roemer et al. (1993) PM10
Study of children with
chronic respiratory
symptoms in
Wageningen, The
Netherlands
Hoek & Brunekreef PM10,
(1995) Study of sulfates
respiratory symptoms in
PM. fug/m3)
Mean Minimum Maximum Other Pollutants
Measured
6 days above 1 10 jig/m3 SO2 and NO2
means not given
48 13 124 ozone,
36 11 136 nitrate
Other
Weather & Pollutants
Other Factors in Model
(not given) none
trend, day of none
week,
humidity
RR per 50 |tg/m3
increase*
(Confidence Interval)
Cough
(not given)
Upper respiratory
symptoms
Logistic regression
300 children in Deane &
Enkhulzen, The
Netherlands
ADULTS
Ostro et al. (1991) Study
of adult asthmatics in
Denver, Colorado
November 1987 to
February 1988
PM
12.5
22
0.5
73
nitric acid,
sulfates, nitrates,
SO,, and
hydrogen ion
day of survey,
day of week,
gas stove,
minimum
temperature
none
00
coefficient
•0.0014
(-0.0032 - 0.0004)
Similar results for
lower respiratory
symptoms
Cough
1.09(0.57,2.10)
* Relative risk calculated from parameters given by author assuming a 50 jig/m3 increase in PM,0 or 100 jig/m3 increase in TSP.
** 10th percentile.
*** 90th percentile.
**** Odds ratio for increase is shortness of breath for a 56 fig/m3 increase in PM10.
+ Statistically significant with 95 percent confidence interval.
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TABLE V-16. EPIDEMIOLOGICAL STUDIES OF ACUTE RESPIRATORY DISEASE
Study
Pope et al. (1991),
asthmatics age 8-72 in
the Utah Valley, winter
1989-1990
Ostro et al. (1993) Study
of non-smoking adults in
Southern California
Dusseldorf et al. (1994)
Study of adults near a
steel mill in The
Netherlands
PM,n (uefm3)
PM Mean Minimum Maximum
Indicator
PM10 46 11 195
sulfate 82 37
fraction
andCOH
PM10, iron, 54 4 137
sodium,
silicon, and
manganese
Other Pollutants
Measured
NO2, SOj, and
ozone. Values
were well below
the standard
ozone, mean =
7 pphm,
range = 1 to 28
Geometric mean
iron = 501
ng/m3,
manganese = 17
ng/m3, silicon =
208 ng/m3
Other
Weather & Pollutants
Other Factors in Model
Variables for none
low
temperature
and time trend
temperature, none
rain humidity
(not given) none
RR per 50 ^g/m3
increase41
(Confidence Interval)
Upper respiratory
0.99 (0.81, 1.22)
Lower respiratory
1.01 (0.81, 1.27)
Sulfates:
Upper respiratory
0.91 (0.73, 1.15)
Lower respiratory
1.48(1.14, 1.91)
Cough +
1.14(0.98, 1.33)
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positive significant associations with PM with one or more symptoms. Two of the studies
evaluated respiratory symptoms in asthmatic children (Pope et al., 1991, Ostro, 19955) and
found significant positive associations with PM, although in the Ostro (19955) study, the
effect could not 5e separated from ozone. A study of symptomatic and asymptomatic
children found significant positive associations with all symptoms in the symptomatic
children, and positive, 5ut not significant associations in the asymptomatic children (Pope
and Dockery, 1992). The four studies in adults were inconsistent. Therefore, these studies
suggest that vulnera51e individuals, such as symptomatic children or children with asthma,
may have aggravation of symptoms associated with PM.
ii. Controlled Exposures to La5oratory Aerosols
In general, 5ronchoconstriction and associated symptoms may 5e induced 5y chemical
or mechanical irritation 5y inert dusts, re-suspended ur5an dust, coarse organic dusts, fine
acid aerosols, and fine particles in com5ination with pollutant gases (U.S. EPA, 19825).
Specifically, exposure to high levels of re-suspended dust consisting of dust particles ranging
in size from 0.5-10 /zm diameter with a composition consisting of crustal material, sulfates,
and volatile material has also 5een shown to induce 5ronchoconstriction (U.S. EPA, 1982a).
In controlled human clinical and animal studies, acidic aerosols have 5een a primary
focus of research of PM effects. Ta51e 11.2 of the CD provides a summary of the controlled
human exposures to acid aerosols and other particles and shows acid aerosol effects from
short-term exposures (less than 24 hours). Most of the human clinical studies examine the
effect on lung function from exposure to H2SO4 aerosols. The endpoints most commonly
measured are symptoms and pulmonary function tests which are well standardized in regard
to their use in these studies (Utell et al., 1993). The advantages of such studies include the
opportunity to study the species of interest (humans), and the ability to control exposure in
regard to pollutant concentration, aerosol characteristics, temperature, and relative humidity
(CD, Chapter 11).
In these studies healthy young subjects seem to tolerate relatively large concentrations
of H2SO4 particles without deleterious effect; whereas, asthmatics experience decrements in
lung function at relatively low concentrations. Asthma severity in studies of acid aerosols
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and other particles are presented in Table 11-3 of the CD. Asthmatic subjects appear to be
more sensitive than healthy subjects to the effects of acid aerosols on lung function (Utell et
ah, 1982), but the reported effective concentration differs widely among studies (CD,
Chapter 11). Adolescent asthmatics may be more sensitive than adult asthmatics and may
experience small decrements in lung function in response to H2SO4 at exposure levels only
slightly above peak ambient levels (e.g., less than 100 /*g/m3) (Koenig et al., 1989; CD,
Chapter 11). Lung function effects in asthmatic subjects are correlated with hydrogen ion
content of the sulfate aerosol (CD, Chapter 11) and affected by neutralization by oral
ammonia (Utell et al., 1983b; 1989) and buffering capacity of the aerosol (Fine et al.,
1987b). In addition, results from recent studies have suggested aerosols of submicron
particle size may alter lung function to a greater degree than large particle aerosols in
asthmatic subjects (CD, Chapter 11; Avol et al., 1988a,b,; Utell et al., 1983b) albeit at
larger concentrations than found to affect adolescent asthmatics. Human studies have also
suggested potentiation of effects (airway responsiveness) of H2SO4 aerosol exposure with
ozone exposure (Linn et al., 1994; Frampton et al., 1995; CD, Chapter 11).
However, studies cited in an Acid Aerosols Issue Paper (U.S. EPA, 1989) have not
demonstrated synergistic or interactive effects between sulfates and SO2 exposure (CD,
Chapter 11). Indeed, given the low solubility of SO2 in acid aerosol, significant interactions
would not be anticipated in the deeper regions of the lungs, to which SO2 alone has difficulty
penetrating (U.S. EPA, 1994c). Reflex bronchoconstriction by high peaks of SO2 could,
however, increase the deposition of particles in the tracheobronchial region by narrowing the
conductive airways.
As described in the CD, human studies of PM are limited as they tend to use
pulmonary function as the endpoint of response and do not examine airway inflammation or
other more sensitive indicators related to pulmonary function changes. There are also limits
as to the kind of experiments which can be done using human subjects as exposures must be
without significant harm.
Many laboratory animal studies have also been conducted using acid aerosol
exposures with the most recent studies on effects on pulmonary mechanical function
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November 1995 V-34
presented in Table 11-4 of the CD. Some other earlier work is also presented. The CD
suggests that acidic sulfates exert their action throughout the respiratory tract with response
and location of effect dependent on particle size, mass, and number concentration (CD,
Chapter 13). In regard to the particle size, the CD suggests, that at high concentrations
which are above lethal threshold, large particles are more effective in eliciting response,
while at sublethal levels, smaller particles are more effective (CD, Chapter 11). Issues of
dosimetry and use of an inappropriate dose metric hinder interpretation of such work (see
Appendix D for further discussion).
In contrast to mortality as an endpoint, the dyspneic response in a sensitive sub-
population of guinea pigs to relatively lower concentrations of H2SO4 is similar to the asthma
response in humans (e.g., rapid onset with similar obstructive lung function changes) (CD,
Chapter 11). In addition, in controlled animal experiments, both acute and chronic exposure
of laboratory animals to H2SO4 at exposure well below lethal ones have been shown to
produce functional changes in the respiratory tract (CD, Chapter 11) and, therefore,
whatever the underlying mechanism, the results of pulmonary function studies indicate that
H2SO4 is a broncho-active agent.
b. Long-Term Exposure to PM
i. Chronic Pulmonary Function Changes
A number of epidemiological studies investigated the association between long-term
exposure to PM and pulmonary function change (Table V-17). The results are equivocal
with three studies reporting no association and one finding a decrease in lung function
associated with increasing PM levels. In regard to experimental animal studies, long-term
exposure to H2SO4 is also associated with alteration in pulmonary function (changes in
distribution of ventilation and respiratory rates in monkeys) albeit at high concentration (CD,
Chapter 11). In addition hyper-responsive airways have been induced with repeated
exposures to 250 /*g/m3 H2SO4 in rabbits (CD, Chapter 11).
ii. Chronic Respiratory Disease
Table V-18 summarizes studies investigating the association between chronic
respiratory disease and long-term exposure to PM. Four of the studies reported an
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Do Not Quote or Cite
TABLE V-17. EPIDEMIOLOGICAL STUDIES OF CHRONIC PULMONARY FUNCTION CHANGES
PM Type &
Study No. Sites
CHILDREN
Neas et al. (1994) PM2J, sulfate
Study of lung function in fraction
children in 6 cities in the U.S.
Data collected from 1983-1988.
Dockery et al. (1989) PM,,, sulfate
Study of lung function in fraction
children in 6 cities in the U.S.
Survey done 1980-1981.
Ware et al. (1984) TSP
Study of lung function in
children in 6 cities in the U.S.
Survey done 1974-1977
ADULTS
Ackermann-Liebrich et al. (in TSP, PM,0
press) Study of 9,651 adults in 8
areas of Switzerland done in
1991
Other
PM Mean Pollutants
& Range Measured
Not given SO2, NO2, and
ozone
PM|5 means SO2, NO2
ranged from
20 to 59
/ig/m3
TSP means SO2, NO2
ranged from
39 to 114
/tg/m3
PM|0 mean SO2, NO2, TSP,
was 21.2, O3
ranged from
10.1 to 33.4
Weather &
Other
Factors
City, gender parental
education, history of
asthma, age, height,
weight
City, gender, parental
education, history of
asthma, age, height,
weight
City, gender, parental
education, history of
asthma, age, height,
weight
Height, weight, age,
gender, atopic status
Decrease*
(Confidence Interval)
FVC and FEV, not changed.
Values could not be converted
to mis.
No significant relationship
found with PM10
Non-significant changes of
0.06% (-0.27, 0.39) for first
round and -.09% (-0.42, 0.24)
for second round
A significant 3.4% decrease
in FVC and a 1.6% decrease
in FEV1 was found in healthy
non-smokers. Similar results
were found for non-smokers
and former smokers.
I
Decreases in lung function calculated from parameters given by author assuming a 50 /ig/m3 increase in PM,0 or 100 fig/a? increase in TSP.
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TABLE V-18. EPIDEMIOLOGICAL STUDIES OF CHRONIC RESPIRATORY DISEASE
Study
CHILDREN
Ware et al. (1984)
Study of respiratory
symptoms in children in 6
cities in the U.S. Survey
done 1974-1977
Dockery et al. (1989)
Study of respiratory
symptoms in children in 6
cities in the U.S. Survey
done 1980-1981
Neas et al. (1994)
Study of children aged
7 to 1 1 from six cites in
U.S. Survey done
1983-1986.
ADULTS
Abbey et al. (1995a,b,c)
Study of ADD**,
bronchitis, and asthma in
adult Seventh Day
Adventist
PM Type &
No. Sites
Daily monitoring
of TSP, SO2,
NO2, and ozone at
each city
Daily monitoring
of PM,3, sulfate
fraction at each
city
PM2.5
Daily monitoring
of TSP, PMIO,
visibility at 9 sites
in northern and
southern
California
PM Mean
& Range
City TSP means
ranged from 39
to 1 14 /*g/m3
City PMI3 means
ranged from 20
to 59 jig/m3
Not given
Not given
Overall
Symptom
Rate
Cough, .08,
Bronchitis
.08,
Lower resp.
.19
Cough, .02 to
.09, Bronchitis
.04 to .10,
Lower resp.
.07 to .16
Not given
AOD = 11.8%
Bronchitis =
7.2%
Model
Type
&Lag
Structure
Logistic
regression
Logistic
regression
Logistic
regression
Multi-
logistic
regression
Other
pollutants
measured
S02, N02,
and ozone
S02, N02,
and ozone
NO,
SO,, 03,
S02, N02
Other
Other pollutants
Covariates in model
age, gender, none
parental
education,
maternal
smoking
age, gender, none
maternal
smoking
household none
smoking, gas
stove, age,
gender
Age, gender, none
education,
previous
symptoms
Result*
(Confidence
Interval)
Cough
2.75 (1.92, 3.94)
Bronchitis
2.80(1.17,7.03)
Lower resp.
2.14(1.06,4.31)
Cough
5.39 (1.00, 28.6)
Bronchitis
3.26(1.13, 10.28)
Lower resp.
2.93(0.75, 11.60)
Cough
1.08 (0.76, 1.53)
Bronchitis
1.32 (0.98, 1.79)
Lower resp.
1.23 (0.98, 1.55)
1.23 AOD**
(0.91, 1.65)
1.39 Bronchitis
(0.99, 1.92)
bstimates calculated from data tables assuming a 50 /tg/nr increase in PM10 or 100 jig/nr increase in TSP.
**Airway obstructive disease (AOD) is defined to include symptoms of chronic bronchitis, emphysema, and asthma.
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association between PM levels and lower respiratory illnesses, chronic cough, and bronchitis.
Three of the studies found associations in children, while one found an association between
PM level and a measure of chronic respiratory disease in adults. The results from these
studies are consistent and supportive of those reported for short-term studies. The
implications of respiratory disease in children is discussed above in section V.B.
iii. Lasting Physiological Effects
Symptoms from long-term exposure to PM in humans include cough, chronic
bronchitis (characterized by persistent cough and phlegm production), and lower respiratory
illness. As stated by the CD, the presence of PM, which increases the risk for respiratory
symptoms and related respiratory morbidity, is important because of associated public health
concerns with regard to both the immediate and longer term symptoms produced and the
longer term potential for increases in the development of chronic lung disease. Specifically,
recurrent childhood respiratory illness has been suggested to be a risk factor for later
susceptibility to lung damage (Glezen, 1989; Samet, 1983; Gold et ah, 1989) and is also
increased by PM exposure. Survivors of the Donora, Pennsylvania pollution episode with
prior chronic disease and those who became acutely ill during the episode, had higher
subsequent rates of mortality and illness (Ciocco and Thompson, 1961).
The 1982 Staff Paper concluded that community epidemiological studies (Ware et ah,
1981; Dockery et ah, 1981; 1989) and occupational studies of bronchitis in workers exposed
to high dust levels (Morgan, 1978) suggested that high concentrations of long-term particle
exposure is associated with an increase in prevalence of bronchitis. A description of
respiratory diseases and related impairments associated with occupational exposures to
particles was presented in Table B-l of the 1982 Staff Paper (Appendix F). Lippmann
(1981), drawing analogies between the effects of cigarette smoke and acids on clearance, has
hypothesized that repeated acid exposure may have a role in the etiology of bronchitis, at
least at concentrations that existed in the historical London episodes.
4. Morphological Damage
Traditional epidemiology has not been used to evaluate the extent to which PM
directly alters lung tissues and components. Morphological alterations associated with
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exposure to acid aerosols are outlined in Table 11-5 of the CD. Single or multiple exposures
to H2SO4 at fairly high levels (> 1 mg/m3) produce a number of characteristic morphological
responses (e.g., alveolitis, bronchial and/or bronchiolar epithelial desquamation and edema)
(CD, Chapter 11). Schwartz et al., (1977) reports that using very high concentrations (>. 70
mg/m3) of H2SO4 at comparable particle size, rats and monkeys were quite resistant while
guinea pigs and mice were the more sensitive species as measured by morphological
endpoints. Animal studies of fine (0.3 ftm) diameter to ultrafine (0.04 /*m) diameter H2SO4
aerosols (300 jtg/m3), have shown lavage fluid to contain increases in lactate dehydrogenase
and protein (markers of cytotoxicity and increased cellular permeability) following a single
exposure to guinea pigs (Chen et al., 1992a).
Silica has long been considered to be a major occupational health hazard where
exposure to crystalline silica is associated with pulmonary inflammation and fibrosis (CD,
Chapter 11). The differing forms of silica (amorphous versus crystalline) are thought to have
differential potential for toxicity but data on amorphous forms is limited (CD, Chapter 11).
There are limited data on ambient concentrations of silica, which is generally found in the
coarse fraction. Based on analyses of the silica content of resuspended crustal material
collected from several U.S. cities as part of the last review, staff concluded that the risk of
silicosis at levels permitted by the current long-term PM,0 NAAQS was low. This earlier
conclusion is supported by the CD based on the integration of occupational and autopsy
findings with ambient silica concentrations.
Some risk of long-term exposure to coarse dusts is suggested by autopsy studies of
farm workers and residents in the Southwest, desert dwellers, and zoo animals and humans
exposed to various crustal dusts near or slightly above current ambient levels. These studies
find that those exposures may result in a silicate pneumonoconiosis. Responses ranged from
the buildup of particles in macrophage with no clinical significance to possible pathological
fibrotic lesions.
5. Altered Clearance and Other Host Defense Mechanisms
Responses to air pollutants often depend upon their interaction with respiratory tract
defenses such as clearance and antigenic stimulation of the immune system. Furthermore,
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either depression or over activation of these systems may be involved in the pathogenesis of
lung diseases (CD, Chapter 11). The effects of acidic sulfates on respiratory tract clearance
are summarized in Table 11-7 of the CD. Relatively high H2SO4 exposure has also been
associated with changes in clearance and macrophage function in experimental animals and in
clearance in humans (CD, Chapter 11). Alteration of mucociliary clearance due to acid
aerosols has also been reported and discussed in an Acid Aerosol Issue Paper (U.S. EPA,
1989). The direction and magnitude of the effect are dependent on the concentration and
duration of the acid aerosol exposure, the size and distribution of the acid particles, and the
region of the airways being examined (CD, Chapter 11). In addition, the acidity of the
aerosol has been reported to affect mucociliary clearance (CD, Chapter 11). Acid aerosols
have been shown to elicit a slowing in clearance that lasts several months following multiple
exposures (Lippmann, 1981). In regard to antigenic stimulation, guinea pigs have been
reported to show increased sensitivity to inhaled antigen (ovalbumin) with concurrent H2SO4
exposure (CD).
Alveolar macrophages not only play a role in defense against bacteria but are involved
in the induction and expression of immune reactions and are capable of release of pro-
inflammatory cytokines (CD, Chapter 11). Studies by Chen et al. (1992a) suggest that
effects in alveolar macrophage function may be dependent on particle size (increased
phagocytosis with fine and decreased phagocytosis with ultrafme aerosols). Other studies
have tried to use animal models to demonstrate an effect of H2S04 exposure on susceptibility
to bacterial infection. In such studies, large concentrations were required to elicit effects in
previously healthy animals. In addition, acute exposures of up to 5 mg/m3 of H2SO4 aerosols
alone have not been demonstrated to enhance susceptibility to bacterially-mediated respiratory
disease in mice (See Table 11-8 in the CD). However, Gardiner et al. (1977) reported
increased susceptibility to infection by first ozone (0.1 ppm) and then H2SO4 (0.9 mg/m3) in
mice.
Fiber optic bronchoscopy with broncho-alveolar lavage (BAL) is a useful technique
for sampling the lower airways of humans in clinical studies and can provide a relatively
sensitive measure of inflammation (CD, Chapter 11). Only one study to date has utilized
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bronchoscopy to evaluate responses to acid aerosols. Healthy nonsmokers were exposed to
acid aerosol and were exercised after oral ammonia was neutralized. No evidence of airway
inflammation or changes in markers for host defense were detected in BAL samples collected
18 hours after exposure (Frampton et al., 1992). Gulp et al. (1995) determined that the acid
aerosol exposure did not alter mucus composition in subjects in the Frampton study.
Metals have been reported to affect clearance and other host defence systems. Nickel
inhalation has been shown to impair macrophage function and increase incidence of
pneumonia in laboratory animals (CD, Chapter 11). Loading of particles with certain
transition metals, such as iron, may have the potential to enhance particle toxicity, acute
inflammation, and nonspecific bronchial responsiveness. Silica particles have been reported
to be rendered more toxic when complexed with iron. Rats fed with iron depleted diets
exhibited less inflammation and fibrotic injury after such exposures (Ohio et al., 1994; 1992;
Ohio and Hatch, 1993). However there is some difficulty in extrapolating the in vitro
experimental paradigms used in these studies to ambient exposure situations.
6. Cancer
Studies of long-term exposure have reported associations between mortality from lung
cancer and PM levels. As reported above, using indicators of fine particle mass, (PM2.5 and
sulfates), increased risk of mortality from lung cancer has been reported. It is not clear
whether such associations relate to causation of the disease, or whether individuals with
cancer are more susceptible to other effects of particles.
Studies of the potential of particles to cause cancer as well as noncancer respiratory
effects have been studied in laboratory animals. All major types of airborne PM may contain
absorbed organic compounds which enhance the toxicity of the particles. Specifically these
compounds may be mutagenic or carcinogenic to animals and may contribute in some degree
to the incidence of human cancer associated with exposure to urban air pollution (CD,
Chapter 11). Polycyclic aromatic hydrocarbons (PAHs) are perhaps the best studied class of
potential carcinogens in PM. As noted in the 1982 Staff Paper, organic extracts with
potential carcinogenic activity are preferentially found in the fine fraction. For example,
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diesel exhaust particles and gasoline engine particles are examples of particles whose organic
extracts have proven to be mutagenic and tumorigenic.
In addition to absorbed organic compounds, particles themselves have been shown to
induce a carcinogenic response. Inhalation of talc (NTP, 1992) and carbon black aerosols
(Stoker and Mauderly, 1994) have been associated with induction of lung tumors.
Furthermore, it has been suggested that the insoluble carbon core of diesel particles is as at
least as important as the organic compounds and possibly more so for lung tumor induction
at high particle concentrations (> 2000 mg/m3) (CD, Chapter 11). However it is not clear
that this effect is seen at lower levels. Extrapolation to human risk from extraction studies
are difficult because of different species and age, route of exposure (e.g., no inhalation
assays in animals), physico-chemical properties of the material, and exposure concentration.
A large body of information has focused on toxicology of other constituents of PM
such as metals, trace elements, and silica. Metals contained in PM are all toxic under
specific conditions of exposure. Many are carcinogens as well as causing decreases in
respiratory function. In addition, silica has been reported to cause lung tumors following
chronic exposures in rats (CD, Chapter 11).
D. Strength and Coherence of Epidemiological Evidence
The majority of the evidence of the effects of PM on health comes from
epidemiological studies. In assessing these studies for review of the primary standard, the
strength and quality of the epidemiological studies must be evaluated. The CD outlines the
major criteria to be used in evaluating the scientific quality of the epidemiological studies and
to assist in interpreting them. These criteria include quality of the aerometric data, clear
definition of study populations and health endpoints, appropriate statistical analysis, adequate
control of confounders, and evaluation of the consistency and coherence of the findings with
other known facts (CD, Chapter 12). The CD addresses each of these issues, including both
the strengths and inherent limitations of such studies. In developing staff conclusions and
recommendations for primary standards, it is important to evaluate the most critical aspects
of the epidemiological studies. Accordingly, the discussion below summarizes the
consistency and coherence of the recent studies as a group, and outlines observations on
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potential confounding by weather, other pollutants, exposure considerations, as well as
sensitivity to model specification.
1. Consistency and Coherence
As noted above, numerous recent studies have evaluated the relationship between PM
and health effects. Figure V-l displays the results of selected studies for a variety of health
effects. These studies have been conducted in a number of geographic locations, using a
variety of air quality measurements and statistical techniques, and with varying temporal
relationships. The strength of the association is enhanced by qualitatively and quantitatively
consistent associations between PM levels and health effects found by different investigators
in different geographical locations. In the early stages of this review, issues were raised
about the reproducibility of the original studies finding effects at low levels in several U.S.
cities. To resolve these issues, the Health Effects Institute (HEI) funded a reanalysis of data
sets from Philadelphia, Utah Valley, Santa Clara, St. Louis, Kingston and Birmingham
(Samet et al., 1995). The HEI reanalyses produced independent results that closely agreed
and confirmed the original investigators' results in all six locations'. Evaluated in isolation,
individual studies may have specific weaknesses, which have been discussed previously in the
CD. When viewed together, however, the studies show consistent effects of PM on health.
In addition, this collection of studies shows substantial coherence in the types of
observed effects. The mortality studies indicate respiratory-related and cardiovascular deaths
are a major contributor to the PM/mortality relationship. These findings are supported by
the morbidity studies finding an association between respiratory and cardiovascular hospital
admissions. Related, but less severe health effects include symptoms and functional changes
indicating aggravation of respiratory diseases such as bronchitis and asthma, as well as acute
respiratory illness as evidenced by cough and other lower respiratory tract symptoms. The
impact of these events are also observed in the association with restricted activity days, work
'Additional observations and insights from the extended HEI analyses are included in subsequent sections.
HEI typically receives half of its funds from U.S. EPA and half from 28 manufacturers and marketers of motor
vehicles and engines in the U.S.
-------
FIGURE V.I. RELATIONSHIP BETWEEN RELATIVE RISK PER 50 ng/m3 PM10 AND SPECIFIC CAUSES OF MORTALITY AND
MORBIDITY IN ADULTS AND CHILDREN
3-
2.6-
Q.
*
8
g.1.8
w
S
1.4-
0.6
+ Adults * All Children
Symptomatic/Asthmatic Children
•M
Tdtal
Mortality
Respiratory
Mortality
Adults
Respiratory
Hospital Admissions
Cough
Lower
Respiratory
Children
Upper
Respiratory
Total Mortality and Respiratory Mortality
Cough. Lower Respiratory, and Upper Respiratory
1. Pope et al. (1992)
2. Schwartz (1993)
3. Styer et al. (1995)
4. Ostro et al. (1995a)
Respiratory Hospital Admissions
1. Schwartz (in press) New Haven, CT
2. • Schwartz (in press) Tacoma, WA
3. Scwartz (in press) Spokane, WA
4. Thurston et al. (1994) Ontario, Canada
Hoek and Brunekreef (1993)
Schwartz et al. (1994)
Pope et al. (1991), asthmatic children
Pope and Dockery (1992), symptomatic children
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loss days and school absences. Such a coherence of effects adds to the strength and
consistency of the association (Bates, 1992).
2. Model Sensitivity
Chapter 12 of the CD discusses concerns that have been raised regarding the extent to
which the observational results are sensitive to the statistical modeling approach used to
analyze the data. Investigators have applied a variety of statistical techniques to evaluate the
relationship between observed health effects and variations in short-term exposure to PM
(Table C.I, Appendix E) with almost all approaches indicating consistent positive
associations. The investigators from the recent analyses sponsored by the HEI developed a
new statistical method for analyzing data. Using this technique, corrected t-statistics were
reported to be greater than those reported by the original investigators. This result would
indicate that the original investigators underestimated the statistical significance of the
PM/mortality relationship. They confirmed the PM,(/mortality relationship was relatively
insensitive to statistical technique.
3. Exposure Misclassification
A significant difficulty in interpretation of the epidemiological studies, particularly for
quantitative purposes, is the determination of uncertainties and possible biases introduced by
using outdoor monitors to estimate population exposures. It is important to examine the
possible effect that exposure misclassification may have on the reported associatins in the
studies, as it may bias the results in either direction. Unfortunately, most studies provide
only qualitative assessments of this issue, as opposed to their more formal treatment of
weather and some other confounders. The discussion below focuses on the relationship
between the monitored pollutant levels and the actual exposure and on how the error in the
measurements might bias the reported associations.
Chapter IV discusses the overall relationship between outdoor monitors and personal
exposure and the properties of fine particles. Apart from errors associated with the outdoor
measurements themselves, questions have been raised about the number of monitors needed
to represent the population. Because fine particles are spatially homogeneous, the
uncertainties associated with studies using a limited number of monitors to represent daily
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fluctuations in community concentrations are reduced. In contrast, the coarse fraction which
is less spatially homogeneous across a city, is not as well represented by a limited number of
monitoring stations.
Moreover, because some of the sensitive populations in the short-term mortality and
hospital admissions studies (i.e., the elderly and those with pre-existing disease) may spend
even more time indoors than the general population, the extent to which outdoor fluctuations
are found to affect indoor and personal exposures is of particular importance. Examination
of indoor and personal exposures calculated on a group level provide equivocal results.
Correlations are often poor because they mainly reflect variation between subjects (Janssen et
al., 1995, CD, Chapter 7). However, as discussed in Chapter IV and the CD, studies of
serial correlations are more relevant in determining how well personal exposure can be
represented by a monitoring station for short-term exposure studies. At least two exposure
studies that used serial correlations (Janssen et al., 1995; Lioy et al., 1990) noted good serial
correlations between outdoor PMJO and personal exposures (e.g., R2 of 0.4 to 0.53 for
children), and even better serial correlations for outdoor and personal exposure for PM25
(e.g.,R2 of 0.74 for children) (Janssen et al., 1995). The strength of this correspondence
between outdoor concentrations and personal exposure levels on a day-to-day basis reduces,
but does not completely eliminate concerns about the use of outdoor monitors in the short-
term studies.
Given the potential error in pollution and other covariate measurements, consideration
should be given to the effect of these errors on the association between exposure and
outcome. This measurement error can often bias the association toward the null. However,
the association can also be influenced by the relationship between paniculate matter and the
other covariates, which can bias the association in either direction. For example, Schwartz
and Morris (in press) address this issue in their study of cardiovascular hospital admissions
•
and PM, CO, and weather in Detroit, MI. In this case, the correlation between CO and the
weather variables and PM was small. In addition, the correlation between PM and weather
variables was also small. Such low correlations may imply that it is likely significant
portions of bias comes from the errors in measuring the pollutants, which would decrease the
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association between paniculate matter levels with hospital admissions. The authors point out,
however, that this does not mean that the estimated magnitude of the associations was
unbiased.
It is possible that the reported associations would be biased upward if there is a
significant positive correlation between the covariates. Such bias would result in an
increased chance of finding a false positive finding. Thus, when reviewing the potential for
exposure misclassification, it is important to consider potential correlation between the
covariates, since it can influence the effect estimate. Schwartz (1994b) reviewed the reported
correlations between PM, temperature, and SO2. The correlations between PM and
temperature were less than 0.5 in 9 of the 10 study areas. Similarly, the correlations with
SO2 in 5 of the 8 study areas were less than 0.4. Consistent with the implications of the
previous example (Schwartz and Morris, in press), these low correlations suggest that much
of the error results from the measurement of PM.
While the precise effect that measurement error will have on the paniculate
matter/health effect associations is unknown, it is possible to estimate the likely influences
measurement error will have on the association, and thereby exclude unlikely scenarios.
Given the good correlation between ambient monitors and personal exposure, these
observations suggest that the association is more likely to be biased downward.
Nevertheless, a comprehensive, formal treatment of exposure misclassification in paniculate
matter effects studies is an important research need.
4. Confounding in Short-term Studies
Potential confounders of the PM/health effects relationship are those independent risk
factors related to both PM concentrations and the health effect of interest. Inadequate control
for confounding can result in incorrect interpretations assuming the effect is a result of the
observed risk factor, when a third variable (the confounder) is really responsible. In short-
term exposure studies, major covariates associated with daily changes in health effects, such
as weather, season and other pollutants (e.g., SO^) correlated with PM need to be
considered. In contrast, as discussed in the next section, the long-term prospective cohort
studies and cross-sectional studies need to consider risk factors that may vary among
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communities (e.g., smoking levels). A number of methods are used by epidemiologists to
address or reduce confounding, with varying degrees of success. A summary of the major
issues relevant to recent PM studies is outlined below.
a. Weather
Weather is an important confounder in short-term PM studies because fluctuations in
weather are associated with both changes in PM levels and health effects observed in the
studies. The relationship between weather and mortality often follows a U-shaped curve with
increases in mortality in cold and hot weather conditions. PM levels can be high under
either temperature regime; some areas have peak levels in the summer (e.g., Los Angeles),
and some in the winter (e.g., Utah Valley). The independent effect of PM separate from
weather can be ascertained both by evaluating multiple studies conducted in areas with
varying weather and by assessing the methods individual studies use to adjust for weather.
Taken together, positive consistent associations between PM and mortality and morbidity
effects have been observed in dry and humid climates (e.g., Los Angeles versus
Birmingham), cold and warm climates (e.g., Toronto versus Birmingham) and areas where
PM is highest in the winter (e.g., Utah Valley, Minneapolis), and the summer (e.g.,
Birmingham), or are elevated in both seasons (e.g., Los Angeles) (Schwartz et al., 1994b).
On an individual study basis, investigators have used a variety of approaches to
separate the effects of PM and weather. For example, some studies have excluded a portion
of the extreme weather days, as defined by temperature and/or humidity, from the analysis
(Schwartz, 1994a; Schwartz and Morris (in press). Many investigators use statistical
methods to adjust for weather when modelling the PM and health effect relationship. In
several of these studies (Schwartz, 1993a, 1994a, 1994d, 1994e, 1994f) nonlinear functions
have been used that can reflect the complex relationship between weather and health effects
(e.g., the effect of temperature in Birmingham, Alabama (Schwartz, 1993a). In other
studies, linear and categorical variables were used (e.g., for very high temperature days) to
adjust for routine fluctuations in weather and extreme conditions (Kinney et al., 1995; Pope
et al., 1992). Finally, an examination of the sensitivity of the PM10/health effect relationship
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to varying degrees of control for weather has been examined (Schwartz (in press), Schwartz
et al., in press, Kinney et al., 1995). Several studies reported that the effects of weather had
on mortality were distinct but largely separate from the effects of PM in the areas studied;
elimination of all weather variables from the PM-mortality models did not substantially affect
the size of the observed associations between PM and mortality (Schwartz et al., in press;
Schwartz and Dockery, 1992a, 1992b). All the studies use some method to adjust for
weather, and report consistent, positive associations between PM and health effects.
The HEI analysis included a careful evaluation of the sensitivity of the mortality/TSP
association to specification of weather in their reanalysis of Philadelphia (Samet et al., 1995).
The investigators used a nonparametric surface to model the relationship between mortality
and temperature and dewpoint, and compared it to the linear terms used by Schwartz and
Dockery (1992a). They found association between mortality and TSP was relatively
insensitive to the specification of weather in the model.
t"
A number of investigators and commenters believe that the most recent analyses of
short-term PM and mortality have controlled adequately for weather (Moolgavkar et al.,
1995; Schwartz, 1994; Dockery and Pope, 1994). Recommendations have been made,
however, to examine further the use of synoptic classifications (Kalkstein, 1991) associated
with health stress as an approach to assessing weather as a confounder of PM effects.
Analyses of this kind have been recently completed for Utah Valley and are being submitted
for publication. The unpublished results are reported to be consistent with the above
assessment (Pope and Kalkstein, in press).
b. Confounding by Other Pollutants
One of the considerations in evaluating these studies is whether the health effects are
associated with air pollution in general, of which PM is a portion, or whether the health
effects are independently exerted by PM. Suggestive, but not conclusive, support for PM
effects comes from a comparison across multiple areas and studies. If PM is truly acting
independently, then a consistent association should be observed in a variety of locations of
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differing relative proportions of particles and potential gaseous pollution confounders. If
instead the observed PM effect results from confounding from another pollutant, the
associations with PM would be expected to be consistently high in areas with high
concentrations of the confounder, and consistently low in areas with lower concentrations of
the confounder. Figure V-2 shows the reported relative risk of particle effects and
associated levels of SO2, NO2, ozone, and CO for a number of study cities where such data
were readily available. The relative risks are those reported in each of the studies,
unadjusted for the other pollutants. The figure indicates that the association with PM
remains consistent through a wide range of concentrations of these potentially confounding
pollutants. Although further studies are needed in this area, the available body of data
show some associations for these other criteria pollutants, but the results are not as consistent
as for PM. While it is possible that different pollutants may serve to confound particles in
different areas2, it seems unlikely that the confounding would lead to such similar
associations and relative risk numbers for particles. Specific observations relating to the
potential for confounding from SO2, ozone, CO and NO2 are outlined below.
i. Sulfur Dioxide (SO2)
SO2, having been present at high concentrations with PM during some historical
episodes, especially in the well-documented wintertime smogs in London, has long been seen
as a prime candidate for potential confounding. Reanalyses of the London data (Schwartz
and Marcus, 1986) provided some support for the suggestion of Mazumdar et al., (1981) that
at lower SO2 values in London, mortality effects may be associated with PM alone. The
more recent studies, in particular short-term exposure mortality studies, have applied several
approaches to address SO2 confounding, including exclusion (studies in areas with low SO2
levels) and more direct means. Other pertinent information comes from SO2 and PM air
^ia this interpretation of the results, CO, for example, would lead to a false association with particles in
Utah Valley where SO2 was low, and SO2 would lead to a false particle signal in Philadelphia, where CO levels
were more modest. Such a serendipitous combination of variable confounding would make the more ubiquitous
pollutant, particles, appear to be consistently associated with the effect. In this event, at least two other
pollutants, or an unidentified substances) correlated with them, would be associated with mortality and other
effects.
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FIGURE V-2. RELATIONSHIP BETWEEN RELATIVE RISK OF MORTALITY ASSOCIATED WITH PM10 AND LEVELS OF SO2, CO, NO2,
AND OZONE.
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Data on SO* CO, NO2 and Oj are from the EPA Trends Report, except for annual averages of SO2 and NO2 in Kingston and St Louis, which are from Dockery et a! (1992). The detection limit is
used for cities reporting nondetects (Utah Valley (SO2), and Birmingham (NOj)).
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November 1995 V-47
quality relationships and studies of the penetration of SO2, alone and in combination with
particles, to the respiratory tract.
In areas where the potential for confounding from SO2 is relatively high, investigators
have adjusted for SO2 in the model (Ostro et al., 1995a; Toulomi et al., 1994; Schwartz and
Dockery, 1992a). These studies have also conducted sensitivity analysis of the association
between PM and health effects, by evaluating the association before and after adding SO2 to
the model. These analyses produced inconsistent results. Studies conducted in Santiago
Chile, Philadelphia, PA and Sao Paulo, Brazil, found the association between PM and
mortality remained positive and significant after the addition of SO2; whereas, the association
between SO2 and mortality became insignificant (Ostro et al., 1995; Schwartz 1992a; Saldiva
et al., 1994). A similar analysis found that after modeling both SO2 and PM, the association
with SO2 remained significant and positive (Touloumi et al., 1994). The estimates of
associations with health effects for both pollutants were reduced, however.
The SO2 confounding issue has been thoroughly explored in Philadelphia through
extensive analysis by several investigators, where SO2 and PM are highly correlated
(Schwartz, 1992a; Moolgavakar, 1995b; Li and Roth, 1990; Samet et al., 1995). In these
studies, investigators have been concerned about the potential for confounding from SO2 in
the observed TSP/mortality association. The original analysis by Schwartz and Dockery
evaluated the association between TSP and mortality in Philadelphia between 1973-1980
(1992a). They found the association between TSP and mortality remained significant after
adding SO2 to their model; whereas, the relationship between SO2 and mortality became
insignificant. Moolgavkar et al., (1995b) evaluated the association between TSP and
mortality in Philadelphia between 1973-1988. They evaluated the associations separately by
season because of potential confounding by season. Modeled individually with mortality,
•
both pollutants were found to be significantly associated with mortality in each season. In
models where TSP and SO2 where included simultaneously, they concluded that TSP was
positively associated with mortality in the summer and fall, and SO2 was positively associated
in all four seasons in Philadelphia.
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HEI evaluated both of these data sets (Samet et al., 1995). Although overall results
were similar to those of the original authors, the techniques used in this study revealed a
more complex, non-linear set of relationships among pollutants, season, and mortality. The
authors concluded that the Philadelphia data showed a relationship between air pollution and
mortality, but that it would be difficult to use the results of this study to attribute such effects
solely to particles. The combined pollutant mortality relationships are of some interest (See
Figure V-13 below in section V.E). The relationship between TSP and mortality indicates a
monotonically increasing response occurs only at particle levels above 100 /xg/m3 TSP. This
result is consistent with either a no observed effects level for TSP at 100 /zg/m3 or a reduced
association caused by a correlation with SO2 at lower concentrations. Conversely, SO2
displays a monotonically increasing concentration response function from the lowest levels to
about 40-60 ppb, where the curve flattens out. It is difficult to find a plausible mechanism
for such a concentration-response relationship for a single pollutant, suggesting confounding
is likely.
The original investigators' response to HEI suggest that TSP and SO2 are indicators of
a more appropriate risk factor, such as fine particles. The facts that fine particle sulfates and
SO2 share a common source in Philadelphia and that the coarse fraction of TSP is poorly
correlated with the fine fraction (Wilson et al., 1995) indicate that either or both pollutants
could reasonably serve as a surrogate for fine particles. In this event, SO2 itself might play
no direct role in causing effects, with only a fraction of TSP participating.
In evaluating the findings in Philadelphia, an important consideration is the evidence
on the mechanisms of toxicity of particles as compared to SO2 alone. Although quantitative
support is lacking, the discussion of controlled human and animal studies of particles indicate
that smaller particles can more effectively penetrate to the portions of the lung where
irritation or other interactions with lung tissues might produce significant effects. (See
section V.A above). Beyond reflex bronchoconstriction observed only at very high peak
levels, however, gas-phase SO2 is generally efficiently removed in the extrathoracic region in
humans (U.S. EPA, 1994c). It is hard to posit significant cardio-pulmonary effects for low
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concentrations of a substance that does not effectively reach the bronchial or alveolar
regions. However, one mechanism by which SO2 can be transported deeper into the lung is
absorption or dissolution onto the surfaces of atmospheric particles (U.S. EPA, 1982b). In
this case, the complex HEI results might be reflecting varying atmospheric interactions of the
two pollutants, rather than a direct SO2 effect.
Given the difficulty in ascribing effects to a single pollutant in Philadelphia, or similar
cities where elevated particles are associated with SO2, confounding by SO2 can be addressed
by exclusion, i.e. by assessing the PM/mortality relationship in areas with low levels of SO2.
Dockery et ah, (1993) found no association between SO2 and mortality in Kingston and St.
Louis, areas with considerably lower SO2 levels (Figure V-2a). As discussed above,
consistent significant associations between particle level and mortality are found in cities of
differing SO2 levels (Figure V.2a). The figure also shows the relative risk of mortality
associated with PM10 remains relatively unchanged in areas of low SO2 versus high SO2,
further supporting the robustness of the association between PM10 and mortality. While
consistent associations between PM and health effects are observed across the different
studies, the reported association between health effects and SO2 can vary widely. In
Steubenville, the association between SO2 and mortality was ten-fold greater than in
Philadelphia (i.e., coefficients of 0.0104 versus 0.00132 per ppb) (Schwartz and Dockery,
19992a,b) although the two areas have comparable SO2 levels.
There are studies in a few cities where SO2 and PM are highly correlated and it is
more difficult to ascribe the observed mortality effects to a single pollutant (e.g.,
Philadelphia). In such cases, consideration of the observed relationships and relevant
information on air quality, dosimetry, and mechanisms suggest that there is not an
independent effect of SO2 that does not involve some particle fractions. Moreover, given the
number of studies using different methods to correct for potential confounding in areas of
high and low SO2 that find an association between PM and mortality, it is unlikely that SO2
is responsible for all of the observed associations between PM and mortality. Similarly,
when the more severe morbidity endpoints such as respiratory-related hospital admissions are
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considered, the presence or absence of SO2 is also seen to have little effect on observed PM
associations (see Table V-ll, Schwartz, 1995a).
ii. Ozone
Increased ozone concentrations in the summer or ozone season is a potential
confounder in areas with concurrent high PM levels, (e.g., large regions of eastern North
America and Los Angeles). In areas where ozone peaks often occur in the same time of year
as high PM concentration, covariate adjustment has often been used to try to distinguish
effects from other pollutants. A number of studies using such methods have found PM to be
a stronger predictor of mortality than ozone (Dockery et al., 1992; Saldiva et al., 1995;
Kinney et al., 1995; Ostro et al., 1995). Adjusting for the presence of ozone did not affect
the associations with PM and mortality. For example, in Los Angeles, which has the highest
concentrations of ozone studied (Figure V-2), the investigators found no significant
association between ozone and mortality in models that included PM (Kinney, 1995). In
Santiago, a negative correlation exists between ozone and PM, and a positive association was
not observed between ozone and mortality across a full year even without PM in the model,
despite summertime values of ozone twice the U.S. standard (Ostro et al., 1995). Finally, in
Utah Valley, ozone and PM were also negatively correlated, resulting in a strengthened PM
effect being observed upon inclusion of ozone as a covariate (Pope et al., 1995, Table V-3).
As discussed above, Figure V-2d shows the relative risk for mortality from exposure
to PM by the 2nd hour maximum ozone value in each of the areas (exception of St. Louis,
where the value is the maximum daily average). The relative risk remains relatively constant
across the studied areas. Additionally, in some locations the potential for ozone to confound
the effects caused by PM is minimized by the low concentrations observed during seasons
which show a robust PM effect. Examples include Utah Valley and Santa Clara, where
ozone levels are minimal in the winter when the PM levels are high (Pope et al., 1992;
Fairley, 1990). The discussion above of confounding by weather notes a number of cities
with cooler climates, where particles are associated with mortality, which would have low
ozone levels.
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There is a higher potential for ozone confounding for the risk of respiratory-related
morbidity, because multiple studies have demonstrated apparent separable associations
between respiratory effects and PM and ozone concentrations. The respiratory-related
hospital admission studies often find ozone and PM are each singularly associated with
respiratory-related admissions (Schwartz, 1994d; Schwartz (in press); Burnett et al., 1994).
Table V-ll shows the relative risk associated with a 50 ug/m3 increase in PM!0 and hospital
admissions before and after inclusion of ozone in the model in New Haven, CT and Tacoma,
WA (Schwartz, in press). When both pollutants are modeled together, the association
between PM and respiratory-related admissions in general remains relatively unchanged,
indicating a separable effect independent of ozone. Potential for ozone confounding for
cardiac-related hospital admissions appears to be much less. Two studies have reported that
PM is associated with cardiac hospital admissions but ozone is not (Burnette et al., 1995;
Schwartz and Morris, in press).
iii. Carbon Monoxide (CO)
The lethality of high concentrations of CO is well documented; as such, it must be
considered as a potential confounder in community studies (U.S. EPA, 1991). Three of the
short-term PM exposure studies examined the effect of CO on the PM/mortality relationship.
A study in Athens found a significant association between mortality and CO and PM when
each pollutant was considered separately (Touloumi et al., 1994). When considered
together, only PM remained significantly positively associated with mortality. However,
there was a high correlation between CO and PM. Similarly in Los Angeles, where CO and
PM were also correlated, positive associations between each pollutant and mortality were
reported when both were evaluated simultaneously (Kinney et al., 1995). However, in
Chicago, insignificant associations were reported between CO and mortality (Ito et al.,
1995). The results from these studies are inconsistent. Because of the nature of urban
sources of CO as well as indoor sources, exposure misclassification may introduce significant
problems. In addition, while cardiovascular effects are plausibly linked to CO, controlled
studies do not suggest CO is a respiratory irritant (U.S. EPA, 1991). It is therefore unlikely
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to confound studies reporting respiratory related mortality, hospital admissions, or
aggravation of conditions such as asthma, all of which are linked to PM.
The potential relationship of CO and PM to cardiovascular effects was examined in
Schwartz and Morris's study (in press) of hospital admissions for cardiovascular diseases in
Detroit. They found an association between CO and PM and ischemic heart disease and
congestive heart failure admissions when evaluating each pollutant separately. When
evaluated together, CO was no longer associated with ischemic heart disease admissions, but
the association with admissions for congestive heart failure for both pollutants remained
relatively unchanged, suggesting each pollutant had a separable, independent association with
congestive heart failure.
iv. Nitrogen Dioxide (NO2)
By comparison, fewer of the mortality studies have directly assessed NO2 as a
potential confounder of PM10 effects. Several such studies have reported high correlations
between NO2 and PM in Los Angeles, CA; Toronto, Canada; and Santiago, Chile (Kinney,
1991, Ostro, 1995, Ozkaynak, 1994). Mixed results were reported concerning the
association between NO2 and mortality. Kinney and Ozkaynak (1991) found a statistically
significant relationship with NO2 and mortality in Los Angeles, but reported that these results
were interchangeable with CO and PM, since the correlations were so high between these
pollutants. In Los Angeles and some other Western U.S. cities, nitrogen oxide emissions
are themselves a major source of fine particles and nitric acid. The Santiago study found,
however, that NO2 was not associated with mortality when included in the model of PM and
mortality (Ostro et al., 1995. Furthermore, the association between PM and mortality
remained relatively unchanged after addition of NO2 to the model. Similar results were
found in the Sao Paulo study, where NO2 was not associated with mortality in adults after
including PM10 in the model (Saldiva et al., 1995). All these studies were conducted in areas
of relatively high NO2 levels; Santiago had the lowest mean level of 0.0556 ppm. A study in
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St. Louis, with a lower mean level of 0.02 ppm, found no significant association between
mortality and NO2 (Dockery et al., 1992).
While the association between NO2 and health effects in these studies is inconclusive,
the association between PM and health effects remains positive and consistent, both across
study areas with varying levels of NO2 (Figure V-2c) and after controlling for NO2 in the
model (Ostro et al., 1995; Saldiva et al., 1995; Schwartz et al., 1994).
c. Summary of Short-Term Confounders
Evaluated individually, each study has potential confounding problems. Concerns
continue relating to treatment of weather, other pollutants, and particularly, measurement
errors and exposure misclassification. However, there are over 50 studies finding positive,
significant associations between short-term PM levels and mortality and morbidity endpoints.
Many of these studies have been conducted in areas across the U.S. and Canada, where
meteorological and pollution patterns vary distinctly. Yet, the studies find a consistent,
positive association between PM and mortality and morbidity effects. The breadth of these
studies and insights drawn from air quality and controlled effects studies suggest that it is
unlikely that the PM effect can be entirely attributed to one or more of the known potential
confounders. Moreover, although the available evidence can not be conclusive, it also
seems unlikely that the effect is due to some unknown non-particulate confounder.
5. Confounding in Long-term Exposure Studies
In the long-term studies, differences in health effects are evaluated across
communities with differing levels of pollution. Unlike the short-term exposure studies,
which must consider confounders that fluctuate temporally with PM levels, these studies need
to consider confounders that may vary among communities and that are important risk factors
for the health effect of interest. The studies evaluate a range of health effects from mortality
to morbidity endpoints, but mostly focus on respiratory and cardiovascular related endpoints.
The recent cohort studies represent a substantial advance in the study of the effects of long-
term exposure to air pollutants, because individual information on potential confounders such
as age, sex, smoking habits, education, occupation, and other risk factors can be taken into
account. Several specific risk factors are discussed below:
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1) Smoking represents the largest potential confounder since it is highly associated with
the same effects observed with PM. Smoking has either been controlled for by
adjusting for the presence of smoking and pack-years smoked in the analysis, or by
exclusion of smokers from the analysis. Increased risk of mortality is seen after
adjusting for smoking. In addition, associations between mortality and morbidity
effects and PM continue to be observed when the analysis is restricted to never
smokers (Pope et al., 1995; Dockery et al., 1993) or involve only non-smokers
(Abbey etal., 1991-5).
2) Similar to smoking, individuals with occupational exposure to PM (e.g., dust, gases,
fumes, asbestos, chemical acid solvents, coal or stove dust) appear to be at increased
risk from particle effects ((Dockery et al., 1993; Abbey et al., 1991, 1995), although
the relationship continues to hold after adjustment for occupational exposures
(Dockery et al., 1993; Pope et al., 1995). Pope et al. (1995) also found that once the
analysis adjusted for cigarette smoking, adjustments for occupational exposure made
little difference in the observed PM-mortality associations.
3) Weather is a potential confounder in short-term exposure studies, because short-term
fluctuations in weather are associated with health effects. Since long-term exposure
studies evaluate changes in health effects over longer periods of time, short-term
variations in weather are less a concern in these studies. However, if there is a
difference in total mortality over the year due to different cumulative impacts of
weather and season in differing locations, this could lead to some potential
confounding. Pope et al. (1995) found that daily high, low, or mean temperature was
not correlated with PM2 5 concentrations across the fifty cities he studied, and that
inclusion of indicator variables for generally "hot" and "cold" cities did not
substantially affect the paniculate matter/mortality associations.
4) The possibility of confounding by other potential confounders needs to be assessed in
relationship to the controls that were used. For instance, individual controls on body-
mass index and education would serve as substantial controls on the most relevant diet
and lifestyle factors.
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In regard to residual confounding, those studies using a larger number of cities
or locations would be expected to provide better estimates of effects, since the
chances that a potential confounder would be substantially associated along the same
gradient as the pollutant in question should be expected to decrease as the number of
additional areas and distinctive locations increases.
5) With regard to copollutants, mortality effects associated with long-term exposures to
air pollutants were more strongly associated with the levels of inhalable, fine, or
sulfate particles than with the levels of sulfur dioxide or nitrogen dioxide (Dockery et
al., 1993). In addition, no apparent relationship with long-term ozone concentrations
was observed, although the small differences in ozone levels among the cities limited
the power to detect ozone-health effects associations (Dockery et al., 1993). The
Seventh Day Adventist study found that both the development and aggravation of
chronic respiratory disease symptoms was associated with long-term exposures to
several indicators of particles (TSP and estimated PM10 and PM2.5) (Abbey et al.,
1995b). In contrast, long-term exposures to sulfur dioxide or nitrogen dioxide did not
have effects on chronic respiratory disease symptoms, while ozone was associated
with aggravation of asthma symptoms, but not the development of aggravation of
chronic bronchitis (Euler et al., 1988; Abbey et al., 1993, 1995). The lack of
independent effects for copollutants at the levels observed in these long-term studies
indicate that these copollutants are not likely to be confounding the effects observed
between particles and mortality and morbidity.
E. Concentration-Response Relationships
This section presents a staff assessment of quantitative information on concentration-
response relationships between health effects and ambient PM. As discussed below for short-
and long-term studies, the staff has focused on selected individual studies to gain insight, to
the degree possible, from the available concentration-response information as to where a
clear and consistent increase in risk may be discerned. This assessment is intended to
provide information useful in deriving appropriate ranges of concentrations for consideration
in selecting ambient air quality standard levels. In so doing, the staff does not intend to
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imply that such an assessment can or should be used to attempt to identify a threshold of
effects below which there is no increased risk. Such population thresholds may not exist
within the range of ambient PM concentrations, and, as previously discussed,
epidemiological studies are limited in their ability to discern such thresholds even if they do
exist.
Further, the staff recognizes that the inherent uncertainties in each individual study,
such as those associated with specification of relevant exposures and potential confounding by
other environmental and/or personal variables, substantially limit the conclusions that can
appropriately be drawn from any one study. Thus, in this assessment, the staffs interest is
ultimately on the coherence of results from all the studies rather than solely on each study
considered independently. This quantitative assessment of concentration-response
relationships is considered in context with the entire body of health effects and air quality
evidence in identifying a quantitative basis for drawing conclusions and recommendations
about appropriate ranges of levels for consideration in setting PM standards, as presented in
Chapter VI.
1. Criteria for Assessment
The epidemiological studies of short- and long-term exposures to PM are most
straightforwardly interpreted as indicating whether a general, global association exists
between health effects and the varying concentrations of particulate concentrations observed
in the studies. However, to gain additional insight useful in assessing policy alternatives for
standard setting, staff has looked to several types of information from the studies in assessing
concentration-response relationships between exposures to PM and health effects. As
discussed below, such information includes the range of PM concentrations over which the
general relationship between particles and health effects are observed, the central tendency of
that range, and the pattern and consistency of increases in risk observed within the range of
PM concentrations.
1) Information on the range of concentrations observed in the study helps bound
the particle concentrations with which there is a possible association with the
observed health effects. However, it is often not possible to make clear
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inferences as to whether the observed risk of health effects is uniformly
associated with increasing particle concentrations, or is more strongly
associated with concentrations of PM above a certain level.
2) Information on the central tendency (median or mean) of the range can provide
an indication where the observed association between particles and health
effects has the least statistical uncertainty, although this value may not reflect a
point at which risk is clearly elevated, especially if the relationship between
health effects and particle concentrations is substantially non-linear.
3) The most useful information for the assessment of concentration-response is
provided by presentations of the observed relationships between risk and
particle concentrations for various segments of the overall range. Such
presentations typically take the form of dividing the data into smaller
percentile ranges (such as quartiles or quintiles) and reporting the associated
risk for each division of the range, or nonparametric smoothed curves that
apply weighted averages of the effects around a particular concentration. Both
of these approaches allow the existence of substantial nonlinearities in the
observed relationship to be assessed, and have been used by some investigators
to identify concentrations associated with elevated health risk (e.g., Samet et
al., 1995; Schwartz, 1993a).
However, for reasons discussed in the CD, the staff recognizes that
these approaches have inherent limitations and need to be interpreted with
caution. For example, observed differences in risk across discrete or
continuous segments of the concentration range may be more reflective of
relatively smaller numbers of observations in one or more of the segments than
of real differences in observed risk.
The specific studies considered in this assessment were selected on the basis of the evaluation
of the quality of the studies presented in the CD, findings of significant associations between
PM exposures and health effects, and the availability in the study of information that
provides insight into the pattern of concentration-response within the range of the study.
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2. Concentration-Response Relationships from Short-Term Studies
The selected studies listed in Table V-19, which report associations between short-
term (24-hour average) exposure to PM and health effects, provide quantitative
concentration-response information showing the pattern of increased risk within the range
over which increased relative risk is reported. Included in this list of selected studies are
studies that report associations between PM, as measured by PMIO, PM2.S, sulfates, and TSP,
and mortality, hospital admissions, and respiratory symptoms. These selected studies are
part of the much larger number of studies that have been evaluated in the CD and
summarized in section V.C. They are discussed below with regard to the nature of the
concentration-response relationships observed in the studies and the insights that can be
gained with regard to the PM concentrations where clear and consistent increases in risk can
be discerned.
a. PM,n/PM-, 5 Studies
The most recent investigation of the effects of daily PMi0 and PM2 5 concentrations on
mortality examined the associations between several indicators of particles and daily mortality
in six cities (Schwartz et al., in press). As discussed above in section V.C. and summarized
in Table V-6, PM2 5 showed the strongest and most consistent association with mortality,
coarse fraction particles did not show a statistically significant3 association, and the
statistically significant association observed between PMIO and mortality has been interpreted
by the authors as resulting primarily from fine particles (Schwartz et al., in press). Positive
associations between PM? s and mortality were observed for each of the six cities, and this
association was statistically significant for the three cities experiencing the highest daily
mortality in the study. Although concentration-response curves were not presented for each
city, the authors reported an additional analysis that excluded all PM2 5 concentrations of 30
/zg/m3 and above in all the cities (approximately the top 10% of values). The association
remained statistically significant when concentrations of 30 /ig/m3 PM2 5 and above were
excluded.
Statistical significance is reported at the 95% level throughout this section unless otherwise noted.
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V-58a
TABLE V-19. CONCENTRATION-RESPONSE INFORMATION
FROM SELECTED SHORT-TERM EXPOSURE STUDIES
Study
Mean or Median
Measured
Concentration
(/tg/m3 of
measured
pollutant)
Concentration
Range
(/tg/m3 of
measured
pollutant)
Minimum Clear
Increased Risk
Level
Gig/m1 of measured
pollutant)
Mortality - 6 Cities
Schwartz et al., in press: PM-2.5
PM-10
Mortality — St. Louis
Dockery et al., 1992: PM-10
PM-2.5
Sametetal., 1995: PM-10
PM-2.5
Mortality - Utah Valley
Pope etal., 1992: PM-10
Sametetal., 1995 PM-10
Mortality — Birmingham
Schwartz, 1993a,1994g: PM-10
Sametetal., 1995 PM-10
Hospital Admissions — Birmingham
Schwartz etal., 1994e: PM-10
Hospital Admissions — Detroit
Schwartz, 1994d: PM-10
Hospital Admissions — Detroit
Schwartz and Morris, in press PM-10
Respiratory Symptoms — 6 Cities
Schwartz et a!., 1994: PM-10
PM-2.5
Respiratory Symptoms — Utah Valley
Pope and Dockery, 1992: PM-10
18
25 (median)
28
18
H
ft
47
48
M
45
48
48
30
18 (median)
76 (mean)
<4 - >44
8-69
1-97
1-75
up to 297
M
up to 163
a
19-77
22-82
22-82
<13 - 117
<7-86
up to 251
<30
33
. 44
46
50
60
53
20-45
52
37
23
^S^C^J
22 - 338
4-8
jC^fS^i
100
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External Review Draft Do Not Quote or Cite
November 1995 V-59
These results from Schwartz et al. (in press) are generally consistent with the earlier
findings of Dockery et al. (1992). Dockery et al. (1992) reported an earlier analysis of one
of six cities, St. Louis, that included only one-fifth of the observations for this location that
were later included in the Schwartz et al. (in press) study. Positive associations were
reported between PM2 5 and mortality that reached marginal statistical significance, but the
strongest associations over the study period were reported between PM,0 and mortality.
Concentration-response information for PM,0 was presented in the form of a quintile plot
showing the association between daily particle concentrations and mortality (Figure V-34).
Examination of this information suggests that risk may not increase in a clear and consistent
pattern until the fourth quintile, with a mean concentration of approximately 33 /xg/m3 PM10.
A reanalysis of these data (Samet et al., 1995), which associated quintiles of PM10 with
mortality in a slightly different manner, reported that risk was not elevated until perhaps the
highest quintile (Table 22 in Samet et al., 1995), with a mean concentration of approximately
44 fjig/m3 PM10 (as reported in the original study). A positive but marginally significant
association was also reported with PM25, although no PM2.5 concentration-response
relationship was presented.
Pope et al. (1992) reported an association between PMIO and mortality in the Utah
Valley, as shown in Figure V-4. Although generally linear, risk does not appear to clearly
and consistently increase until the third quintile, with a mean concentration of about 46
/ig/m3 PM10. Reanalysis of the Utah Valley data by Samet et al., (1995) found no pattern of
increased risk until the fourth quintile, with a mean concentration of approximately 50 jig/m3
PM10 (Table 28 in Samet et al., 1995). Thus, while the two analyses differ somewhat
concerning risk at the lowest concentrations, where uncertainty would be expected to be
greatest, the analyses appear to agree well concerning the PM10 concentrations, 46-50
associated with a clear and consistent increase in risk.
An association between PM,0 and mortality was also reported for Birmingham
(Schwartz et al., 1993a). The concentration-response relationship was reported as a
4Figures V-3 through V-18 in this section include annotations as presented in the original references.
-------
V-59a
FIGURE V-3.
RELATIONSHIP BETWEEN RELATIVE RISK OF MORTALITY
AND PM-10 IN ST. LOUIS AND EASTERN TENNESSEE
(DOCKERY ET AL., 1992)
1.10
1.05
1.00
0.95
10
-J t-
ZO
30
PMiO
40
50
Relative risk of mortality of quinliie of PM ,0 concentrations on the pro tous day. separately
for St. Louts (A,) and eastern Tennessee (V). The lowest quimile in each area is taken as the reference
category. Straight line is the weighted mean regression.
FIGURE V-4.
RELATIONSHIP BETWEEN RELATIVE RISK OF DEATH AND
PM-10 IN THE UTAH VALLEY (POPE ET AL., 1992)
v
Q
o
«
•-«
o
Pi
||
1.1
£ 1.0
0.9
20 40 60 80
PMIO Concentration
100
Relative risk of death, by quiniile of PM,. concentration.
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External Review Draft rjo ffot Quote or Cite
November 1995 V-60
nonparametrically smoothed plot, with a presentation in a subsequent publication showing the
95% confidence limits (Schwartz, 1994g), as shown in Figure V-5. This plot shows an
increase in relative risk over the range of approximately 20-40 /*g/m3 PM,0, with a flattening
in the concentration-response relationship between approximately 40-60 /*g/m3. Risk
appears to increase in a clear and consistent pattern at concentrations of 60 /*g/m3 and above.
A reanalysis of this study which presented information in terms of quartiles found risk to be
elevated for the third and fourth quartiles (Table 31 in Samet et al., 1995), with the third
quartile having a mean concentration of approximately 53 /*g/m3 PM,0.
Three recent studies have reported concentration-response information for associations
between PM10 and respiratory hospital admissions for pneumonia and COPD, primarily in the
elderly. Schwartz (1994d) reported an association between PM10 and respiratory hospital
admissions for pneumonia and for COPD in Detroit. A quartile plot of pneumonia
admissions in the elderly, Figure V-6, appears to suggest that clear and consistent risk from
PM10 is associated with the third quartile, with a mean of approximately 52 /*g/m3. For
COPD admissions, which are less frequent than pneumonia admissions, the concentration-
response relationship is less consistent (Figure V-7). Increased risk is apparent at the second
quartile, with a mean of approximately 34 /*g/m3 PM,0, decreases but is still elevated for the
third quartile (52 /ig/m3 PM10), and clearly increases above the third quartile. Thus, for
respiratory hospital admission in Detroit, risk appears to clearly and consistently increase at
52 /xg/m3 PM10 and above, with a likelihood of elevated risk occurring at concentrations
below that point, especially for COPD admissions.
Schwartz (1994e) reported associations between PM10 and respiratory hospital
admissions in Birmingham. Nonparametric smoothed curves of pneumonia admissions in the
elderly (Figure V-8) and COPD admissions (Figure 6 in Schwartz, 1994e) appear to show
increasing risk throughout the range of the concentration-response relationship. When
nonlinear terms were compared with a linear term for PM10, no statistical significant
improvement in model fit was seen (Schwartz, 1995e). Taking into account the lack of
nonh'nearities, staff considers that a clear and consistent increase in risk can most
appropriately be judged as occurring within the lower range of concentrations from 45
-------
V-60a
FIGURE V-5.
RELATIONSHIP BETWEEN RELATIVE RISK OF DEATH AND
PM-10 IN BIRMINGHAM (SCHWARTZ, 1993a)
ra O
41 •
O
«. o
o: —
M 40 60 60 100 120 140
PM10 (mfcragraoisAneter cubed)
The smoothed plot of the relative risk of death versus nclO in Birmingham, Alabama,
after controlling for smoothed fractions of time, tempenmrc, and dew-point temperamre
(and day-of-week dummy variables) in a, generalized additive modeL Pointwise one-
standaid-enor mnfMnK^ intervals are also shown.
FIGURE V-6.
RELATIONSHff BETWEEN RELATIVE RISK OF PNEUMONIA
ADMISSION AMONG THE ELDERLY AND PM-10 IN DETROIT
(SCHWARTZ, 1994d)
c
o
1.08
106
c
o-
102
1.00
0.98
30
50 60 70 80 90
The relative risk otpneumoniaaJmi&sioos in the ekteriy in Deooit.
Michigan, by quartle of PM« is shown. The pW is after adjusting tor all
other covariates. A stepped response with increasing dose is evident, with
no evidence for a threshold.
-------
V-60b
FIGURE V-7.
RELATIONSHIP BETWEEN RELATIVE RISK OF COPD
ADMISSIONS AMONG THE EU)ERLY AND PM 10 BV
DETROIT (SCHWARTZ, 1994d)
1.15
c
I 1.11
£
1.07
O
o
c
- 1.03
0£
o
• 0.99
o
0.95
20 30 -10 50 60 70 80
The relative risk of COPO admissions in the eWerty in Detroit,
Michigan, by quartfle at PM* is shown. Tha plot is after adjusting for all
other covariaies. A steoped response with increasing dose is evident, with
no evidence for a threshold.
FIGURE V-8.
RELATIONSHIP BETWEEN RELATIVE RISK OF PNEUMONIA
ADMISSIONS AMONG THE ELDERLY AND PM-10 IN
BIRMINGHAM (SCHWARTZ, 1994e)
Nonparametric smooth of counts of pneu-
monia admissions (persons per day) versus «h« con-
centration o( airborne paniculate matter with an aero-
dtametef o< S10 ^ (PMJ after controttnfl by
regression kx tong-««rm temporal jPf^1?,*^
weather. The oointwise 95 perwrrt confidence fcmrts of
the smooth curve are also shown.
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External Review Draft Do Not Quote or Cite
November 1995 V-61
pcg/m3, the median concentration, down to 20 /*g/m3, where the lower 95% confidence
interval for this nonparametric smoothed curve includes no increase in risk. Additional
uncertainty in the relationship may result from the lack of inclusion of ozone as a covariate,
although ozone was not found to have a statistically significant association with hospital
admissions in Birmingham (Schwartz, 1994e). The nonparametric smoothed curve for
COPD admissions is similar but steeper to that for pneumonia admissions, although COPD
admissions are a more infrequent outcome.
Cardiac hospital admissions have also been associated with PM,0 for the elderly in
Detroit (Schwartz and Morris, in press). Figure V-9 shows a quartile plot of the relationship
between PM10 and hospital admissions for ischemic heart disease, controlling for carbon
monoxide and other covariates. Increased risk is apparent at the second quintile, with a
mean of approximately 37 ^ig/m3 PM10.
Schwartz et al. (1994) reported associations for PM10 and PM2 5 with respiratory
symptoms in children, including cough and lower respiratory symptoms, across six cities.
The nonparametric smoothed plot presented in the study for the PM10 relationship with cough
is shown in Figure V-10. Cough incidence increases throughout the range, and the slope of
increase appears to be diminished at the lowest PM10 concentrations. However, the overall
relationships for cough and for lower respiratory symptoms were tested for deviations from
linearity, which was not found to be significant (Schwartz:et al., 1994), implying substantial
nonlinearities were not present in the relationship between PM,0 and cough and lower
respiratory symptoms. Interpretation of this plot is made more difficult by the absence of
confidence intervals. Staff judges that clear and consistent risk can most appropriately be
characterized as occurring at or below the median PM,0 concentration of 30 /xg/m3, where
statistical uncertainty would be expected to be the least. With regard to lower respiratory
symptoms, elevated risk is observed across almost the entire range of PM,0 concentrations
(Figure 3 in Schwartz et al., 1994), but caution in interpretation is appropriate given the
relatively small number of observations for this health endpoint.
Pope and Dockery (1992) found PM10 to be associated with upper respiratory
symptoms, lower respiratory symptoms, and cough in Utah Valley during a winter of
-------
V-61a
FIGURE V-9.
RELATIONSHIP BETWEEN ISCHEMIC HEART DISEASE
ADMISSIONS AMONG THE ELDERLY AND PM-10
(SCHWARTZ AND MORRIS, IN PRESS)
46
45
ri
•O
-------
V-61b
FIGURE V-10.
RELATIONSHIP BETWEEN THE ODDS OF COUGH
INCIDENCE VERSUS PM-10 CONCENTRATION FROM THE
SIX CITY STUDY (SCHWARTZ ET AL., 1994)
f
o
o
«- T
o ,_•
tn
•
a
Q)
cr
20 40
PM10 (ug/m3)
60
Relative odds of incidence of coughing smoothed against 3-d
mean PM,. (ng/m1), controOing tor temperature, city, day o» the week, and
ozone concentration.
FIGURE V-ll.
RELATIONSHIP BETWEEN PERCENT OF CHILDREN
REPORTING SYMPTOMS AND PM-10 IN UTAH VALLEY
(POPE AND DOCKERY, 1992)
MEAN % REPORTING RESPIRATORY SYMPTOMS FOR QUART1LES
OF PM« LEVELS*
Reporting
No. of PMlt
Symptomatic
Asymptomatic
Quartile Days Meant Upper Lower Cough Upper Lower Cough
1
2
3
4
25
25
25
25
25
55
69
141
21
27
27
33
11
13
16
20
12
16
18
24
17
16
15
16
10
11
10
14
8
11
11
16
• Tha quanta* wan faasad on feday moving avwagad Pl^ Wv*. «Mch canffad ftora13 to 208 w^i". wtth the l«t. 2nd. and
3rd quartlte* equal to 39, 67, end 107 iig/m1. <««p«ctlv«ly.
.
t Thte «qu*b th« m»«n PM^ lev«< for the 25 days Jo *ad) quartto.
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November 1995 V-62
relatively high particle concentrations. The associations were stronger for children identified
as having a history of mild respiratory symptoms. Figure V-l 1 shows the percent incidence
of health effects by quartile of PM,0. Risk for all three respiratory symptom categories
increases consistently for children with symptomatic histories at the second quartile of PMi0,
which averaged 55 jtg/m3, with risk not increasing in asymptomatic children until the fourth
quartile.
b. Sulfate Studies-
Sulfates and acid aerosols have been reported in a number of studies to be associated
with respiratory hospital admissions, as summarized in Table V-9. Two studies particularly
useful for assessing quantitative concentration-response relationships have reported an
association between sulfates and hospital admissions for all ages while simultaneously
controlling for ozone (Burnette et al., 1994, 1995). In these studies, sulfates were reported
to be associated with respiratory and cardiac hospital admissions in 168 hospitals across
Ontario. Figure V-12 shows a decile plot of daily respiratory admissions and sulfate level
from these studies. By inspection, this plot suggests that the observed risk for respiratory
hospital admissions becomes more clearly and consistently elevated within a concentration
range of 4-8 /tg/m3 as sulfate. From a separate analysis, the daily average hospital admission
rates for respiratory and cardiac illness, associated with the third quartile of sulfate
concentrations (averaging 4.1 fig/m3) were reported to be significantly different from the
corresponding rate for the lower 50% of concentrations (averaging 1.5 /xg/m3) (Burnette et
al., 1995).
c. TSP Studies
A number of studies have been conducted examining the relationship between TSP
and various health endpoints, especially mortality. In general, because of the inclusion of
non-inhalable particles within the TSP indicator, the CD .concludes that TSP is a less reliable
indicator for evaluating health effects of PM. However^ because of the substantial amount of
daily air quality data for TSP and other pollutants available in Philadelphia, several
investigators have extensively reanalyzed this database with respect to associations between
air pollution and premature mortality in Philadelphia (Samet et al., 1995, Moolgavkar et al.,
-------
V-62a
FIGURE V-12.
RELATIONSHIP BETWEEN RESPIRATORY HOSPITAL
ADMISSIONS AND SULFATE CONCENTRATIONS IN
ONTARIO (BURNETTE ET AL., 1994)
O 112
no
o 108
OT 106
102
0 2 4 6 B 10 12 M 16 l« 20
Daily Average Sufphote Level (yg/m*), lagged One day
Avenge number of adjusted respiratory admissions among all 168 hospitals by decile of the daily average sulfate level
) lagged I day'
FIGURE V-13. RELATIONSHIP BETWEEN RELATIVE MORTALITY AND TSP
OR SO2 IN PHILADELPHIA (SAMET ET AL., 1995)
PMtdelpfcta Mortally. Tottl
PMadaipMa Mortafity. Total
I-
e.
'I'
» WO 1«9 J[ 0 8 40 « « «w
TSP «yq
Plots of cdimatad BonparanMtric •Sacti of TSP and SO,
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External Review Draft £)o /yo/ Quote or Cite
November 1995 V-63
1995, Schwartz and Dockery, 1992; Dockery, Schwartz and Pope, 1995; Li and Roth,
1990).
Samet et al. (1995) reanalyzed the Philadelphia dataset used by Schwartz and Dockery
(1992), covering the years of 1973 -1980, to examine in detail the relationship between TSP
and other covariates such as weather, season, time trend variables, and SO2 in explaining
variations in daily mortality. The authors largely confirm the findings of Schwartz and
Dockery (1992) concerning the association between TSP and daily mortality in Philadelphia,
with important differences concerning the effects of season and the relative effects of TSP
and SO2. In terms of concentration-response relationships, Samet et al. (1995) find some
evidence that a nonlinear, nonadditive surface of TSP and SO2 better predicts mortality than
the linear additive models used by the original investigators. When TSP and SO2 were
considered simultaneously in an additive model but allowed to vary nonlinearly, TSP was
associated with log-relative mortality most clearly at concentrations of 100 /ig/m3 and above,
while SO2 exhibited a roughly linear increase in the log-relative mortality rate until about 40
parts per billion, after which there was little change (Figure V-13). The authors themselves
do not interpret the possible significance of an association with SO2 that is restricted to the
lowest concentrations.
Drawing from the discussion of confounding in section V.D., the staff believes it
would not be plausible to interpret these results as indicating an association between SO2
acting alone and mortality. Dockery et al. (1995) suggest that the most parsimonious
interpretation is that both pollutants are likely serving as surrogates for the real pollutant of
concern. They suggest fine particles are likely to be more closely associated with the
observed health effects. Given that TSP by definition includes particles too large to be
inhaled, and, thus, is clearly an imperfect surrogate for particles of interest for respiratory
effects, it would not be surprising that other indicators such as SO2, often associated at low
concentrations with fine particles, might be better associated than TSP with observed health
effects. Further, they suggest that if two variables are serving as proxies for a third, local
nonlinearities, apparent interactions, or both are likely to occur.
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November 1995 V-64
Samet et al. (1995) further examined the effects of simultaneously regressing TSP and
SO2, and found that both TSP and SO2 had independent effects, or, in models with more
extensive controls for long-term time trends, that TSP remained significant but SO2 did not
[the original findings of Schwartz and Dockery (1992)]. Furthermore, although graphs of
the concentration-response relationship for the later period, 1981-1988, are not provided,
Samet et al. (1995) report that the association between TSP and mortality is stronger over
this period than the association between SO2 and mortality. Based on the analyses and
interpretations discussed above, to the extent that TSP can serve as a surrogate for inhalable
or fine particles that may be associated with the observed mortality effects, analyses of TSP
in Philadelphia do not appear to suggest a clear and consistent increase in mortality risk until
concentrations of approximately 100 ^g/m3 TSP.
3. Concentration-Response Relationships from Long-Term Studies
Several studies reporting associations between long-term (annual average) exposure to
PM and health effects, listed in Table V-20, also provide quantitative concentration-response
information showing the pattern of increased risk within the range over which increased
relative risk is reported. Included in this list of selected studies are studies that report
associations between PM, as measured by PM25, PM15, and TSP, and mortality and
aggravation of chronic respiratory symptoms. These selected studies are part of the much
larger body of studies that have been evaluated in the CD and summarized in section V.C.
They are discussed below with regard to the nature of the concentration-response
relationships observed in the studies and the insights that can be gained with regard to the
PM concentrations where clear and consistent increases in risk can be discerned.
As discussed in section V.D., studies of long-term exposures are subject to different
types of confounders and employ different means of controlling for confounding than short-
term exposure studies. In addition, the evaluation of concentration-response relationships
•
specifically from studies of health effects due to long-term exposures is subject to additional
uncertainty related to specification of relevant exposures.
With regard to controlling for confounding variables in long-term studies, the recent
prospective cohort studies represent a substantial advance in study design in comparison with
-------
V-64a
TABLE V-20. CONCENTRATION-RESPONSE INFORMATION
FROM SELECTED LONG-TERM EXPOSURE STUDIES
Study
Concentration Range
(/ig/m3 of measured
pollutant)
Minimum Clear
Increased Risk Level
Oig/m3 of measured
pollutant)
^"^^^•-^^ss* *V >- - ^^^r^V^^tsSxv^-"*'*^ *-#^ ' ^^^^^^^^^^^^''^^^^^&:^^M^^:\
-.^""•x^3^ 1MUT "SjfjWliGfi ^ " ^ "f'»%\<*'s """"-yy "• ~~ * S f ' ^f^-f^f ffjfff v * "V1 ^ *• % -x \f -^jy^s f' ^s ^. s\, s\ j.
Mortality — 6 Cities
Dockery et al., 1993
Mortality - ACS 50 Cities
Pope et al., 1995
11 -30
9-33
15 - <30
>15
^^fM^ll^i^ i; " v, ^g-JC -^ *> ^ '^ " '>1'^^'" ^^'"^v^^^Cr^' '"X-fiT .c-^*'
-r%^M^^SM»Stufl[y<;V\ .^/* f>^ -< ** - -^ , ^ ^,- , ',, ,y^, .^ %
Bronchitis in Children — 6 Cities
Dockery et al., 1989: PM-15
PM-2.5
20-59
12-37
38
22'
TSP Study
Chronic Bronchitis — 53 Cities
Schwartz etal., 1993
48 - 130
75
'PM-2.5 concentration provided in the study for city (St. Louis), with minimum long-term concentration
showing clear and consistent risk (Figure V-16).
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External Review Draft Do Not Quote or Cite
November 1995 V-65
previous cross-sectional studies in that information about each subject's age, body-mass
index, lifestyle habits, etc., can be taken into account. This improvement is important since
these studies are not restricted to one area, but rather compare relative risks in terms of
measures of air quality from different cities. As a result, a number of risk factors that can
vary across locations are introduced by including subjects from different geographic areas,
with potentially different diets, exposures to other environmental variables, age distributions,
and other population characteristics. Studies that involve a large number of locations or
cities (e.g., Pope et al., 1995, Schwartz et al., 1993) or that assign individual exposure
estimates to each member of the cohort (Abbey et al., 1995a) may have a greater likelihood
of minimizing residual confounding from unaddressed variables.
With regard to uncertainties in specifying relevant exposures, questions arise as to the
significance and levels of air quality concentrations prior to the study period, and as to the
appropriateness of the averaging time used by the investigator. Given the decreasing patterns
of PM concentrations observed over this century, associating risk observed in a recent study
period solely with contemporaneous air quality could serve to magnify, on a /tg/m3 mass
basis, the apparent risk of current PM levels. This uncertainty is addressed in the CD in
terms of the potential implications of using longer historical periods of exposure in analyzing
long-term relative risks.
a. PM,_« Studies
The most significant recent studies concerning long-term effects of exposure to PM
are two prospective cohort studies that have directly examined the relationship between PM2 5
and mortality in cohorts of individuals across a number of U.S. cities. In a study of
mortality over a 14-16 year period involving 8,111 adults living in six U.S. cities, Dockery
et al. (1993) reported an association between the average PM2.5 concentrations in these cities
and mortality. Concentration-response information from this Harvard Six City study was
provided in the form of a plot of increased risk of death by city as a function of the annual
average PM2.5 concentration (Figure V-14). This plot shows the relationship between PM2.5
concentrations and differences in death rates across the cities among the cohorts after
controlling for confounders. The observed association is highly significant (p< 0.005), with
-------
V-65a
FIGURE V-14.
RELATIONSHIP BETWEEN MORTALITY RISK RATE RATIOS
AND PM-2.5 IN THE SIX CITY STUDY (DOCKERY ET AL.,
1993)
1.4 r
1.3
DC
to
15
1.1
1.0
W
H
10 15 20
Fine Partides
25
30
35
FIGURE V-15.
RELATIONSHIP BETWEEN ADJUSTED MORTALITY AND PM-
2.5 IN THE AMERICAN CANCER SOCDZTY STUDY (POPE ET
AL., 1995)
o 1000
o
o
o
o;
JE
o
£ 800
1 • < 1 1
1
1
.1 •
1 •
1 • ^ t
!• • ^. «f«
i • •
€ * 1*^ ** •
* , • '
H 1 - • «!
o:
O
Q 700
y,T
rr\
'. i-
' t
600
I
5 10 -f 20 25 30 35
FINE PARTICLES (micrograms per cubic meler)
Age-, sex-, and race-adjusted population-based mortality rates
for 1980 plotted against mean fine partioulate air pollution levels for 1979
to 1983. Data from, metropolitan areas that correspond approximately to
areas used in prospective cohort analysis.
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November 1995 V-66
apparent linearity across the cities, and the comparison of differences in death rates between
the highest and lowest cities (1.26) is in exact agreement with the relative risk from the
reported regression equation. The clearest increased risk is observed for Steubenville, at 30
Hg/m3 long-term PM25 concentration, the only city for which statistical significance on an
individual city basis was obtained. However, the highly significant relationship identified
across all six cities suggests that increased risk of mortality in this study is likely to be
associated across a wider portion of the range than only for the city which independently was
statistically significant. From this plot, it appears that a clear and consistent pattern of
increased risk is evident for the four cities with the highest annual average PM2.5
concentrations. Of the four cities showing clear increase in risk, the lowest concentration
among these four cities is associated with Watertown, MA, which has an average
concentration of approximately 15 /ig/m3 PM2 5.
A particular strength of this study is the long period of air quality measurements it
incorporates, and the fact that these measurements came from monitors specifically sited to
represent the exposure of the cohort as a whole. For fine particles, 6 to 9 years of PM2 5
concentrations were available, beginning in 1980 (four to six years into the study), and
ending in 1985-1988 (three to seven years before the end of the study). While it would be
ideal to have air quality monitoring extend throughout the period of study as well as
considerably before, only approximately one-fifth of the deaths had occurred in the cohort
before fine particle monitoring had begun. For other particle indicators evaluated in this
study, such as TSP, measurements went further back in time, but measurements of PM2 s
extended furthest into the later years of the study, in which mortality was the greatest
(Figures 1 and 2 in Dockery et al., 1993).
Questions remain as to whether previous fine particle concentrations for these cities
varied substantially from concentrations monitored in this study. Nearly all the cities showed
a slight decrease in fine particle concentrations over the course of the study (Figure 1 of
Dockery et al., 1993). Assessment of historical levels of fine particles, as indicated by
airport visibility measurements discussed in the CD, suggests that, unlike indicators of larger
particles which may have been at dramatically higher concentrations in several cities during
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External Review Draft DO fjO( Quote or Cite
November 1995 V-67
the 1960s, fine particles are likely to have been roughly equal to or only somewhat higher
than the concentrations measured during the study. This comparison is necessarily uncertain
due to the use of airport visibility data as a surrogate for PM2J and the potential for
significant variability in long-term PM2 5 trends among cities. Nevertheless, even if longer-
term historical concentrations are relevant for a substantial portion of the cohort, it is not
expected that inclusion of historic PM2.5 concentrations would substantially alter the nature of
the associations between PM2 5 and mortality risks seen in the study, although the impact on
quantitative study results is uncertain.
A large-scale study by Pope et al. (1995) involving from three hundred thousand to
half a million adults living in from fifty to one hundred fifty cities nationwide also reported
associations between PM2 5 and mortality. The ACS study sought to determine if the
relationship between mortality and fine particles, as measured by PM2 5 and sulfates,
observed in the Harvard Six City study, could be confirmed in a larger study including ten to
thirty times the number of locations and thirty to seventy times the number of cohort
members. The ACS study also collected detailed information on a greater number of
potential confounding risk factors than in the Harvard Six City study.
In the ACS study the association between mortality and PM2 5 concentrations was
evaluated in fifty cities. The PM2 5 concentration-response information from the ACS study
(Figure V-15) is based on a simple ecologic analysis, rather than a full cohort analysis,
including adjustments only for differences among cities in age, sex, and race. In contrast,
the concentration-response assessment in the Harvard Six City study used the strength of the
prospective cohort approach, comparing PM25 concentrations against the adjusted mortality
rate for each city's cohort, with the adjustment based on the outcome of the control of
important risk factors on an individual basis for each individual in the cohort. Thus, the
PM2 5 concentration-response information for mortality risk in the ACS study does not
incorporate the degree of control for confounding that the Harvard Six City study does, even
though the full ACS study cohort analysis incorporates control for more potential risk factors
on an individual basis than in the Harvard Six City study.
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November 1995 V-68
In further comparison to the Harvard Six City study, the estimates of long-term PM2.S
concentrations in the ACS study are likely to be somewhat more uncertain because the
duration of monitoring was not as long, and the monitors used had not been sited with the
population exposure of the cohort in mind. Data from the inhalable particle network for the
period 1979-1983 was used to estimate long-term exposure of the cohort in relation to
mortality in the cohort occurring from 1982-1989.
While recognizing these uncertainties, the ecological analysis from the ACS study
does appear to suggest that risk increases clearly and consistently at median PM2.5
concentrations above 15 jttg/m3 PM2 5. Given the uncertainties inherent in its analyses of
concentration-response information, the ACS study, drawing from a much larger number of
cities, can be characterized as supporting the findings of Dockery et al. (1993) concerning
clear and increased risk above 15 /ig/m3 PM2 5.
b. Supporting Studies With Other Indicators
Two additional long-term studies using other indicators of PM, including PM15 and
TSP, provide concentration-response information for associations with respiratory illness in
children and adults. Although these studies appear more uncertain or potentially less useful
for assessing concentration-response relationships with fine particles, they are included here
to provide information on whether the ranges of increased risk observed from the cohort
mortality studies are consistent with relevant findings from other studies of associations
between long-term exposure and chronic morbidity.
The effects of long-term exposures to particles on respiratory symptoms in children in
the six cities has been studied in relation to a number of PM indicators (Dockery et al.,
1989). PM15 was observed to be statistically significantly associated with increased acute
bronchitis symptoms among the entire cohort, with PM2 5 showing the second strongest but
marginally significant association (95% CI for Odds Ratio = 0.8 to 5.9). When a subset of
children with a history of asthma or persistent wheeze was analyzed separately, PM,5 and
PM25 showed consistent, marginally significant associations (CI= 0.9 - 15.5 for PM,j-, 0.9 -
13.2 for PM2.5). This study used the same monitoring network as did Dockery et al. (1993),
which was specifically sited to measure the cohort's exposure to fine particles. Because this
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study is restricted to children 7-11 years of age, concerns about the relevance of previous air
quality are diminished.
Given that in five of the six cities PM2 5 comprises between 58 to 68% of the PM,5
mass, PM2 5 most likely contributes at least partially to the PM15 associations seen with
bronchitis symptoms. Speizer (1989) suggests that the effects on bronchitis symptoms
observed in this study might be most strongly associated with acid aerosols (H+), a
component of the fine particle fraction (Figure 3 in Speizer, 1989; Figure 12-16 in the CD).
This may be especially true for the cities with the highest particle concentrations. However,
the one city that shows relatively large coarse particle contributions, Topeka, has an elevated
prevalence of bronchitis as well.
Figure V-16 shows a plot of the prevalence of bronchitis versus PM15 concentration,
with the solid line representing those with a history of asthma or persistent wheeze. The
cities with the three highest concentrations, where the magnitude of increased risk is greatest,
had annual mean PMI5 concentrations ranging from 37 - 58 /xg/m3 and PM2 5 concentrations
ranging from 22 - 37 /xg/rn3, although the pattern of increased risk is not consistent across
these three cities.
A cohort study involving information from the First National Health and Nutrition
Survey (NHANES) of 6000 adults in 53 cities adults reported associations between chronic
bronchitis and a physician-diagnosed respiratory illness and TSP (Schwartz et al., 1993).
Figure V-17 shows the relative risk of chronic bronchitis versus TSP concentration, and
Figure V-18 shows the relative risk of doctor diagnosed respiratory illness versus TSP. In
both, risk appears to be increasing clearly and consistently at the second quartile, with a
mean concentration of approximately 75 /tg/m3 TSP.
This study is based only on the TSP concentrations from the year prior to the
NHANES assessment of effects. To the extent that chronic bronchitis prevalence may
involve longer exposures, and that past TSP concentrations were potentially much higher in
some of the study area cities, these concentration-response relationships may contain
significant uncertainty in the specification of relevant exposures. To the extent that TSP may
be serving in part as a surrogate for fine particles, however, the uncertainties in the
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V-69a
FIGURE V-16.
RELATIONSHIP BETWEEN BRONCHITIS PREVALENCE AND
PM-15 IN THE SIX CITIES STUDY (DOCKERY ET AL., 1989).
50
40
I
o
2
o
cr
m
id
CJ
2
LU
HI
cr
OL
30 4
p~l
10 20 30 40 50 60
City-specific prevalence of reported bronchitis versus annual mean PM,, concentrations (wg/rn1) stratified
by reported asthma or persistent wheeze. Upper curve
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V-69b
FIGURE V-17.
RELATIONSfflP BETWEEN RELATIVE RISK OF CHRONIC
BRONCHITIS AND TSP FOR NHANES I SURVEY SUBJECTS
(SCHWARTZ, 1993b)
2.0
1.5
o
t.
6
«»
o
1.0
0.5
40
60
80
100
120
ToUl Suspended P«rtioles (ug/m3)
The relative risk of chronic bronchitis by quartiles of TSP exposure, after controlmg for age,
race, sex, and cigarette smoking.
FIGURE V-18.
RELATIONSHIP BETWEEN RELATIVE RISK OF
RESPIRATORY ILLNESS AND TSP FOR NHANES I SURVEY
SUBJECTS (SCHWARTZ, 1993b)
2.0
£ IS
CL
V)
V
1.0
0.5
40
60
80
100
120
Tcttl Suspended Particles (\ig/m3)
The relative risk of a diagnosis of respiratory illness by the examining physician by quartile
of TSP exposure, after controlling for age, race, sex, and cigarette smoking.
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concentration-response relationships would be expected to be less, given the smaller variation
seen in historical fine particle trends.
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VI. STAFF CONCLUSIONS AND RECOMMENDATIONS ON PRIMARY NAAQS
This chapter presents staff conclusions and recommendations for the Administrator to
consider in deciding whether to retain or revise the PM NAAQS. Drawing from the
information and analyses discussed in Chapters IV and V, this chapter addresses the major
components needed to specify an ambient standard: averaging time, form, pollutant
indicator, and level. Staff conclusions and recommendations on each of these interrelated
components are based on considering how the components of an individual standard and how
a suite of standards operate together to protect public health with an adequate margin of
safety.
In recommending a range of options for the Administrator to consider, the staff notes
that the final decision is largely a public health policy judgement. A final decision must
draw upon scientific information about health effects and risks, as well as judgements about
how to deal with the range of uncertainties that are inherent in the evidence and analyses.
The staffs approach to informing these judgments is based on a recognition that the available
health effects evidence generally reflects a continuum consisting of levels at which health
effects are likely through levels at which scientists generally agree that effects may occur but
the likelihood and magnitude of the response becomes increasingly uncertain. This approach
is consistent with the requirements of the NAAQS provisions of the Clean Air Act and with
how EPA and the courts have historically interpreted the Act. These provisions do not
require the Administrator to establish a NAAQS at a zero-risk level but rather at a level that
avoids unacceptable risks and, thus, protects public health with an adequate margin of safety.
A. Averaging Time and Form of the Standards
The current primary PM NAAQS include both a 24-hour standard with a statistical
form and an annual standard with an arithmetic mean form. These standards were intended
jointly to protect the public against the health effects associated with both short-term and
long-term exposures to PM based on epidemiological and other health studies available at
that time. Since the last review, numerous researchers have extended the epidemiological
database linking health effects with both short-term (from less than 1 day to up to 5 days)
and long-term (from generally a year to several years) exposures to PM. This body of
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evidence, summarized in Chapter V, provides increased support for both short-term and
long-term standards, as discussed below.
1. Short-term Standards
a. Averaging Time
The current 24-hour averaging time is consistent with the majority of the results from
community epidemiological studies, which have reported associations of 24-hour
concentrations of PM,0, fine particles, and TSP with an array of health effects.
Nevertheless, because some such studies have found a stronger association with a multiple
day average (Pope et al., 1992; Ostro et al., 1995; Pope and Dockery et al., 1992), the staff
considered whether a multiple day averaging time would be more appropriate. In some
geographic areas the observed health effects are associated with same day or previous day
PM concentrations. For example, such associations are shown by mortality studies in Los
Angeles, CA; Birmingham, AL; St. Louis, MO; Toronto, Canada; Santiago, Chile; Athens,
Greece; and London, England. Further, most hospital admissions studies show associations
with same day concentrations. The 24-hour averaging time effectively protects against
episodes lasting for several days while also protecting sensitive individuals who may
experience effects after a single day of exposure. Thus, the staff concludes that a longer
averaging time, such as 3 to 5 days, would not provide more effective protection than a 24-
hour average.
The staff has also considered the evidence regarding effects associated with PM
exposures of durations less than 24 hours; Some investigators prior to the 1987 review
(Lawther et al., 1970) speculated that the observed health effects might be largely due to
short-term peaks on the order of an hour. Controlled human and animal exposures to
specific components of fine particles, such as acid aerosols, also suggest that some effects,
such as bronchoconstrictioir, can occur after exposures of minutes to hours. Some
epidemiological studies of exposures to acid aerosols have also found changes in respiratory
symptoms in children using averaging times less than a 24-hour period (e.g., 12 hours).
However, it is not clear whether the majority of effects that have been associated with daily
exposure to PM, including mortality and various measures of morbidity, would occur after
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only short duration exposures. Moreover, a 24-hour average can be expected to provide
significant protection from potential effects associated with short duration peaks in most
urban atmospheres. Thus, although some study results may be suggestive of short duration
effects, the staff does not believe that the reported results provide a satisfactory quantitative
basis for setting a general particle standard with an averaging time of less than 24 hours.
Further, the staff believes that additional research is needed to examine short duration
exposures.
Based on the above discussion, the staff recommends that consideration be given to
retaining the current 24-hour averaging time as the most appropriate to address health effects
associated with short-term (from less than 1-day to up to 5-day) exposures to PM.
b. Form
As part of the last review, the 24-hour standard was changed from a deterministic
form, in which the standard was not to be exceeded more than once per year, to a statistical
form. The statistical form was selected to be a one-expected-exceedance form, averaged
over 3 years. The basis for this change in the form of the standard was that a statistical form
can offer a more stable target for control programs and, with reasonably complete data, is
less sensitive to truly unusual meteorological conditions than the deterministic form (U.S.
EPA, 1982b). The staff continues to believe that this rationale is sound and, thus,
recommends that consideration be given to retaining the current statistical form for a 24-hour
PM standard.
2. Long-term standards
a. Averaging Time
As summarized in Chapter V, community epidemiological studies have reported
associations of annual concentrations of PM2 5, sulfates, PMIO, and TSP with an array of
health effects, notably increased mortality (Dockery et al., 1993, Pope et al., 1995) and
respiratory symptoms and illness (e.g., chronic bronchitis and cough in children). The CD
recognizes the importance of the presence of PM in the lungs because of associated public
health concerns about both immediate and longer term symptoms produced and the long-term
potential for increased risk of chronic lung disease. Specifically, recurrent childhood
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respiratory illness has been suggested to be a risk factor for later susceptibility to lung
damage (Glezen, 1989; Samet, 1983; Gold et al., 1989) and is also increased by PM
exposure. Therefore, serious health consequences are associated with long-term PM
exposures.
In addition, human lung deposition data show that both coarse and fine fractions of
PM10 are able to penetrate and deposit in the gas exchange portion of the lung, an area in
which insoluble particles are retained for long periods (i.e., months to years). Given that
particles can be retained in the lung for long periods of time, several of the plausible
mechanisms of toxicity support the need for a long-term averaging time to protect against
health effects. Specifically, it is possible that accumulation of large lung burdens of particles
over time could be a possible mechanism or that long-term exposures could lead to impaired
respiratory defenses. Moreover, chemically active substances on particle surfaces, such as
acids or carcinogens, could cause damage before they are cleared, which, if not repaired,
could lead to cumulative damage. Although the specific mechanisms of toxicity of PM
remain speculative at this time, the staff believes that information on lung deposition and
clearance provides additional support for concern with long-term PM exposures.
The staff has also considered whether, for some effects (e.g., chronic mortality),
relevant exposure periods might better reflect the cumulative effects of PM exposures over a
number of years. In such cases, an annual average would provide effective protection
against long-term exposures to PM that exceed a year. Further, the staff has considered that
air quality studies show significant seasonal variability in exposures to PM. However, the
staff believes that the available community studies do not support a clear association for
seasonal exposures that would be distinct from 24-hour or annual exposures.
As discussed above, the staff believes that an annual averaging time is consistent
with the effects observed in community epidemiological studies, as well as insights into
potential effects of long-term exposure from studies of toxicology and dosimetry. Further,
the staff does not believe that multi-year or seasonal averaging times would be more effective
or supportable than an annual averaging time. Thus, the staff recommends that consideration
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be given to retaining the current annual averaging time as the most appropriate to address
health effects associated with long-term exposures to PM.
b. Form
As part of the last review, the annual standard was changed from a geometric mean to
an arithmetic mean of the daily averages. This change in the form of the standard was based
on an arithmetic mean being 1) more directly related to dose, which is associated with
observed health effects, 2) more sensitive to repeated short-term peaks, and 3) more
consistent with other annual NAAQS (U.A. EPA, 1982b). The staff continues to believe that
this rationale is sound and, thus, recommends that consideration be given to retaining the
current arithmetic average form for an annual PM standard.
B. Particulate Matter Indicator
1. General Considerations
Faced with clear evidence of adverse health effects in heavily polluted areas in the
decades after World War II, public health authorities in the U.S. and Great Britain pushed
for reductions in general particulate matter as indexed by available monitors, despite the fact
that the identity of causative agents and mechanisms was not well understood. That these
efforts were successful is evidenced in the elimination of classical pollution episodes, greatly
improved air quality, and reduced health risks (U.S. EPA, 1982b). As the review of U.S.
air quality trends in Chapter IV indicates, these improvements have continued under the
current PM10 standards, in areas with differing combinations of particulate and gaseous air
pollution. Furthermore, concentrations of some of the more innately toxic components
(e.g., trace metals, benzo(a)pyrene (BaP)) also declined in previously polluted areas (U.S.
EPA, 1982b). Previous decisions to control particles as a general class, although
heterogeneous in physical and chemical composition, appear to have been good public health
policy even though "paniculate matter" is lexicologically undefined. Based of the
evaluation of the updated scientific information in this review, the staff continues to believe
that separate general PM standards (as opposed to combined PM and SO2 standards) remains
an appropriate policy choice for protecting public health.
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The most recent summary of scientific information in the CD and outlined in Chapters
IV and V also continues to support past staff and CASAC recommendations regarding
selecting size specific indicators for PM standards. More specifically, the staff believes that
the following conclusions reached in the 1987 assessment remain valid:
1) Health risks posed by inhaled particles are influenced both by the penetration and
deposition of particles in the various regions of the respiratory tract and by the
biological responses to these deposited materials.
2) The risks of adverse health effects associated with deposition of ambient fine and
coarse fraction particles in the thorax (tracheobronchial and alveolar regions of the
respiratory tract) are markedly greater than for deposition in the extrathoracic (head)
region. Maximum particle penetration to the thoracic region occurs during oronasal
or mouth breathing.
3) The risks of adverse health effects from extrathoracic deposition of general ambient
PM are sufficiently low that particles which deposit only in that region can safely be
excluded from the standard indicator.
4) The size specific indicator(s) should represent those particles capable of penetrating to
the thoracic region, including both the tracheobronchial and alveolar regions.
Based upon the above considerations as well as the available information on human
dosimetry of particles, in the previous review the staff and CASAC recommended a size
specific indicator that included particles less than or equal to a nominal 10 /im "cut point,"
termed PM,C. The recent information on human particle dosimetry contained in the CD
provides no basis for changing 10 fim as the appropriate dividing line for particles capable
of penetrating to the thoracic regions.
The large body of new community studies and improvements in human exposure and
air quality presented in the CD and outlined in Chapters IV and V above, however, have
significantly expanded the information regarding associations between contemporary
community air pollution containing particles and morbidity and mortality in sensitive
populations. Even with the presence of other pollutants in the airsheds studied, PM is
independently associated with the observed health effects. While earlier studies mainly relied
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on BS, TSP, and sulfates as particle indicators, the recent work has added information on
PM10, fine particles, coarse fraction particles, and acid aerosols. Because statistical
associations between these indicators and health indices have been observed at concentrations
below the current standards, the adequacy of both the indicator and the levels for the PM,0
standards have been questioned (Schwartz and Dockery, 1992a; Dockery et al., 1993;
Lippmann and Thurston, 1995). If the constituents other than the most harmful fractions of
PMJO are captured by samplers and targeted for reduction by health protection strategies, less
effective health protection will occur. Therefore, proper identification of the components of
PM,0 most likely responsible for the observed health effects is critical to maximize health
protection strategies. The indicator is used to target and monitor health protection strategies,
and the choice is key to overall health protection provided by the PM NAAQS. Given these
concerns and the expanded information, the staff believes it is appropriate to reexamine the
question of whether the PM10 indicator should undergo additional refinement to provide for
more effective protection of public health.
2. Alternative Refinements for PM,0 Indicator
The staff bases its conclusions and recommendations for indicator(s) on the integration
of information in three key areas:
• Assessment of the totality of the evidence from epidemiology, toxicology and
human clinical studies;
• Consideration of the information on dosimetry and potential mechanisms of
toxicity; and
• Air quality and exposure analyses related to interpretation of the health studies.
Key aspects of each of these related areas have been drawn from the studies contained
in the CD and summarized in Chapter V. Based on these consideration as well as the earlier
assessment of indicators (U.S. EPA, 1982b; 1986b), the staff has identified the following
major policy options for further refinements to the PM10 indicator:
• Specifying an additional size division based on the observed bimodal ambient
air size distribution, that is, between fine and coarse fraction particles less than
10 fxm; and,
Adding a chemical class indicator based on sulfates and aerosol acidity.
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Each of these approaches is discussed and evaluated briefly below. The
Administrator must select the appropriate indicator(s) and consider how the indicator will
relate to providing health protection in conjunction with the other components of a standard
(i.e., averaging time, form, and level).
a. Indicators for the Fine and Coarse Fractions of PM^
Recognition that ambient particle mass and volume are typically distributed bimodally
has long led to the suggestion that the health (and other) effects of the two modes should be
treated separately (NAS, 1977; Miller et al., 1979; Wilson and Suh, 1995; Pope et al., 1995;
Schwartz et al., 1995). From an atmospheric chemistry perspective, the two modes can be
thought of as separate pollutant classes with distinct properties and origins. Although both
size fractions are implicated in health effects, the important differences in their physical and
chemical properties make it less clear whether the relative risk presented by the two modes
should be considered to be equivalent. In the previous review, staff gave serious
consideration to separating the two classes, ultimately concluding that the limited number of
and nature of the community epidemiology studies available at that time could not be used to
support more than a single size specific indicator (U.S. EPA, 1982b; 1986b).
In this review, the staff concludes that the significantly expanded community
epidemiology exposure and air quality information provide a sufficient basis for considering
separation of fine and coarse fraction particles. In addition, the experience in implementing
the PMIO standards provides insights as the relative effectiveness and efficiency of standards
based on that indicator in limiting the risks presented by fine and coarse fraction particles.
As outlined above, staff continues to believe that both fractions of PMIO present health risks
that must continue to be addressed by ambient standards. Key considerations regarding
indicators for each of these fractions are discussed below,
i). Fine Particles
The staff assessment of the basis for a separate fine particle standard is summarized
as follows.
1) The fundamental physical and chemical characteristics of the fine fraction are
summarized in Chapter IV. Fine particles tend to originate from nucleation (i.e.,
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formation of particles from low vapor pressure substances, produced either from
combustion or from chemical reaction of gases) and condensation of gases onto
existing particles. As a result of their physical properties, fine particles share a
number of properties important to assessing health risk. These include physical
properties such as high surface area and number, a more uniform distribution in urban
and regional scales, long atmospheric lifetimes, and increased ability to infiltrate
indoors. Although fine particles are chemically heterogenous, as a group they are
generally acidic and a major fraction is soluble and hygroscopic, while the coarse
fraction is generally basic and insoluble.
These differences in sources and properties also have a profound influence on
the nature of control strategies. Conceptually, the PM,0 indicator was intended to
provide adequate protection from both fine and coarse fraction particles. Areas which
exceed the current PM NAAQS have significant amounts of coarse fraction mass.
Specifically, the PM10 indicator registers a substantial amount of coarse particle mass
(e.g., up to 70 percent in the western half of the country where most exceedances of
the current standards occur and around 35 percent in the eastern U.S.). In practice, it
is often easier for sources and regulators to control preferentially the locally generated
coarse fraction. Therefore, it is not clear that a PM10 indicator, unless set at an
unnecessarily stringent level, provides adequate, efficient protection from the effects
of fine particles.
2) Although only qualitative information exists on potential mechanisms of toxicity,
both past and current assessments in this area suggest that the distinct physical and
chemical properties of fine particles may contribute to enhanced risk for several
possible mechanisms. The enhanced effects with decreasing size in some toxicologic
studies of laboratory generated aerosols and the substantial surface area for potential
adsorption of irritant gases has long been noted as a reason for increased concern for
fine particles (Natush and Wallace, 1974; U.S. EPA, 1982b; NAS, 1977a). Although
the relevance of the particle composition can be questioned, recent reports of the
acute toxicity of freshly generated ultrafme particles at low concentrations show that
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severe pulmonary inflammation and death are observed in rats after brief exposures
(Oberdorster et al., 1995). In this case, the large number of particles per unit mass
may have been critical. Preliminary work using an ambient particle concentrating
device developed by Sioutas et al. (1995) finds lethal effects in compromised animals
from ambient aerosol between 0.2 and 2.5 /*m at much lower concentrations than
reported for pure compounds in other laboratory studies.
That common physical properties (surface area and number) shared by fine
particles in disparate areas might be instrumental in particle toxicity is also indirectly
supported by one of the most interesting features of the recent body of epidemiologic
literature. As noted in Chapter V, a large number of studies conducted in cities in
the U.S., Europe, and South America have found strikingly similar relative risks for
particles when normalized to a comparable indicator and concentration. Substantial
differences are observed (or reasonably expected) in the chemical composition of fine
and coarse fraction particles and pollutant gases among such areas. Although far
from conclusive, this similarity is suggestive that some consistent characteristic of all
particles, such as surface area, might be involved if these associations are causal. In
this respect, fine particles would present a greater risk than coarse fraction particles.
Several chemical classes of concern such as most of the acids and sulfates are
found predominantly in the fine fraction. In general, acids are found to be more
acutely irritating than are materials in the coarse fraction. Kleinman et al. (1995)
reported the relative toxicity of high concentrations of fine particle components
(sulfate and nitrate) in animal tests to be greater than resuspended road dust. Some
transition metals and organics associated with the fine fraction have been shown to
cause effects in lexicological experiments. Loading particles with certain transition
metals such as iron, vanadium, or nickel may have the potential to enhance particle
toxicity, acute inflammation, and non-specific bronchial responsiveness. Adsorbed
organic compounds may also enhance toxicity of particles. Diesel exhaust particles
and gas engine particles are examples of particles whose organic extracts have been
proven to be mutagenic and tumorigenic in animals.
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3) As noted above, particle deposition in the tracheobronchial and alveolar regions of the
human lung is of greatest concern. For quiescent breathing in normal adults, most of
the mass of insoluble fine particles tend to penetrate to the alveolar region, where
they may accumulate over time. Hygroscopic fine sulfates and acids, however, grow
in the respiratory tract, resulting in significant deposition in the tracheobronchial
region. Furthermore, soluble particles that deposit in the alveolar region are available
to cause damage before they are cleared, damage which if not repaired can contribute
to cumulative effects. Both tracheobronchial and alveolar deposition of fine particles
may be enhanced for sensitive populations such as individuals with chronic or acute
respiratory disease, and for small children. Fine particles penetrate and deposit more
efficiently in the alveolar region.
4) Direct epidemiological evidence distinguishing the relative effects of fine versus
coarse fraction particles is limited. Nevertheless, a coherent body of epidemiology
studies has shown associations of health effects with fine particles measured by PM2 5,
BS, KM, CoH, and with classes of compounds found mostly in the fine fraction, such
as sulfates and associated acids. Associations with fine particles have been reported
across the full spectrum of health effects described in Chapter V, including mortality
associated with short-term and long-term exposures, hospital admissions, respiratory
symptoms, decreases in lung function, school absences, and work absences. These
data alone provide a substantial basis for quantitative assessments needed to establish
a standard level. In addition, staff believes that the large epidemiological database
relating to associations between health effects of short-term elevations of PM10 is best
interpreted as primarily representing risks from fine particles, as discussed below.
Historical pollution catastrophes such as those in London, England, in the 1950's
were most likely caused by increases in levels of fine particles.
Several recent studies have shown stronger relationships for PM2 5 than PM10
with both excess mortality and hospital admissions (Dockery et ah, 1993; Pope et ah,
1995; Thurston et ah, 1994; Schwartz 1995). Studies examining other morbidity
endpoints reported statistically significant associations with PM,0, although the
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associations with PM2 5 were suggestive of a trend but not statistically significant
(Dockery et al., 1989). The most direct comparison of the acute effects of fine and
coarse fraction particles is provided by the analysis of daily mortality in six cities by
Schwartz et al., (1995). In this analysis, both PM2J and PM,0 were positively and
significantly associated with fine particles, while the association with coarse particles
was small and insignificant. While this does not show that coarse particles do not
cause acute effects, it does indicate the mortality effects are best related to the fine
fraction.
Because of their physical properties, fine particles are more likely than coarse
particles to contribute to exposures measured in the epidemiology studies.
Examinations of air quality aspects of the time series PM10 mortality studies' also
support this suggestion:
• As described in Chapter IV, air quality properties of PM2 5 in the areas studied
imply that daily measures of PM]0 are driven by underlying changes in PM2 5
levels. First, PM2 5 is highly correlated with PMi0 in study locations.
Furthermore, the day-to-day variation of PM2 5 concentration is predominantly
greater than the day-to-day variation in coarse fraction concentration in these
areas; thus, day-to-day variations in PM,0 levels are driven by variations in
fine particle levels, and the coarse fraction is much less variable. Finally, in
the Eastern U.S., where most studies were conducted, PM2 j represents a large
fraction of the PM10 mass (63 percent of mass on average in the Eastern U.S.).
In specific Western U.S. cities studies, fine particles were used as
measurements (e.g., Los Angeles, CA; Santa Clara County, CA; Denver, CO)
or fine particles tend to dominate the PM10 measurements (e.g., woodsmoke
communities in winter and stagnation conditions of low wind speed in
conjunction with combustion sources).
'As described in the Criteria Document (Chapter 12), time series analyses attempt to use statistical
techniques to relate short-term variations in air quality measurements (o short-term variations in health endpoints
over time, typically using a 24-hour period as a unit of measure (e.g., daily PM concentrations and daily
deaths or hospital admissions) while controlling for confounding factors.
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• Epidemiological studies associate outdoor levels of PM to health endpoints. In
general, stationary monitor fine particles levels are better related to personal
exposure measures than are coarse fraction levels. The spatially homogeneous
nature of fine particles means community-oriented monitors on which most
studies are based may better represent fine than coarse particles. Coarse
particles are higher near sources and then levels drop off with distance from
the source. Thus, the community-based monitor may not represent exposure
to coarse particles as well as exposure to fine particles.2
Moreover, outdoor-origin fine particles are better able to infiltrate
indoors in air conditioned or heated areas than are coarse particles; once
inside, fine particles will remain suspended for longer periods of time. Thus,
outdoor fine particles contribute more to exposure because people spend a
significant amount of time indoors. It follows that time series associations
between variations in particle concentrations at outdoor monitors and both
personal exposures and related health effects in populations that spend most of
their time indoors are more likely due to fine particles. The recent time
series studies providing a direct comparison between outdoor PM,0 and PM2.S
and personal exposure show that both indicators are significantly related to
variations in personal exposure, but that fine particles show substantially
stronger associations (Janssen et al., 1995). By inference, the coarse fraction
association must be smaller even than for PM,0.
Consequently, daily fluctuations in PM10 concentrations measured in the
epidemiology studies are likely to be better associated with fluctuations in fine
particle concentrations. However, insufficient monitoring data prevent this
conclusion ftpm being tested directly in most areas. In most of the areas
where the relative health significance of fine and coarse fraction particles were
2This does not imply that the coarse fraction does not contribute to the observed health effects, only
that the time series studies would not be the most effective tool to elucidate coarse fraction associations.
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• examined directly, fine particles were more statistically significant and stable
predictors of the health effects than coarse fraction particles.
ii. Coarse Fraction of PM,0
As noted above, the staff continues to believe in the need to provide against the
potential health effects of coarse fraction particles. Coarse fraction particles deposit in both
the tracheobronchial and alveolar region. Long-term deposition of insoluble coarse fraction
particles in the alveolar region may have the potential for enhanced toxicity in part because
clearance from this region of the lung is significantly slower than from the tracheobronchial
region.
Although none of the available community epidemiology studies has been able to
isolate high concentrations of coarse fraction particles, occupational studies, laboratory
exposures and autopsy studies suggest a number of concerns remain about potential risks
from the coarse fraction. Occupational studies suggest that some effects, specifically
industrial bronchitis, may be associated with prolonged occupational exposure to coarse
particle insoluble mineral dusts (e.g., greater than 5 £im aerodynamic diameter) (U.S. EPA,
1982b; Morgan, 1978). Laboratory studies of potential mechanisms find that high levels of
coarse insoluble dusts can result in responses such as bronchoconstriction, altered clearance,
and alveolar tissue damage (U.S. EPA, 1982b). Autopsy studies of animals and humans
exposed to various ambient crustal dusts at or slightly above ambient levels typical in the
Western U.S. suggest those exposures result in silicate pneumonoconiosis (U.S. EPA,
19825). Responses ranged from build up of particles in rnacrophages with no clinical
significance to possible pathological fibrotic lesions.
Although much of the recent epidemiology suggests greater effects from fine particles,
it is premature to ascribe all of the effects observed in the PMIO studies to fine particles.
This is particularly true for effects in children (Schwartz et al., 1994; Dockery et al., 1989),
who spend more time in outdoor activity and hence receive less protection from both building
and nasal removal mechanisms. In such studies, however, it is not possible to provide
separate estimates for coarse fraction effects levels. 3n addition, the existing ambient data
base for coarse fraction particles is quite small. On the other hand, the monitoring network
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for PM,0 is large, and some of the epidemiological studies can be used to assess PM,0 levels.
If fine particle standards were established, then PM,0 would serve as a de facto indicator for
coarse fraction particles. As noted above, in many areas, this is already the case with
respect to control strategies. Because coarse fraction particles in such areas contribute
significantly more mass than smaller particles, risk managers have incentives to focus
reduction measures on particle sources that contribute the most by mass. Therefore, if a fine
particle indicator were chosen, the staff would still recommend retention of PMIO as the
indicator to protect against the risks of coarse fraction particles.
b. Chemical Class Indicators — Sulfates and Acid Aerosols
Another option for a PM indicator is a chemical class such as sulfates and acids
aerosols, metals, and organics. Each of these classes is predominantly found in the fine
fraction. Following the conclusion of the last PM standards review, the CASAC
recommended that special consideration be given to only one of these classes — acid aerosols.
Accordingly, EPA prepared a comprehensive review of acid aerosols, including sulfate
aerosols (U.S. EPA, 1989). The review concluded that the scientific and technical basis was
not sufficient to support a separate NAAQS for acid aerosols. The more recent information
in the CD prompted reexamination of this issue.
As presented in the CD and Chapter V, there are substantial health data concerning
sulfates and acid aerosols. This section examines their potential use as PM indicators. Both
sulfates and acids reside almost exclusively in the fine particle fraction and are usually
closely associated with each other.
Sulfates have a long, well-documented history of associations with health effects.
Some of the earliest reports of health effects from PM in the United States used sulfate as the
air quality measurement. Sulfates and fine particle mass are highly correlated in many areas
of the country, especially in the Eastern U.S. As discussed in the CD and Chapter V,
epidemiology associations have been reported between sulfates and mortality and serious
morbidity endpoints such as hospital admissions.
Toxicological studies and human clinical studies of pH neutral or nearly neutral
sulfate salts, however, have not been able to reproduce the health effects observed in the
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epidemiological studies, even at relatively high concentrations (Lippmann and Thurston,
1995). Sulfate aerosols containing strong acids such as sulfuric acid (H2SO4) do produce
functional and structural changes in healthy subjects consistent with the effects observed in
the epidemiological studies (CD, Chapter 11-13). Consequently, although sulfate itself is not
innately of health concern, it is closely linked to acid species which have been shown in
toxicological, human clinical, and epidemiological studies to be of concern. Based on these
factors, some investigators (Lippmann and Thurston, 1995) suggest that sulfates would be an
appropriate indicator for PM.
A sulfate indicator would not capture all of the potential agents of concern as
effectively as a fine particle indicator. PM associations with daily mortality have been
observed in locations where sulfate concentrations would be expected to be low (Fairley,
1990; Schwartz, in press (Spokane); Schwartz et al., 1993). A sulfate indicator would not
address these risks as effectively as a general fine particle standard although a sulfate
indicator might capture some of the contributing components. While sulfates might be a
useful proxy for acidic species in the fine fraction, it would only include these classes.
Concern exists for the potential role of transition metals, organic compounds, ultrafine
particles, particle surface area, or number. PM25, on the other hand, would effectively
capture all of these agents.
Acid aerosols are currently regulated to varying degrees by current NAAQS for PM,
sulfur dioxide, and nitrogen oxides. Recent epidemiology studies have reported associations
between acid aerosols and health effects (See CD Table 12-3). However, several PM
epidemiological studies in areas where acid concentrations are low or minimal have still seen
consistent particle effects (Fairley, 1990; Pope, 1991; Pope, 1992; Dockery et al., 1992).
While several studies show acids to be as well or even more strongly correlated with health
effects than particle mass measurements, some other studies have found general particle
measures to be better correlated (Dockery et ah, 1992; Schwartz, et a!., 1994).
An acid standard would focus health protection measures on acids, leaving out control
of organics, transition metals, non-acidic ultrafine particles, and other components of PM of
potential concern. While fine or ultrafine acid aerosol clearly may play a role in the
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observed health effects associations, the data do not provide support for any single
mechanism or pollutant. Therefore, using sulfates or other acid indicators would not address
these risks as effectively as a general fine particle standard. Moreover, because sulfates
form such a large fraction of fine mass in the Eastern U.S., an appropriate fine particle
standard would focus attention on control of sulfates and associated acids.
This review suggests that a large number of different paniculate substances may
produce a variety of responses in animals and humans. Identification and control of each of
the many ambient aerosol components would be difficult to accomplish, time-consuming, and
would place excessive monitoring, compliance, and other requirements on effected agencies
and industries with no clear potential for improving public health protection over general
particulate regulation. Given current knowledge and technical capabilities, separate national
standards for chemical classes, including sulfates and acid aerosols, would be difficult to
support and implement, again with no obvious advantages for improving health protection
over an appropriately set fine particle standard.
3. Staff Conclusions and Recommendations for a Particle Indicator
Based on the above assessments and the scientific information in the CD, the staff
draws the following conclusions:
1) Ambient particles capable of penetrating to the thoracic region represent the
greatest risk to health. Previous staff and CASAC recommendations for 10
/im as the appropriate cut point for such particles remain valid. The recent
health evidence and implementation experience with PMIO have, however,
prompted the staff to reconsider previous conclusions regarding further
refinements to the indicator.
2) Any refinement of the PM10 indicator should be based on the integration of the
totality of the evidence from epidemiology, toxicology and human clinical
studies; consideration of respiratory tract deposition data and potential
mechanisms of toxicity; and air quality and exposure analyses.
3) The staff finds that the available information is sufficient to further refine the
indicator for the current primary standard indicator, PM10. In order to provide
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more effective and efficient health protection, the staff recommends a
distinction be made between standards for fine particle and for coarse fraction
particles.
4) Movement to chemical class indicators is not advisable during this review. Of
the paniculate chemical classes, most is known about sulfates and acids. In
the past reviews, staff has concluded that insufficient data exist to set a
separate national sulfate or acid aerosol standard (U.S. EPA 1989; 1986b;
1982b). The staff continues to concur with these judgments. Additional
components of fine particles have also been demonstrated to be of health
concern. Because sulfates form such a large fraction of fine mass in many
areas, an appropriate fine particle indicator would result in control of sulfate-
related species.
Based on these conclusions, the staff makes the following recommendations with
respect to reviewing the adequacy of the current indicator for PM:
1) The PM,0 indicator should be retained. PM10 is the most appropriate surrogate
for additional protection from potential risks of coarse fraction particles. A
separate coarse particle indicator is not appropriate because of the much larger
data base associated with PMI0.
2) A fine particle indicator should also be added to provide more effective
protection against the risk posed by fine particles.
As discussed in Chapter IV and Appendix A, the minimum particle diameter between
the fine and coarse modes lies between 1 and 3 j*m, and the scientific data support a cut
point to delineate fine particles in this range. Because of the potential overlap of fine and
coarse particle mass in this intermodal region, specific cut points are only an approximation
of fine particles. Thus, the decision within this range is largely a policy judgement. Based
on considerations of consistency with health data, the limited potential for intrusion of coarse
particles into the fine fraction, and availability of monitoring technology, the staff
recommends using a PM2.5 gravimetric measurement, which will be further specified in the
Federal Reference Method and equivalency program.
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From a public health perspective, PM2.5 captures all of the potential agents of concern
in the fine fraction. For example, PM2 5 captures most sulfates, acids, fine particle metals,
organics, and ultrafine particles and accounts for most of surface area, and particle number.
PM2.5 has been used directly in many health studies as described in the CD and Chapter V.
PM2.s has some potential for intrusion of particles generated by grinding or crushing (i.e.,
coarse mode particles) into the daily PM2 s measurement. A sharper inlet for the Federal
Reference Method may help to minimize the intrusion of coarse mode particles into the PM2 5
measurement. Although intrusion of coarse mode particles into daily PM2 5 measurements is
not anticipated to be significant in most situations, if subsequent data reveal problems in this
regard, this issue might be better addressed on a case-by-case basis in the monitoring and
implementation programs. Furthermore, PM2 s measurement technologies are widely
available and have been in use since the 1970s.
PM,, on the other hand, has not been used in health studies primarily due to lack of
available monitoring data. PM, could reduce possible intrusion of coarse mode particles in
some situations, but it might not capture all of the fine mode in other situations. PM,
sampling technologies have been developed; however, the PM, samplers have not been
widely field-tested to date. Thus, the staff recommends the use of PM2^ as the fine particle
indicator.
C. Level of the Standards
Selecting a suite of PM ambient air quality standards that provide an adequate margin
of safety remains a difficult challenge for the decision maker despite recent new studies and
analyses since the last review that provide significant relevant information and insights.
Although we can now somewhat better characterize PM, it remains a pollutant class with
chemical and physical characteristics that vary with geographic location, source mix,
meteorology, and time. Tijis aspect of PM inherently makes interpretation of
epidemiological evidence difficult and diminishes the utility of controlled human and animal
studies in making quantitative judgments about appropriate ranges of standard levels. In
addressing this issue, the staff recognizes, as in past reviews, that although the scientific
literature supports the notion that various mixes of particles pose risks to health, the basis for
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any general PM standards is largely a public health policy judgment. The staff believes that
by considering policy alternatives that focus control on those particles with the greatest
potential for causing health effects of concern, primarily through PM2.5 standards as
recommended above, a more effective and efficient policy response would result than that
associated with the current suite of standards.
1. General Considerations and Approach
In developing an approach to formulating recommendations on appropriate ranges of
standard levels, the staff has taken into account the following considerations:
1) Recent new epidemiological studies are noteworthy in their scope and efforts
to account for potential confounding and other uncertainties (e.g.,
characterization of exposure). However, each individual study has inherent
and methodological limitations and interpretation of these findings is the
subject of ongoing debate within the scientific community. Thus, the staff
views its assessment of each individual study in the context of the overall body
of epidemiological evidence (with mechanistic support from lexicological and
dosimetry studies) and the consistency and coherence of results across studies
and effects.
2) As noted in the last review, it continues to be the case that even the best
epidemiological studies can do no more than observe site-, time-, and monitor-
specific associations between levels of a given pollutant and health responses.
Further, such studies cannot be expected to provide clear evidence of
population thresholds of response. Thus, the staff recognizes that attempting
to identify "lowest observed effects levels" and adding margins of safety
below such levels is not an appropriate approach in this case. Instead, the
staff has attempted to assess the nature of health risks, and the associated
uncertainties, along a continuum of exposures using the full range of available
health and exposure data from the specific key and supporting studies.
3) Relative to other single pollutants for which NAAQS have been set,
establishing appropriate ranges of levels for general PM standards involves
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unusually large uncertainties. While recent studies help to reduce the
uncertainties that were present in the last review, they do not change this basic
observation relative to other NAAQS. To better address these uncertainties
over time, the staff believes that research should continue into the more
difficult problem of identifying and assessing potential health effects that may
be associated with specific chemical and physical characteristics within the
mixture of particles. However, even without any additional chemical-specific
evidence, the staff believes that the large uncertainties inherent in setting
general PM standards do not preclude our identifying appropriate ranges of
policy alternatives from which specific PM standards can be selected to
effectively and efficiently protect public health with an adequate margin of
safety.
Taking these considerations into account, the staffs approach to formulating
recommendations on appropriate ranges of standard levels for the recommended indicators
and averaging times is based on: 1) staff assessments of the quantitative concentration-
response relationships suggested by specific epidemiological studies identified in the CD as
appropriate for quantitative assessment purposes; 2) consideration of how these studies may
be applied in developing ranges specifically for PM2 5 and PM,0 standards; and 3) qualitative
consideration of the uncertainties and other key factors that affect the margins of safety
associated with ranges of standard levels. This approach recognizes that final decisions about
appropriate PM standard levels must draw not only on scientific information about health
effects and risks, but also on policy judgments about when observed effects become adverse
from a public health perspective and how to deal with the range of uncertainties that are
inherent in the evidence and assessments.
These staff assessments and considerations are discussed below for both 24-hour and
annual PM2 5 standards, as well as for PM,0 standards. The following discussions are based
on information in the CD and in Chapters IV and V of this Staff Paper.
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2. Specific Considerations and Conclusions for PM25 Standards
a. 24-Hour PM? < Standard
i. Levels of Interest from Short-term Epidemiological Studies
As discussed in section V.E, selected epidemiological studies provide quantitative
concentration-response information useful in developing an appropriate range of standard
levels for consideration in setting a new 24-hour PM2.5 standard. In the last PM standards
review, studies were not available that directly used the PM,0 indicator that was established
based on that review. In this review, by contrast, several studies are available that directly
use the currently recommended PM25 indicator (Schwartz et al., in press; Dockery et al.,
1992; Schwartz et al., 1994). A larger number of studies using PMIO, as well as reanalyses
of some datasets by independent reviewers, are also now available to provide concentration-
response information (Pope et al., 1992; Schwartz, 1993a, 1994g; Schwartz et al., 1994e;
Schwartz, 1994d; Schwartz and Morris, in press; Pope and Dockery, 1992; Samet et al.,
1995). These key PM25 and PM10 studies are supported by other studies that used sulfates
and TSP as indicators of exposure (Burnette et al., 1994, 1995; Samet et al., 1995). These
selected studies were the basis for staffs assessment to discern concentrations of the
measured pollutants at which risk increases in a clear and consistent pattern in these studies,
as presented in Table V-19.
To gain insight into the coherence of these short-term studies with regard to estimated
24-hour PM2 5 concentrations at which clear and consistent increases in risk may occur, staff
converted all such estimates in terms of the measured pollutants into estimates of PM25,
shown in Table VI-1. In so doing, staff is aware that this approach is premised on assuming
that PM2 5 concentration-response relationships for these studies would be similar to those
observed for other measured particle indicators. Further, staff recognizes that translating
exposures measured in terms of one particle indicator to PM2 5 exposures incorporates
additional uncertainties beyond those inherent in specifying exposures directly in terms of a
measured particle indicator. To minimize this uncertainty to the extent possible, site-specific
conversion factors were used wherever available. Taking into account these caveats, staff
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VI-22a
TABLE VI-1. ESTIMATED LEVELS OF MINIMUM CLEAR INCREASED RISK
IN TERMS OF MEASURED OR ESTIMATED PM2^ (24-HOUR AVERAGE)
Study/PM Indicator
MORTALITY - 6 Cities - PM-2.5
Schwartz et al., in press
MORTALITY - St. Louis - PM-2.5/PM-10
Dockery etal., 1992
Sametetal., 1995
MORTALITY - Utah Valley - PM-10
Pope et al., 1992
Samet et al., 1995
MORTALITY - Birmingham - PM-10
Schwartz, 1993a, 1994g
Samet et al., 1995
MORTALITY - Philadelphia TSP
Samet et al., 1995
HOSPITAL ADMISSIONS - Birmingham - PM-10
Schwartz etal., 1994e
HOSPITAL ADMISSIONS - Detroit - PM-10
Schwartz, 1994d
HOSPITAL ADMISSIONS (Cardiac) - Detroit - PM-10
Schwartz and Morris, in press
HOSPITAL ADMISSIONS - Ontario - Sulfate
Burnetteetal., 1994, 1995
RESPIRATORY SYMPTOMS - 6 Cities - PM-2.5
Schwartz etal., 1994
RESPIRATORY SYMPTOMS - Utah Valley - PM-10
Pope and Dockery, 1992
Minimum Clear Increased Risk
Level for PM^
(/ig/m3 of measured or
estimated PMU)
<30
21'
28'
272
292
343
303
344
11 -263
335
23s
13 - 18*
<;187
322
'Concentration to PM-2.5 from PM-10 quartile done by using a site-specific PM-2.5/PM-10 ratio for the period
of study (0.64).
Inversion to PM-2.5 used nationwide PM-2.5/PMT10 ratio for all seasons (0.58) from SAI, 1995, because
urbanized Utah Valley judged not well represented by other Southwest sites.
3Minimum clear risks indicates lowest concentration on nonparametric smoothed curve where a clear and
consistent increase in risk is evident. Conversion to PM-2.5 done using the PM-2.5/PM-10 ratio for Southeast
region from SAI, 1995 (0.57).
^Conversion to PM-2.5 done by applying median PM-2.5/TSP ratio available for 1982 in Philadelphia (0.34),
using data from the inhalable particle network.
'Conversion to PM-2.5 done using PM-2.5/PM-10 ratio (0.63) for central U.S. from SAI, 1995.
*Conversion to PM-2.5 done using site-specific regression equations to convert from sulfate to PM-10 for the
three major cities in the study and converting the PM-10 values to PM-2.5 using a nationwide PM-2.5/PM-10
regression equation for Canada (CEPA/FPAC Working Group, 1995; Brook et al., in press). The results agree
closely with those obtained using a sulfate/PM-2.5 ratio for Toronto from Thurston et al., 1994.
'Conversion to PM-2.5 from PM-10 done by using site-specific ratio for the period of study (0.6).
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believes that this approach provides useful insight beyond that which can be obtained by only
looking at each study independently.
As seen in Table VI-1, the selected short-term PM25 and PMIO studies most useful for
evaluating quantitative concentration-response relationships appear to show strong coherence
in terms of measured and estimated PM2 5 concentrations at which the risk of observed
mortality and morbidity effects appears to clearly and consistently increase. From the
mortality studies, risk appears to clearly and consistently increase at PM2 5 concentrations
somewhat below 30 ^g/m3. The morbidity studies show a wider range of estimates for
concentrations of clear and consistent risk, ranging from somewhat below 20 /xg/m3 to
somewhat above 30 ftg/m3. When the sulfate and TSP studies are considered as surrogates
for PM2 5, these studies yield estimates of PM2 5 concentrations where risk increases in a
clear and consistent pattern that are within the range of that seen in the PM2 5 and PM10
studies. Thus, this staff assessment suggests that, when considered together, the short-term
epidemiological studies are quantitatively coherent and support the judgment that evidence of
increased mortality and morbidity risks become more apparent when daily PM2,
concentrations reach approximately 20 jcg/m3 to somewhat below 30 /*g/m3.
The above discussion of 24-hour PM2 5 levels at which increased risks of various
health effects are likely is based on interpreting the quantitative study results as being
primarily attributable to changes in PM2 5 levels. The staff believes such an interpretation is
reasonable in light of the entire body of evidence and given efforts in the original studies and
reanalyses to control for potential confounding and to characterize exposures in terms of
PM2 5 concentrations in selected studies where such information was available. However, the
staff recognizes that various issues have been raised that call into question using these study
results directly as a basis for establishing a range of levels for a 24-hour PM2 s standard.
Alternative interpretations of the studies, for example, raise the possibility that the observed
effects may in part be more appropriately attributed to specific components within the
mixture of PM or to other pollutants in the mixture of ambient air in general, despite
extensive efforts to control for such confounders. Further, limitations on matching exposures
of the population subgroup experiencing effects to the ambient measurements of PM, and the
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conversions of measured concentrations of other indicators into PM2.5 concentrations that
have been used in developing exposure-response relationships for PM2 s call into question the
specific levels at which effects are likely to be experienced. Finally, the degree of
prematurity of death observed in the mortality studies is an issue in regard to the extent to
which such prematurity — if it is, for example, on the order of a few days — should be
considered a matter of public health concern.
These issues are discussed further below. Taking into account all such questions,
however, the staff considers it appropriate at a minimum to interpret the short-term
quantitative studies as a body of evidence that, when taken together with information from
controlled human and animal studies, supports the following conclusion: adverse public
health effects, including premature mortality and increased morbidity, are likely to occur in
various sensitive population subgroups at 24-hour PM2 5 concentrations below those that
occur when the current 24-hour PM,0 NAAQS is attained. Thus, the staff concludes that a
PM2.5 concentration that is approximately equivalent to 150 jtg/m3 PM10 represents a clear
level of concern where health effects can with confidence be attributed to PM exposures.
This approximately equivalent PM2 s concentration varies from about 55 to about 95 /zg/m3
for western regions and eastern regions, respectively, across the U.S., with the national
average conversion yielding a 24-hour PM2 5 level of about 85 ftg/m3 as the approximate
equivalent of the current 24-hour PM10 NAAQS. Setting a 24-hour PM2 5 standard at this
level would give maximum weight to the issues and uncertainties mentioned above by, in
essence, completely discounting the quantitative study results, and no weight to the coherence
of the entire body of evidence that has become available since the last review of the PM
standards. Such a standard could not be construed as being at all precautionary in nature,
nor to provide any identifiable margin of safety. Instead, the staff believes that the issues
and uncertainties mentioned above should be considered in the context of deciding what
standard within the range recommended below will, in the Administrator's judgment, provide
an adequate margin of safety.
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ii. Margin of Safety Considerations for a 24-Hour PM2 5 Standard
As discussed above, there are a number of issues that the staff believes are relevant
and appropriate to consider in deciding what standard will provide and adequate margin of
safety.
An effect of rtair pollution" on mortality is now broadly accepted by the scientific
community (Moolgavkar, 1995, Samet et al., 1995), but differing views remain as to the
degree to which the risk of premature mortality can be quantitatively associated with PM.
Further, associations between air pollutants other than PM have been well-established for
some of the morbidity effects linked to PM, resulting in uncertainties in the degree to which
the risk of observed morbidity effects can be quantitatively associated with PM. As
discussed in section V.D, when the health effects of PM are evaluated across the entire body
of evidence, not just looking at each study independently, concerns are lessened by the
absence of consistent and plausible confounding by other candidate pollutant(s). Further,
investigations into plausible mechanisms, elucidating how exposure to ambient levels of PM
may result in the observed effects have not yet established definite pathways from exposure
to effects at ambient PM concentrations. Therefore, substantial uncertainty will remain
concerning the agent(s) responsible for the observed associations.
A related uncertainty concerns the degree to which effects associated with PM can be
attributed primarily to the fine particle fraction of PM. Although the existing health
literature contains more studies using PM10 as a general indicator of particles than it does
studies of PM2 s, the staff concludes that the existing PM2 5 studies strongly implicate fine
particles, and as discussed in Chapter V, that much of the larger body of PM10 studies can be
interpreted as linking effects to the fine particle component of PM,0. Further, there are
differing views as to the degree to which specific chemical classes within PM2.5 may be
primarily associated with observed effects. The staff believes this issue concerning specific
chemical classes should be considered in judging the desirability of a more general surrogate
indicator (i.e., one that is likely to include the various physical properties and chemical
constituents causally linked to effects) as a practical guide to the development of effective
and efficient control strategies.
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Another relevant factor concerns the uncertainties associated with using fixed-point
outdoor monitoring networks, and area-wide conversions between a measured indicator and
estimates for another indicator of PM exposure, to specify exposures in quantitative analyses
of exposure-response relationships. Although recent studies have become more sophisticated
in the application of central, fixed-site monitoring to community-wide measures of health
effects, significant uncertainties necessarily remain. As discussed in Chapter IV, the
importance of this uncertainty is lessened for fine particles, which have good serial
correlation between central monitors and personal exposure (Janssen et al., 1995), are
generally more uniformly distributed across a community than other PM indicators, and
penetrate more efficiently indoors where much of individual exposures to PM occur.
Uncertainties in specifying exposures carry over into analyses of the exposure-
response relationships directed toward gaining insight into patterns of increasing risk over
relevant PM concentration ranges. The staff has attempted to minimize the impact of such
uncertainties concerning concentration-response by evaluating available information from
individual studies to attempt to discern where the clearest and most consistent patterns of
increased risk are evident, and, further, to consider the coherence of these analyses in the
context of the entire body of evidence.
Another factor to be addressed in margin of safety considerations includes the
uncertainties and differing views with regard to the degree of life shortening that is reflected
in the mortality events associated with short-term PM exposure. The extent of life
shortening in these studies is difficult to specify, with some authors reporting that at least a
portion of the mortality effects from short-term exposures may involve little displacement of
mortality (Spix et al., 1993). Other findings from short-term exposure studies (Pope et al.,
1992) and from long-term exposure studies (Dockery et al., 1993; Pope et al., 1995) suggest
that substantial displacement of mortality may be occurring in some cases. The staff believes
that assessing the public health significance of this effect ultimately involves a general policy
judgment that should be made in the context of considering what standard will provide an
adequate margin of safety.
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b. Annual PM2 5 Standard
i. Levels of Interest from Long-term Epidemiological Studies
Staff has used the same approach to identify concentration levels of interest for an
annual PM2.5 standard as described above for a 24-hour PM2 5 standard. Although only four
long-term studies were judged to provide quantitative concentration-response information
useful in developing an appropriate range of consideration for an annual PM2.5 standard, two
of these studies directly examined the effects of PM2.5 exposure on mortality (Dockery et al.,
1995; Pope et al., 1993). These PM2J mortality studies are supported by studies of
morbidity effects (e.g., chronic bronchitis in children and adults) using PM,5 and TSP
(Dockery et al., 1989; Schwartz et al., 1993). These selected studies were the basis for
staffs assessment to discern concentrations of the measured pollutants at which risk increases
in a clear and consistent pattern in these studies, as presented in Table V-20.
To gain insight into the coherence of these long-term studies with regard to estimated
annual PM2 5 concentrations at which clear and consistent increases in risk may occur, staff
converted all such estimates in terms of the measured pollutants into estimates of PM2 5,
shown in Table VI-2. In so doing, staff is aware that this approach is premised on assuming
that PM2 5 concentration-response patterns would be similar to those observed for other
measured particle indicators. Further, staff recognizes that translating exposures measured in
terms of one particle indicator to PM2 5 exposures incorporates additional uncertainties
beyond those inherent in specifying exposures directly in terms of a measured particle
indicator. Taking inlo account these caveats, staff believes that this approach provides useful
insight beyond that which can be obtained by only looking at each study independently.
The two strongest studies of the effects of long-term exposures to PM2 5 are the
Harvard Six City (Dockery et al., 1993) and ACS (Pope et al., 1995) mortality studies. As
seen in Table VI-2, the Harvard Six City study suggests a range of clear and consistent risk
of from 15 ^g/m3 to below 30 /xg/m3 PM25. Available concentration-response information
from the ACS study, which examined cities with a similar range of long-term particle
concentrations to the Harvard Six City study, provides evidence of clear risk at
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VI-27a
TABLE VI-2. ESTIMATED LEVELS OF MINIMUM CLEAR INCREASED RISK
IN TERMS OF MEASURED OR ESTIMATED PM^ (ANNUAL AVERAGE)
Study/PM Indicator
MORTALITY - 6 Cities - PM-2.5
Dockery et al., 1993
MORTALITY - ACS 50 Cities - PM-2.5
Pope et al., 1995
BRONCHITIS IN CHILDREN - 6 Cities - PM-2.5/PM-10
Dockery et al., 1989
CHRONIC BRONCHITIS - 53 Cities - TSP
Schwartz etal., 1993
Minimum Clear Increased Risk
Level for PM^j
(/ig/m3 of measured or estimated
PMW)
15 - <30
>15
22
23'
'Derived from applying conversion factors for PM-10/TSP (0.5) and PM-2.5/PM-10 (0.6) for late 1970's -
early 1980's data and previous as given in the 1986 SPA (pgs. 8 & 11) (U.S. EPA, 1986b.) Ratios may have
differed somewhat over the study period (1970-1974).
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concentrations above 15 Mg/rn3 PM2S. Thus, the ACS study provides support that effects
may be occurring at the lower end of the Harvard Six City study range.
The findings of these mortality studies, which associate PM2 5 with mortality of
sufficient prematurity to give rise to differences in overall annualized mortality rates, lessens
the likelihood that mortality events associated with PM2 5 solely involve only very brief
shortening of life. Further, the ability to look across regions of substantially different PM
composition allows for more confident focus on PM2 5 as being primarily responsible for the
observed effects (Dockery et al., 1993). Staff notes that questions raised in the CD about the
appropriate exposure period to use in examining long-term mortality effects add to the
uncertainty in interpreting the magnitude of risk and the concentration at which risk increases
in a clear and consistent pattern suggested by these studies. Staff believes that these
important uncertainties dealing with mortality effects should be addressed as part of the
margin of safety considerations.
Coherence between the mortality and morbidity studies is more difficult to judge
because the morbidity effects can be less confidently ascribed primarily to PM2 5 and require
uncertain conversions from other PM indicators to arrive at estimates of PM2.5. However,
when expressed in terms of PM2 5, the morbidity studies suggest estimates of minimum PM2 5
concentrations of clear and consistent risk from 22 to 23 /xg/m3. These morbidity studies
support the judgment that clear and consistent risk from long-term exposures to PM2 5 is
likely to occur well below 30 jtg/m3 annual average PM2 5.
ii. Margin of Safety Considerations for an Annual PM2 5 Standard
Staff has identified several factors that are relevant and appropriate to consider in
assessing margin of safety considerations, as discussed below.
Similar to the short-term studies, uncertainties in attributing observed effects
specifically to PM, rather than to other co-pollutants, and more specifically to PM2 s, are an
important factor in margin of safety considerations. Several long-term studies have found
PM to be a stronger indicator for many health effects from long-term exposures than other
potentially confounding pollutants (Abbey et al., 1995c; Dockery et al., 1993; Dockery et
al., 1989), as well as PM25 being an equal or better indicator than other measures of PM
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November 1995 VI-29
(Dockery et al., 1993; Abbey et ah, 1995c). However, as long as mechanistic investigations
have not established definite pathways from exposure to effects, uncertainty will remain
concerning the agent(s) responsible for the observed effects. Further, uncertainties about
specific causal agents should be addressed in considering the desirability of a more general
surrogate indicator; i.e., one that is likely to include the various physical properties and
chemical constituents causally linked to effects, as a practical guide to the development of
effective and efficient control strategies.
With regard to specifying exposures, long-term studies have the same uncertainties as
do short-term studies concerning the use of centrally-located, fixed-site monitors, generally
compounded by the comparison across different urban areas. The current long-term
mortality and morbidity cohort studies address this problem by controlling other potential
confounding risk factors. Some also site monitors with a goal of characterizing the study
population exposure (Dockery et al., 1989; 1993) or use fixed monitoring information broken
down on a subject-by-subject basis (Abbey et al., 1991; 1993). However, uncertainties with
regard to specification of exposures necessarily remain for long-term studies.
An important uncertainty involves whether cumulative effects from a long period of
exposure to PM pollution, not fully captured in the monitoring done for a study, might be
most relevant for some of the observed health effects. If a large proportion of subjects were
responding to cumulative exposures over a period of years, and the air quality concentrations
prior to the studies were substantially higher than during the studies, this circumstance could
lead to an overestimate of the effects of PM on health. Examination of historical visibility
records suggests that historical levels of fine particles do not appear to be substantially higher
than that used in a key mortality study (Dockery et al., 1993). Further, some morbidity
studies addressed this question by either testing the effects of particle concentrations several
years previous to the effecjt (Abbey et al., 1995b) or by restricting their study population to
young children (Dockery et al., 1989). In general, however, the current lack of knowledge
concerning the most relevant exposure periods for the effects associated with long-term
exposure to PM suggests that exposure estimates for long-term studies incorporate greater
uncertainty than those from short-term studies.
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Another factor to be considered is the uncertainty relating to the degree to which the
long-term studies are detecting additional increased risk of chronic mortality or other
endpoints, or are just measuring the cumulative impact of associations with short-term
exposures. Given uncertainties concerning the measure of exposures, both current and
historical, for the long-term studies, as well as corresponding uncertainties in the short-term
exposure studies, a comparative assessment of the magnitude of risk observed by both study
approaches is difficult. However, any mortality resulting from short-term exposures that is
substantially premature should be reflected in the mortality events measured in long-term
studies. Thus, the long-term studies can be interpreted as indicating either that a significant
portion of the mortality associated with short-term exposures involves significant prematurity,
or, more likely, that the mortality associated with long-term exposures includes both chronic
and acute mortality effects.
3. Staff Recommendations for PM2 5 Standards
The following staff recommendations are based most directly on the above discussion,
but take into account the entire body of evidence presented in the CD and in Chapter V.
These recommendations suggest ranges of levels for 24-hour and annual PM2 5 standards that
the staff believes would protect against the various adverse health effects associated with
exposures to PM that have been reported in a large number of epidemiological studies and
supported by evidence from controlled human and animal studies.
a. 24-Hour PM, 5 Standard
With regard to a 24-hour PM2 5 standard, the staff offers the following
reco m mendation s:
1) The upper end of the range of consideration for a new 24-hour PM25 standard
should be below the PM2 5 concentration that is approximately equivalent to the
level of protection provided by the current PM,0 standard. An approximately
equivalent 24-hour PM2 5 concentration, about 85 jig/m3 on average in the
U.S., contains no identifiable margin of safety and should not be considered as
an appropriate standard alternative While the uncertainties inherent in the
most recent epidemiological studies are important margin of safety
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considerations, the staff believes there is no basis for discounting the
quantitative results from these studies completely in selecting an upper end of
range of consideration. Thus, staff recommends that weight be given to the
coherence of the entire body of epidemiological evidence, with support from
controlled human and animal studies, in limiting consideration to a level below
85 fig/in* for a new 24-hour PM2 5 standard.
2) The lower end of the range of consideration for a new 24-hour PM2.S standard
be 25 fig/m3. The key and supporting epidemiological studies relied upon to
assess the point at which increased risks of adverse health effects can be
clearly seen, taken together, suggest a range of levels from somewhat below
20 /xg/m3 to somewhat over 30 /xg/m3. In considering a 24-hour PM2.S level of
25 jig/m3 as the lower end of the range, the staff places significant weight on
the coherence of the study results, even in light of inherent uncertainties and
alternative interpretations possible for each study considered independently.
The staff believes that a 24-hour PM2 5 standard set at this level would be
precautionary in nature in protecting against a full range of short-term effects
associated with the identified sensitive subgroups of the population, giving less
weight to concerns that the relied-upon studies may not have completely
controlled for all potential confounding variables nor fully accounted for all
limitations in the exposure data.
3) In selecting a level for a 24-hour PM2 5 standard within this range, the
Administrator should consider the degree and nature of protection that will be
afforded by a new annual PM2 5 standard. The joint protection provided by a
suite of standards that includes both 24-hour and annual PM2 5 standards should
be considered in selecting the levels for each standard. One possible policy
approach would be to view an annual PM2 5 standard as serving as the primary
driving force for control programs that would effectively lower the entire
distribution of PM2 5 concentrations, thus serving to protect not only against
long-term effects but also short-term effects as well. With this approach, the
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24-hour PM2.5 standard would be set so as to protect against the occurrence of
peak 24-hour concentrations that would likely not be controlled by areas
attaining a new annual PM2.5 standard. Thus, in conjunction with an annual
PM2 5 standard, the Administrator may judge that the 24-hour standard should
be set so as to limit only those peak 24-hour concentrations that are likely to
persist upon attainment of the annual standard. The comparative air quality
data presented in Chapter IV (Table IV-8) shows approximately 90% of the
monitored PM25 annual-peak-to-mean ratios below 3.34 on average nationwide
(with a range from 3.1 in the southeast to 3.8 in the northwest). Thus,
considering the joint protection afforded by both 24-hour and annual standards
suggests, for example, that a 24-hour PM2 5 level of about 65 /tg/m3 might be
an appropriate complement to a 20 ftg/m3 annual PM2 5 standard.
b. Annual PM2 5 Standard
With regard to an annual PM2 5 standard, staff offers the following recommendations:
1) Staff recommends that the upper end of the range of consideration for a new
annual PM2 5 standard should be below 30 ^g/m3. This level, which is
approximately equivalent on average across the U.S. to the level of the current
annual PM10, contains no identifiable margin of safety and should not be
considered as an appropriate standard alternative. While the uncertainties
inherent in the most recent epidemiological studies are important margin of
safety considerations, staff believes there is no basis for discounting the
quantitative results from these studies completely in selecting an upper end of
range of consideration. Thus, the staff recommends that weight be given to
the coherence of the entire body of long-term epidemiological evidence, with
mechanistic support from controlled human and animal studies, in limiting
consideration to a level below 30 /*g/m3 for a new annual PM2 5 standard.
2) Staff recommends that the lower end of the range of consideration for a new
annual PM2 5 standard be 15 ^g/m3. A standard set at this level would place
greater weight on the full range of exposure-response relationships from the
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key mortality studies and on the staffs assessment of the levels at which
mortality risk clearly increases. In recommending this lower level of
consideration, staff recognizes that this level does not represent a threshold
below which there is no risk of premature mortality. Rather, the staff judges
that below this level the uncertainties in historical air quality and relevant
periods of exposure, as well as potential confounding by other environmental
and/or personal lifestyle factors, become sufficiently great as to serve as an
appropriate bound for a policy choice intended to avoid unacceptable risk.
3) The staff recommends that in selecting a level for an annual PM2 5 standard
within this range, the Administrator consider the degree and nature of
protection that will be afforded by a new 24-hour PM2 5 standard. The joint
protection provided by a suite of standards that includes both 24-hour and
annual PM2 5 standards should be considered in selecting the levels for each
standard.
4. Staff Conclusions and Recommendations for PMi0 Standards
The following staff conclusions and recommendations are based on a reexamination of
the previous conclusions regarding PM10 standards in light of the above recommendations
regarding fine particle standards and the body of evidence presented in the CD and Chapters
IV and V of this paper. The staff makes the following conclusions and recommendations
regarding PM10 standards:
1) Assuming a fine particle standard is established, the major function of the
PM10 standard is to protect against the known and anticipated effects associated
with coarse fraction particles in the size range of 2.5 to 10 /*m. It is difficult
to discern the incremental effects of coarse fraction particles from fine
particles in available community epidemiology studies.
2) Based on the assessment of the available studies, the staff finds that the best
evidence for drawing quantitative conclusions for PM10 comes from a long-
term cohort study of acute bronchitis in children in the Harvard Six City study
(Dockery et al., 1989). This study found somewhat better associations with
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PM15 than with PM2 5 over the entire cohort. This suggests that coarse
fraction particles, in combination with fine particles, may have influenced the
observed effects. From a mechanistic perspective, it is possible that prolonged
deposition of coarse fraction particles could be elevated in children, who are
more prone to be active outdoors than adults. Moreover, the major site of
thoracic deposition, the tracheobronchial region, would be expected to be the
region involved in the effects. It is of note that Dockery et al. (1989) is an
update of the study by Ware et al., (1986), which formed the main basis for
the level of the current annual PM10 standard. The staff concludes there is no
basis in the more recent study to alter the level and form of current annual
PM10 standard, which is 50 fig/m3, annual arithmetic mean.
3) The staff also considered other potential effects of annual coarse particle
exposures that were not evaluated in community epidemiology studies. These
include altered clearance, industrial bronchitis, and alveolar tissue damage;
such effects have been reported at levels much above those that would be
permitted under the standard. At levels nearer, but likely above the level of
the standard, autopsy studies found silicate pneumoconiosis associated with
particles that by analyses were consistent with exposure to crustal materials.
While these findings support retention of the current PM10 standard, they
provide no basis for changing the level.
4) The level of the current 24-hour PM]0 standard (150 /xg/m3) was based in large
measure on the London mortality and morbidity studies. As noted above, the
present assessment of the more numerous recent short-term studies has led to
the staff conclusion that such effects are far more likely to be associated with
fine particles. Accordingly, the staff recommends that these effects should be
addressed with a fine particle standard.
5) Available community studies conducted in areas with elevated coarse fraction
concentrations suggest that short-term effects occur at concentrations well
above the current standard. Johnson et al., (1992) found that an episode of
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very high concentrations of volcanic ash had little effect on pulmonary
function in a panel of school children. Hefflin et al., (1994) studied hospital
admissions in an agricultural community in eastern Washington. Short-term
exposures to PM,0 were associated with increased respiratory effects across the
year, which included both fine and coarse exposures. During a two week
period in which two windblown dust episodes occurred with particle levels
exceeding 1,000 /ig/m3, only hospital admissions for upper respiratory
infections showed an increase of even marginal significance. The authors
conclude that dust in the community has only a small effect on general
respiratory health.
6) Based on the lack of clear evidence for short-term effects of coarse fraction
particles at or near the level of the current PM10 standard, the staff examined
the relative protection afforded by the annual standard. Based on the typical
24 hour to annual ratios in Chapter IV, the annual standard would be expected
to provide substantial protection against the occurrence of high coarse fraction
concentrations. Using the average ratio of 3 (Table IV-6), an annual average
of 50 Atg/m3 would have a daily maximum of 150 jig/m3 or less. In areas with
more variability, the ratios can be larger, but are still likely to limit the peak
concentrations of coarse fraction particles from human derived activities to
levels below those expected to be associated with adverse health effects.
Using the data from Table IV-7, 95% of areas with an annual mean of 50
/tg/m3 would have 24-hour maxima below 250 /tg/m3.
7) In summary, the staff recommends retention of the current annual PM10
standard of 50 /xg/m3, annual arithmetic mean. This standard is judged to
provide adequate protection against the long-term and short-term effects
associated with the presence of coarse fraction particles.
D. Summary of Staff Recommendations
The major staff conclusions and recommendations made in sections VI.A-C above are
briefly summarized below:
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1) General PM standards remain a reasonable public health policy choice.
2) While the current PM10 standards provide protection from both fine and coarse
mode particles that are capable of penetrating to the most sensitive regions of
the human respiratory tract, the tracheobronchial and alveolar regions, the staff
concludes that the fine fraction of PM|0 is more likely to contain those physical
and chemical properties and components associated most strongly with a broad
array of adverse public health effects, including premature mortality as well as
various measures of increased morbidity in children and other sensitive
populations. Further, retaining PMIO as the sole indicator of PM would
continue to direct control efforts towards coarse fraction particles, which
available evidence suggests are of lower risk to health than the fine fraction.
Thus, a new fine particle indicator is recommended, to include those particles
with an aerodynamic diameter less than a nominal 2.5 ^m, in addition to
retention of a PM10 indicator to continue to limit coarse mode particle
pollution.
3) Staff recommends replacing the current 24-hour PM10 standard with a new 24-
hour PM25 standard, with a statistical expected exceedance form, and
supplementing the current annual PM10 standard with a new annual PM2 5
standard, with an arithmetic average form. This suite of indicators and
averaging times is judged to be sufficient to address all the components of PM
that have been associated with adverse health effects.
4) Based on the staffs assessment of the short-term epidemioiogical data, the
range of 24-hour PM2 5 levels of interest is 25 to less than 85 jig/m3. Given
the coherence of the body of short-term epidemioiogical evidence for increased
risk in areas where the current standard is attained and the seriousness of the
potential health effects, the upper end of the above range is judged to represent
a clear level of concern with no identifiable margin of safety and should not be
considered as an appropriate standard alternative. Although some degree of
increased risk to public health below 25 «g/m3 cannot be excluded,
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consideration of the entire body of epidemiological and controlled human and
animal studies do not suggest increased health risks of consequence below this
level. The uncertainties inherent in the epidemiological evidence, in particular
with regard to potential confounding by other environmental factors,
limitations on quantifying exposures, and differing judgments as to the public
health significance of the degree of prematurity of death observed in the
mortality studies, should be considered in evaluating margins of safety
associated with alternative 24-hour PM2 5 standards in the range of 25 /xg/m3 to
somewhat below 85 jtg/m3.
5) Based on the staffs assessment of the long-term epidemiological data, the
range of annual average PM2.5 levels of interest is 15 to less than 30 ^cg/m3.
Given the recent large-scale studies directly associating long-term PM2.5
exposure with premature mortality, the supporting evidence from other chronic
morbidity studies, and the seriousness of the potential health effects, the upper
end of the above range is judged to represent a clear level of concern with no
identifiable margin of safety and should not be considered as an appropriate
standard alternative. Although some degree of increased risk to public health
below 15 jig/m3 cannot be excluded, when uncertainties in historical exposures
and relevant exposure periods are considered, the epidemiological evidence
does not suggest increased risk of consequence below this level. The
uncertainties inherent in the epidemiological evidence, in particular with regard
to potential confounding by other environmental and personal/lifestyle factors
and limitations on quantifying exposures, should be considered in evaluating
margins of safety associated with alternative annual PM2 5 standards in the
range of 15 /*g/m3 to somewhat below 30 ftg/m3.
6) When selecting final PM2 5 standard levels, consideration should be given to
the joint protection afforded by the 24-hour and annual standards taken
together. For example, an annual PM2 5 standard at 20 /xg/m3 would be
expected to result in substantially reduced 24-hour levels, potentially limiting
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maximum 24-hour levels to less than about 65 /ig/m3 in approximately 90% of
the areas, thus adding to the protection against short-term effects afforded by a
24-hour standard.
7) Based on staff assessments of air quality, lexicological, and epidemiological
evidence available since the last review, retention of the current annual PM10
standard is recommended to provide ongoing control of coarse mode particles
for protection against known and anticipated adverse health effects associated
with both 24-hour and annual exposures.
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VH. CRITICAL ELEMENTS IN THE REVIEW OF THE SECONDARY STANDARD
FOR PARTICULATE MATTER
A. Introduction
This chapter presents critical information for the review of the secondary NAAQS for
particulate matter drawing upon the most relevant information contained in the CD. The
welfare effects of most concern for this review are visibility impairment, soiling, damage to
man-made materials, and damage to and deterioration of property. For each category of
effects, the chapter presents (1) a brief summary of the relevant scientific information and (2)
a staff assessment of whether the available information suggests consideration of secondary
standards different than the recommended primary standards. Staff conclusions and
recommendations related to the secondary standard for PM are presented at the end of the
chapter.
The chapter does not address in detail the effects of particles on climate change. As
discussed in the criteria document, particles (in the submicrometer size range) can result in
perturbations of the radiation field that are generally expressed as radiative forcing.
Radiative forcing due to aerosols has a cooling effect on climate through the reflection of
solar energy. This is in contrast to "greenhouse gas" that produces a positive long wave
radiative forcing which has a warming effect. Given the complex interaction of these two
phenomena and the present state of the science, it is the staffs judgment that these effects
should not be addressed in this paper, but should instead be considered in the broader context
of global climate change.
B. Effects of PM on Visibility
1. Types of Visibility Impairment
Visibility effects are manifested in two principal ways: (1) as local impairment (e.g.,
plumes and localized hazes) and (2) as regional haze. Local-scale impairment is defined as
impairment that is "reasonably attributable" to a single source or group of sources. This
type of impairment is considered to be an effect primarily due to nearby sources, although it
can be part of a larger, regional impairment. Visibility impairment in some urban areas can
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be dominated by local rather than regional sources, depending on site-specific geographical
and meteorological factors.
The second category of impairment, regional haze, is produced from a multitude of
sources and impairs visibility in every direction over a large area, such as an urban area, or
possibly over several states. Objects on the horizon are masked and the contrast of nearby
objects is reduced. In some cases, the haze may be elevated and appear as layers of
discoloration. Multiple sources may combine over many days to produce haze, which is
often regional in scale. The fate of regional haze is a function of meteorological and
chemical processes, sometimes causing fine particle loadings to remain suspended in the
atmosphere for long periods of time and to be transported long distances from their sources.
2. Social Valuation of Visibility
Visibility is an air quality-related value essential to people's enjoyment of daily
activities in all parts of the country. Survey research on public awareness of visual air
quality using direct questioning typically reveals that 80% or more of the respondents are
aware of poor visual air quality (Cohen et al., 1986). Individuals value good visibility for
the well-being it provides them directly, both in the places where they live and work, and in
the places where they enjoy recreational opportunities. Thousands of Americans appreciate
the scenic vistas in national parks and wilderness areas annually. Visibility is also highly
valued, however, because of the importance people place on protecting nationally significant
natural areas, both now and in the future. Many individuals want to protect such areas for
the benefit of future generations, even if they personally do not visit these areas very
frequently (Chestnut et al., 1994). Society also values visibility because of the significant
role it plays in air transportation. Serious episodes of visibility impairment can lead to
increased risks in the air transportation industry, particularly in urban areas with high traffic
levels (U.S. EPA, 19825).
Many contingent valuation studies have been performed in an attempt to quantify
benefits (or individuals' willingness to pay) associated with improvements in current visibility
conditions. The results of several studies are presented in table VII-1. As an example of the
potential value attributable to improvements in visibility, a recent study estimates visibility
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VII-2a
Table VII-1. Comparison of Residential Visibility
Valuation Study Results
Study
Eastern CVM Studies
McCleUand et al.5
Tolley et al.4
TolleyetaP
ToUey ctal6
Tolley et al*
Tolley et al6
ToUeyetal6
Tolley et a?
Rae7
California CVM
Studies
Brooksirc et al.'
Lochman et ar
California Property
Value Sutdy
Trijonis et aln
Trijonis et al'°
Chy
Atlanta and
Chicago
Chicago
Atlanta
Boston
Mobile
Washington, DC
Cincinnati
Miami
Cincinnati
Los Angeles
San Francisco
•
Los Angeles
San Francisco
MeanWTP
($1990)
Unadj. $39
Partial $25
Full $18
-$318
$305
$379
-$265
$255
$381
-$196
$187
$231
-$212
$227
$266
-$314
$323
$410
-$78
$77
$86
4134
$120
$141
$175
$115
$294
$161
-$186
$109
Suiting VR
(miles)
17.6
9
9
9
12
12
12
18
18
18
10
10
10
15
15
15
9
9
9
13
13
13
11.4
2
2
12
18.6
16.3
Ending VR
(miles)
20
4
18
30
7
22
32
13
28
38
5
20
30
10
25
35
4
19
29
8
19
29
16.4
12
28
28
16.3
18.6
b
coefficient
305
196
140
367
414
372
275
560
106
226
531 '
105
1172
WTPfor
20% changes
VR(3)
$56
$36
$26
$67
$75
$68
$68
$102
$17
$41
$97
$19
$214
$216-$579
$437-$487
Note: VR - Visual Range
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benefits due to reduced sulfur dioxide emissions under the acid rain program to be quite
significant, in the range of $1.7 - 2.5 billion annually by the year 2010 (Chestnut et al.,
1994).
3. Visibility-Impairing Particles
Visibility impairment has been considered the "best understood and most easily
measured effect of air pollution" (Council on Environmental Quality, 1978). It is perhaps
the most noticeable effect of fine particles (i.e., those with an aerodynamic diameter less than
2.5 /*m) present in the atmosphere. Fine particles are effective in impairing visibility
because the mean diameter of fine particles is usually less than or only slightly greater than
the wavelength range of visible light, and light scattering is at a maximum when the
wavelength is comparable to the particle diameter. Fine particles in the size range from 0.1
to 1.0 nm in diameter are more effective per unit mass concentration at impairing visibility
than either larger or smaller particles (NAPAP, 1991).
Air pollution degrades the visual appearance of distant objects to an observer, and
reduces the range at which they can be distinguished from the background. Particles affect
color of distant objects depending upon particle size, composition, scattering angle between
observer and illumination, and optical characteristics of the background target.
Fine particles, which can be emitted directly to the atmosphere through primary
emissions or formed secondarily from gaseous precursors, impair visibility by scattering or
absorbing light. Different types of particles have varying efficiencies in causing visibility
impairment.
The fine particles (and associated paniculate water) principally responsible for
visibility impairment are sulfates, nitrates, organic matter, elemental carbon (soot), and soil
dust. Coarse particles (i.e., those in the 2.5 to 10 ^m size range) also impair visibility,
although less efficiently than fine particles. Sulfates and nitrates readily absorb water from
the atmosphere and grow in size in a nonlinear fashion as relative humidity levels increase.
Soluble organics are considered to be less hygroscopic than sulfates and nitrates (Sisler,
1993). All of these particles scatter light. Light absorption is caused mainly by elemental
carbon.
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Sulfates, nitrates, and some organic particles begin as gaseous emissions and undergo
chemical transformation in the atmosphere. These fine particles and their precursors can
remain in the atmosphere for several days and can be carried hundreds or even thousands of
kilometers from their sources to remote locations, such as national parks and wilderness
areas (NRC, 1993).
4. Metrics for Expressing Visibility Impairment and Light Extinction.
Daytime visibility is determined the competition between transmitted radiance and
path radiance. Transmitted radiance comes from the object being viewed and contains all of
the information about that object available to the observer. Path radiance is scattered by the
atmosphere into the line of sight, and contains no information about the object being viewed.
When path radiance dominates transmitted radiance, as in a dense fog, visibility is poor.
Path radiance is used in models that calculate visibility as a function of particle
concentration, composition, and size.
Light extinction is an optical property of each point in the atmosphere and is closely
linked to air quality. In itself, light extinction is not the best indicator of visibility for a
specific scene. However, light extinction is a useful measure of haze because it represents
the effect that gases and aerosols have on changes in path radiance. Therefore, light
extinction is a useful indicator of visibility for regulatory purposes.
The light extinction coefficient can be defined as the fraction of light lost or
redirected per unit distance through interactions with gases and suspended particles in the
atmosphere. This coefficient is typically expressed in terms of inverse kilometers or
megameters (km'1 or Mm"1). Direct relationships exist between the concentrations of particle
types and their contributions to the extinction coefficient. By apportioning the extinction
coefficient to different particle types, one can estimate changes in visibility due to changes in
constituent concentrations (Pitchford and Malm, 1994).
The extinction coefficient is inversely related to visual range. Conversion from light
extinction coefficient to visual range can be done with the following equation: Standard
visual range (in kilometers) = 3.912 / light extinction coefficient (in M'^CNAPAP, 1991).
Visual range can be defined as the maximum distance (i.e., miles or kilometers) at which one
-------
External Review Draft £)o Not Quote or Cite
November 1995 VII-5
can identify an object against a uniform background. Visual range has been widely used in
air transportation and military operations in addition to its use in characterizing air quality.
Because it is expressed in familiar units and has a straightforward definition, visual range is
likely to continue as a popular measure of atmospheric visibility (Pitchford and Malm, 1994).
Another important visibility metric is the deciview, which measures perceived
haziness. It is designed to be linear with respect to perceived visual changes over its entire
range in a way that is analogous to the decibel scale for sound (Pitchford and Malm, 1994).
Neither visual range nor the extinction coefficient has this property. For example, a 5 km
change in visual range or 0.01 km"1 change in extinction coefficient can result in a change
that is either imperceptible or very apparent depending on baseline visibility conditions.
Deciview allows one to more effectively express perceptible changes in visibility, regardless
of baseline conditions. A one deciview change is a small but perceptible scenic change under
many conditions, approximately equal to a 10% change in the extinction coefficient. The
deciview metric may be useful for defining perceptible changes in future regulatory
programs. Figure VII-1 illustrates the relationships between these three visibility metrics.
5. Overview of Current Visibility Conditions
Visibility conditions vary regionally, as a function of background levels of fine
particles, average relative humidity levels, and generally higher anthropogenic particle
loadings in the East as opposed to the West. An overview of current visibility conditions,
developed from monitored aerosol concentrations and expressed in terms of the light
extinction coefficient, is provided in figure VII-2 (Sisler et ai., 1993). Median standard
visual range in the rural mountain and desert, areas of the Southwest average 130-190 km,
whereas median visual range in the rural areas south of the Great Lakes and east of the
Mississippi River is between 20 and 35 km.
Most of this six-fold difference between East and West is due to greater sulfate
concentrations in the East and the effect of higher humidity levels in the East (NAPAP,
1991). Studies of historical visibility trends have shown a fairly strong correlation between
long-term light extinction levels and sulfur dioxide emissions. Figure VII-3 illustrates this
correlation for the southeastern U.S.
-------
VII-5a
1.6 T,
Extinction Coefficient
• ' Visual Range
20 25 30
Haziness (dv)
Figure VII-1. Visual range and extinction coefficient as a
function of haziness expressed in deciview.
-------
VII-5b
(a). Total light extinction b^ (Mm"1)
(b). Extinction due to coarse particles and fine soil (Mm"1)
Figure VII-2. Average reconstructed light extinction coefficient
(Mm'1) calculated from the aerosol concentrations measured during
the first three years of IMPROVE, March 1988 through February
1991. The various panels of this figure show total extinction
(including Rayleigh scattering due to air) and the contributions
due to the various aerosol components: coarse particles and
soil, sulfate, organic carbon, nitrate, and light-absorbing
carbon.
-------
03
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External Review Draft Do Not Quote or Cite
November 1995 VII-6
The following sections further explain the reasons for regional variability in visibility
impairment.
6. Estimated Background Levels of Fine Particles and Associated Light Extinction
Total light extinction is determined by the combined effects of fine particles from
background (i.e., natural) sources, Rayleigh scattering, and fine particles from anthropogenic
sources. The 1990 National Acid Precipitation Assessment Program report estimated annual
average background levels of fine particles by particle type, and related contributions to light
extinction, expressed in inverse megameters (Mnr1) (NAPAP, 1991). Table VII-2, shows
that background fine particle concentrations are estimated at 3.32 ^g/m3 in the East and 1.47
jtg/m3 in the West.
The contribution of each particle type to total light extinction is derived by
multiplying the estimated average concentration by the extinction efficiency for that particle
type. Extinction efficiencies used in table VII-2 are for "dry" particles only. Associated
water is expressed as a separate particle type.
Other studies have used slightly different extinction efficiencies for dry particles than
those found in table VII-2. For example, Sisler et al. (1993) used the dry extinction
efficiencies in table VII-3 in an analysis of monitoring data collected from the Interagency
Monitoring of Protected Visual Environments (IMPROVE) visibility monitoring network, a
cooperative program in place since 1986 involving several Federal agencies and State
representatives.
7. Role of Humidity in Light Extinction
As mentioned previously, humidity plays a significant role in the impairment of
visibility by fine particles, particularly in the East, where annual average relative humidity
levels are 70-80% as compared to 50-60% in the West (Sisler et al., 1993). Two ways that
the effect of humidity on light extinction can be represented are by including water as a
separate particle type (as is done in table VII-2), or by multiplying particle-specific extinction
efficiencies by correction factors representing ]) the hygroscopic nature of the particle, and
2) the average annual humidity for the relevant location (Sisler et al., 1993).
-------
VII-6a
Table VII-2
Average Natural Background Levels of Aerosols
and Light Extinction
Average Concentration
FINE PARTICLES (<2.5 urn)
Sulfates (as NH4 HSO4)
Organics
Elemental Carbon
Ammonium Nitrate
Soil Dust
Water
East
fig/m3
0.2
1.5
0.02
0.1
0.5
1.0
West
Jig/m3
0.1
0.5
0.02
0.1
0.5
0.25
Error
Factor
2
2
2-3
2
1 '/2 -2
2
Extinction
Efficiencies*
m2/g
2.5
3.75
10.5
2.5
1.25
5
Extinction Contributions
East
Mm'1
0.5
5.6
0.2
0.2
0.6
5.0
West
Mm'1
0.2
1.9
0.2
0.2
0.6
1.2
COARSE PARTICLES (2.5-10 \im)
3.0
3.0
0.6
1.8
1.8
RAYLEIGH SCATTER
TOTAL
12
26 ±7
11
1712.5
'The extinction efficiencies are based on the literature review by Trijonis ct al. (19S6 & 1988). All the extinction efficiencies represent
particle scattering, except for elemental carbon where the 10.5 m2/g value is assumed to consist of 9 m2/g absorption and 1.5 m2/g
scattering. Note that the 0.6 m2/g value for coarse particles is a "pseudo-coarse scattering efficiency" representing the total scattering by
all ambient coarse particles (< 2.5 Jim) divided by the coarse particle mass between 2.5 and 10 ujn.
-------
VII-6b
Particle
Type
sulfates
organics
elemental carbon
nitrates
soil dust
coarse particles
Extinction
Efficiency
(in m2/g)
3.0
3.0
10.0
3.0
1.0
0.6
Source: Sisler et al. 1993
Table VII-3. Dry particle light extinction efficiency values used in 1993
analysis of IMPROVE data.
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External Review Draft Do Not Quote or Cite
November 1995 VH-7
Because annual average relative humidity is higher in the East, the same ambient
concentration of sulfate, for example, will on average lead to greater light extinction in an
eastern location rather than a western one. The top map in figure VII-4 illustrates the
regional variability of annual mean relative humidity nationwide. The bottom map depicts
the variability of the relative humidity correction factor used for sulfates in the IMPROVE
analysis (Sisler et al., 1993). For example, when corrected for humidity, the overall
extinction efficiency for sulfates in the East may exceed 11-12 m2/g, whereas the extinction
efficiency for sulfate in the West may be one-third to one-half of that.
8. Rayleigh Scattering
Table VII-2 shows the contribution to total light extinction from "Rayleigh scatter."
Rayleigh scattering represents the degree of light extinction found in a particle-free
atmosphere, caused by the gas molecules that make up "blue sky" (e.g., N2, 02, CO2 )(U.S.
EPA, 1979). Rayleigh scattering thus can be used to establish a maximum horizontal visual
range in the earth's atmosphere, absent visibility-impairing particles. At sea level, this
maximum visual range is approximately 326 kilometers (equivalent to light extinction of 12
Mm"1). While Rayleigh scattering can be shown to establish this maximum visual range, it
should not be considered to contribute to visibility impairment. Rather, only fine and coarse
particles from natural and anthropogenic sources should be considered responsible for
impairing visibility (from the maximum visual range "baseline" established by Rayleigh
scattering).
Estimated extinction contributions from Rayleigh scattering and background levels of
fine and coarse particles, in the absence of anthropogenic emissions of visibility-impairing
particles, are estimated to result in a visual range in the East of 150+/- 45 kilometers and
230 +/- 40 km in the West. NAPAP (1991) estimated that the major contributors to
nonanthropogenic light extinction levels in the East are Rayleigh scattering (46%), organics
(22%), water (19%), and suspended dust, including coarse particles (9%). The major
contributors in the West are Rayleigh scattering (64%), suspended dust (14%), organics
(11%), and water (7%). Thus, higher levels of background fine particles in the East result
in a fairly significant difference between maximum visual range estimates in the East and West.
-------
JU* 90
VII-7a
(a) Annual mean relative humidity.
3-84.2
Figure VII-4,
(b) F^
Spatial variation in average relative humidity (NOAA, 1978) and the
sulfate RH correction factor Fr
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External Review Draft Do Not Quote or Cite
November 1995 VII-8
9. Significance of Anthropogenic Sources of Fine Particles
The concentrations of background fine particles are generally small when compared
with concentrations of fine particles from anthropogenic sources. The same relationship
holds true when one compares light extinction due to background fine particles with light
extinction due to anthropogenic fine particles. Man-made contributions account for about
one-third of the average extinction coefficient in the rural West and more than 80% in the
rural East (NAPAP, 1991).
This fact is well-documented by data from the IMPROVE visibility monitoring
network (Sisler et al., 1993). Table VH-4 compares total light extinction (from background
and anthropogenic sources) with light extinction due only to natural sources for. several
locations across the country. The table demonstrates the significant role in most parts of the
country of anthropogenic emissions in overall light extinction as compared to background
fine particle levels.
It should be noted that even in those areas with relatively low concentrations of
anthropogenic fine particles, such as the Colorado plateau, small increases in anthropogenic
fine particle concentrations can lead to significant decreases in visual range. National
concern with protecting visibility in the highly valued national parks and wilderness areas in
this region led to the inclusion of specific language in section 169B of the 1990 Clean Air
Act Amendments, requiring EPA to form the Grand Canyon Visibility Transport
Commission. The Commission is required to provide the Administrator with
recommendations for protecting regional visibility in the future.
10. Regional Differences in Anthropogenic Pollutant Levels
While total light extinction levels vary significantly across the country, so does the
mix of visibility-impairing pollutants from region to region. Table VII-5, taken from the
1993 National Academy of.Sciences (NAS) study on visibility, shows the estimated
contribution of various anthropogenic pollutants to visibility impairment for three main
regions of the U.S. The table takes into account relative emissions levels of each pollutant
type within each region. This and other analyses (Sisler et al., 1993) show that sulfates are a
significant cause of visibility impairment in all parts of the country, but particularly in the
-------
VII-8a
REGION
Eastern U.S., estimated
natural light extinction
Appalachian
Boundary Waters
Northeast
Washington, D.C.
Western U.S., estimated
natural light extinction
Colorado Plateau
Cascades
Southern California
Northern Rockies
TOTAL LIGHT
EXTINCTION, 1988-
1991
(in Mm'1)
Annual
26 +/- 7
112
68
71
164
17 +/- 2.5
27
59
63
54
Summer
NA
193
73
88
192
NA
29
68
76
46
VISUAL
RANGE
(in km)
Annual
150 +/- 45
35
58
55
24
230 +/-40
145
66
62
72
Summer
NA
20
54
44
20
NA
135
58
51
85
bource: Sisler a al. 1993
Table VII-4. Comparison of total light extinction to estimated natural light extinction for
several eastern and western locations.
-------
VII-8b
Table VII-5
Visibility Model Results: Anthropogenic Light
Extinction Budgets"
East" Southwest0 Northwest1
Sulfates
Organics
Elemental carbon
Suspended dust
Nitrates
Nitrogen dioxide
65
14
11
2
5
3
39
18
14
15
9
5
33
28
15
7
13
4
"Percentage contribution by specific pollutant to anthropogenic
light extinction in three regions of the United States.
bBased on Table 9, Table 18, Figure 45, Appendix A, and Appendix
E of NAPAP Visibility SOS/T Report (Trijonis et al., 1990). It is
assumed that sulfates (3% natural) account for 60% of non-
Rayleigh extinction, organics (33% natural) account for 18%,
elemental carbon (3% natural) accounts for 10%, suspended dust
(50% natural) accounts for 4%, nitrates (10% natural) account for
5%, and nitrogen dioxide (10% natural) accounts for 3%.
'Based on Table 9, Table 18, Figure 45, Appendix A, and Appendix
E of the NAPAP Visibility SOS/T Report (Trijonis et al., 1990).
It is assumed that sulfates (10% natural) account for 33% of non-
Rayleigh extinction, organics (33% natural) account for 20%,
elemental carbon (10% natural) accounts for 12%, suspended dust
(50% natural) accounts for 23%, nitrates (105 natural) account
for 8%, and nitrogen dioxide (10% natural) accounts for 4%.
dExtinction efficiencies (relative to organics are chosen as 1.5
for sulfates, 2.5 for elemental carbon, 0.3 for fine crustal
materials, and 1.5 for nitrates (Trijonis et al., 1988, 1990).
Coarse dust extinction is assumed to be three times fine dust
extinction (Trijonis et al., 1988, 1990). Natural aerosol
particle fractions are assumed to be one-tenth for sulfates, one-
third for organics one-tenth for elemental carbon, one-half for
crustal materials, and one-tenth for nitrates. These assumptions
are applied using the fine mass concentrations in Trijonis et
al., (1990). The percentage contribution for nitrogen dioxide is
assumed to be 4%.
-------
External Revie\v Draft Do Not Quote or Cite
November 1995 VII-9
East, where they are responsible for about two-thirds of overall light extinction. In the
Southwest and Northwest, organics play a larger role, as does elemental carbon. Suspended
dust is also a major constituent in the southwest. The main source categories responsible for
visibility-impairing fine particle and precursor emissions are listed in table VII-6 (NAS,
1993).
11. Regional Variation in Urban Visibility
Visibility impairment has been studied in several major cities in the past decade (e.g.
Middleton, 1993) because of concerns about fine particles and their potentially significant
impacts (e.g., aesthetic and health-related) on the many residents of large metropolitan areas.
Urban areas generally have higher loadings of fine paniculate matter than monitored class I
areas, and they demonstrate significant variability in the degree to which different pollutant
types contribute to overall light extinction. Table VII-7 illustrates annual average and
second-highest maximum fine PM levels for various cities in the U.S.
Table VII-8 illustrates the difference between percentage contributions of particle
types to annual average total light extinction in the Washington, DC urban area and the
southern California areas. The dominance of sulfate in Washington, DC exhibits a regional
effect stemming from sulfur dioxide emissions outside the metropolitan area. In contrast,
nitrate plays the greatest role in the overall light extinction levels in the mountainous areas
just outside Los Angeles, with most of the nitrate formation in this area coming from
nitrogen dioxide emissions within the urban area.
12. Staff Considerations Pertaining to the Effects of PM on Visibility
Impairment of visibility in multi-state regions, urban areas, and class I areas (i.e.,
certain national parks, wilderness areas, and international parks as described in section
162(a) of the Act) is clearly an adverse effect on public welfare. The staff has considered a
number of factors in assessing an appropriate regulatory response.
An initial question is whether the range of recommended primary standards for fine
PM would provide adequate protection against visibility impairment across the country. The
range being considered for an annual PM-fine standard is J 5 //g/m3 to less than 30 /xg/m3 and
the range under consideration for a 24-hour standard is 25 //g/m7 to less than 85 /zg/m'.
-------
Table VII-6
PERCENTAGE CONTRIBUTION BY SOURCE CATEGORY TO FINE PARTICLE
(AND PRECURSOR) EMISSIONS IN THE EAST. SOUTHWEST, AND NORTHWEST
EAST
Electric utilities
Diesel-fueled mobile sources
Gasoline vehicles
Petroleum and chemical industries
Industrial coal combustion
Residential wood burning
Fugitive dust (on-road/off-road traffic)
Feedlots and livestock waste mgmt.
Miscellaneous
SOUTHWEST
Electric utilities
Diesel-fueled mobile sources
Gasoline vehicles
Petroleum and chemical industries
Copper smelters
Fugitive dust (on-road/off-road traffic)
Residential wood burning
Feedlots and livestock waste mgmt.
Miscellaneous
NORTHWEST
Electric utilities
Diesel-fueled mobile sources
Gasoline vehicles
Petroleum and chemical industries
Residential wood burning
Forest management burning
Fugitive dust (on-road/off-road traffic)
Feedlots and livestock waste mgmt.
Primary metallurgical process
Organic solvent evaporation
Miscellaneous
SOx
78.0
1.5
1.0
4.5
7.0
—
—
—
8.0
SOx
33
12
5
22
19
-
-
-
9
SOx
30
12
4
19
-
-
-
-
8
-
27
Organic
Particles
_
-
34
—
-
20
_
-
46
Organic
Particles
_
5
38
—
-
-
8
-
49
Organic
Particles
-
-
15
-
22
45
-
-
-
-
18
VOC's
_
-
31
11
-
13
—
-
45
VOC's
_
_
42
12
-
-
5
-
41
VOC's
-
-
31
10
25
13
-
-
15
15
6
Elemental
Carbon
_
47
29
_
-
15
—
-
9
Elemental
Carbon
_
52
31
—
-
-
6
-
11
Elemental
Carbon
—
37
16
-
22
20
-
-
-
-
5
Suspended
Dust
_
-
-
—
-
—
100
—
-
Suspended
Dust
_
_
-
_
-
100
-
—
-
Suspended
Dust
—
-
-
-
—
-
100
—
-
_
-
NH3
-
-
-
—
-
—
-
66
34
NH3
_
—
-
—
-
—
-
75
25
NH3
—
—
-
-
-
-
—
81
—
—
19
NOx
39
16
26
—
-
—
—
-
19
NOx
19
23
32
_
—
—
-
_
26
NOx
8
29
36
-
-
-
—
_
-
—
27
Source: National Research Council, Protecting Visibility in National Parks and Wilderness Areas. National Academy Press, 1993.
-------
VII-9b
LOCATION
Archuleta County, CO
Baltimore, MD
Boston, MA
Cleveland, OH
Columbia, SC
Dallas-Fort Worth, TX
Detroit, MI
El Paso, TX
Fresno, CA
Houston, TX
Los Angeles-Long Beach, CA
Minneapolis, MN
Nashville, TN
New York, NY
Philadelphia, PA
Pittsburgh, PA
Portland, OR
Portland, ME
Riverside, CA
Salt Lake City, UT
St. Louis, MO
Steubenville, OH
Syracuse, NY
Winston-Salem, NC
NUMBER
OF
MONITORS
1
2
1
1
2
1
4
1
3
1
2
1
1
4
1
2
5
1
2
3
6
4
2
2
ANNUAL MEAN,
RANGE OF
HIGHEST VALUES
FOR DIFFERENT
MONITORS,
YEARS 1983-1993
(in /ig/m3)
22.7
24.7-26.1
20.2
28.4
22.3 - 33.0*
13.6
17.3 - 25.4*
14.5
15.4 - 26.0
16.6
27.5 - 32.0
13.6
28.6
21.9 - 47.0*
26.0
25.7 - 26.6
10.2 17.2
39.9*
11.0-43.3
14.0 - 52.9*
14.7 16.9
16.6 - 25.7
20.0-40.8*
23.4 24.7
SECOND HIGHEST
MAXIMUM 24-HOUR
VALUE,
RANGE OF HIGHEST
VALUES FOR DIFFERENT
MONITORS, YEARS 1983-
1993 (in Mg/m3)
48
45- 106
55
55
43 -60
37
44-73
58
58 100
37
70 - 88
38
64
51 -91
47
59 82
19-60
50
22 - 114
14-91
38 -49
42- 81
47 -72
51 -56
Source: U.S. EPA, monitored values from AIRS database
*These dau are unreliable due to incomplete and/or unrepresentative monitoring.
Table VII-7 Annual Average and Second Highest Maximum Fine PM Levels for
Selected U.S. Cities.
-------
VII-9c
Location
Wash,
DC
So.
Calif.
Sulfate
49.0
14.4
Nitrate
16.0
44.4
Organics
16.2
18.2
Elemental
Carbon
11.9
9.0
Soil and
Coarse
6.9
13.9
Source: Sisler « al. 1993
Table VII-8. Percentage contributions of particle types to annual
average total light extinction in the Washington, D.C. and southern
California areas.
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External Review Draft DO Not Quote or Cite
November 1995 VII-10
Table Vn-7 presents monitored fine particle annual averages and second highest maximum
levels for several major U.S. cities. Analysis of these data suggests that adoption of an
annual fine particle standard in the lower half of the recommended range, in combination
with adoption of a 24-hour standard in the lower half of the recommended range, would be
expected to lead to reductions in annual average fine particle concentrations in many urban
areas nationally, and possibly in broader areas in the East if regional attainment strategies are
emphasized. To examine any expected visibility improvement resulting from these
reductions requires an understanding of the relationship between fine particle loadings and
visibility. Figure VH-5 shows that visibility change is sensitive to current fine particle
concentrations and their associated extinction efficiency. To achieve a given amount of
visibility improvement, a larger reduction in fine particle concentration is required in areas
with higher existing concentrations, such as the East. Expected reductions in fine particle
concentrations resulting from adoption of the primary fine particle standards in the lower half
of the recommended range is expected to result in maintained or improved visibility in many
urban areas and in a broader area in the East. Improvement of visibility would be greater if
regional fine particle attainment strategies are emphasized. In its 1993 Report to Congress
on the effects of Clean Air Act programs on visibility in mandatory federal Class I areas,
EPA examined the impact of expected regional sulfur dioxide reductions under the acid rain
program (U. S. EPA 1993). This report estimated that regional sulfate levels would be
reduced over a wide area in the eastern U.S. by the year 2010, resulting in potential
improvements in annual average visibility for the region. The analysis projected no expected
improvement in the rural West. Any additional regional strategies to attain fine particle
standards could lead to further visibility improvements, particularly in the East. However,
there is no evidence that adoption of the primary fine particle standards in the lower half of
the recommended range will eliminate adverse impacts of fine particles on visibility.
-------
Vll-lOa
400
bRg = 0.01 km'1
bext/FINE MASS = 0.004 krTT1/Mg/m3
HUMIDITY<60%
ARROWS INDICATE
ADDITION OF 1 //g/m3
OF FINE PARTICLES
10 20 30 40
FINE PARTICLE CONCENTRATION, pg/rrT3
Figure VII-5. Effects of fine particle increments on calculated visual range. Addition of 1
/Ag/m3 to a clean atmosphere reduces visual range by 30 percent. Addition of the same
amount when background visual range is 35 km (20 miles) produces a 3 percent reduction.
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External Review Draft Do Not Quote or Cite
November 1995 VII-11
The staff has also considered whether the adoption of a national secondary standard
would provide adequate protection of public welfare across the country. Due to the regional
variability in background fine particle levels, the staff has concluded that a national
secondary standard could not achieve this objective. The data presented in table VII-4
indicates that current annual average light extinction levels on the Colorado plateau are about
equal to background levels in the East. In other words, a national secondary standard set to
maintain or improve visibility conditions in the Colorado plateau would have to be set at or
below natural background levels in the East. Conversely, a national secondary standard that
would be both attainable and improve visibility in the East would permit further degradation
in the West.
A more promising option is to establish a regional haze program under section 169A
of the Clean Air Act, which would address the existing adverse effects of fine particles on
visibility in both class I and non-class I areas. Section 169A established a national goal of
"the prevention of any future, and the remedying of any existing, manmade impairment of
visibility in mandatory class I areas." The EPA is required to establish programs to ensure
reasonable progress toward the national goal. These programs are to be implemented by the
States and can be regionally specific.
Much progress has been made in technical areas important to the successful
implementation of a regional haze program, including areas such as visibility monitoring,
regional scale modeling, and scientific knowledge of the regional effects of particles on
visibility. The National Academy of Sciences 1993 report on visibility protection confirmed
this point:
Current scientific knowledge is adequate and control technologies are available
for taking regulatory action to improve and protect visibility. However,
continued national progress toward this goal will require a greater commitment
toward atmospheric research, monitoring, and emissions control research and
development.
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External Review Draft Do Not Quote or Cite
November 1995 VII-12
In addition, it is expected that the development of a regional haze program will have
associated benefits outside of mandatory class I areas. The National Academy of Sciences
concluded that:
Efforts to improve visibility in Class I areas also would benefit visibility
outside these areas. Because most visibility impairment is regional in scale,
the same haze that degrades visibility within or looking out from a national
park also degrades visibility outside it. Class I areas cannot be regarded as
potential islands of clean air in a polluted sea.
Based on the above considerations, the staff recommends that the Administrator
consider establishing a regional haze program under section 169A of the Act, in conjunction
with the recommended fine particle primary standards, as the most effective means of
addressing the welfare effects associated with visibility impairment. Together, the two
programs and associated control strategies should adequately protect against the adverse
effects of fine particle pollutants on visibility.
C. Effects of PM on Materials Damage and Soiling
The deposition of airborne particles can become a nuisance, reducing the aesthetic
appeal of buildings and culturally important articles through soiling, and contribute directly
(or in conjunction with other pollutants) to structural damage by means of corrosion or
erosion. These potential effects are discussed more fully below. The relative importance of
particle size, composition, and other environmental factors (i.e., moisture, temperature,
sunlight, and wind) in contributing to the effects is also considered.
1. Materials Damage
Particles affect materials principally by promoting and accelerating the corrosion of
metals, by degrading paints, and by deteriorating building materials such as concrete and
limestone. Particles contribute to these effects because of their electrolytic, hygroscopic, and
acidic properties, and their ability to sorb corrosive gases (principally sulfur dioxide). The
staff review suggests that only chemically active fine mode or hygroscopic coarse mode
(mainly sea or road salt) particles contribute to such effects (U.S. EPA, 1986b). While
particles have been qualitatively associated with damage to materials, there are insufficient
data at present to relate such effects to specific particle pollution levels. The following
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discussion briefly outlines the available information on PM-related effects associated with
each category of material presented in the criteria document.
a. Effects on Metals
The rate of metal corrosion depends on a number of factors, including the deposition
rate and nature of the pollutant; the influence of the metal protective corrosion film; the
amount of moisture present; variability in the electrochemical reactions; the presence and
concentration of other surface electrolytes; and the orientation of the metal surface (CD,
Chapter 9). This section briefly discusses the factors affecting metal corrosion set forth in
the criteria document.
Nriagu (1978) and Sydberger (1977) conducted studies that highlighted the ability
metals have to form a protective film that slows corrosion rates. Metals initially exposed to
low concentrations of SOX corroded at a slower rate than did samples continuously exposed to
higher concentrations. This protective corrosion layer may, however, be affected by either
dry or wet deposition (CD, Chapter 9).
The rate of metal corrosion decreases in the absence of moisture (CD, Chapter 9).
Moisture influences corrosion rates by providing a medium of conduction paths for
electrochemical reactions and a medium for water soluble air pollutants. Schwartz (1972)
established that the corrosion rate of a metal could increase by 20 percent for each one
percent increase in relative humidity above the minimum atmospheric moisture content that
allows corrosion to occur (i.e., critical relative humidity). Later studies by Haynie and
Upham (1974) and Sydberger and Ericsson (1977) supported Schwartz's theory.
While particles alone have some effect on the early stages of metal corrosion, there is
insufficient evidence to relate such effects to specific particle levels. One study (Goodwin et
al. (1969)) reported damage to steel, protected with nylon screen, exposed to quartz particles
larger than 5 jim; but the exposure time and concentration were not reported. Barton (1958)
also found that dust contributed to the early stages of metal corrosion. A number of the
studies evaluated concluded that particulate matter increased the corrosion rate of sulfur
dioxides (Sanyal and Singhania, (1956); Yocom and Grappone, (1976); Johnson et al.,
(1977); Russell, (1976); Walton et al., (1982)). Laboratory studies show mixed results as to
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whether catalytic species or conductance of the thin-film surface electrolyte is the cause of
the increases in corrosion rates (Walton et al., 1982; Skerry et al., 1988 a,b; Askey et al.,
1993).
Results of actual field studies have not established a quantitative relationship between
particles and corrosion. Thus, the independent effect of particles is not evident since SOj is
the controlling factor for determining corrosion rate (U.S. EPA, 1986b). Edney et al. (1989)
exposed galvanized steel panels to actual field conditions in Research Triangle Park, NC and
Steubenville, OH between April 25 and December 28, 1987. The panels were exposed under
the following conditions: (1) dry deposition only; (2) dry plus ambient wet deposition; and
(3) dry deposition plus deionized water. The average concentrations for SO2 and paniculate
matter was 22 ppb and 70 /*g/m3 and < 1 ppb and 32 /tg/m3 for Steubenville and Research
Triangle Park, respectively. The runoff from the steel panel was analyzed and it was
concluded that the dissolution of the steel corrosion products for both sites was likely the
result of deposited gas phase SO^ on the metal surface and not paniculate matter.
Another study conducted by Butlin et al. (1992) also demonstrated that the corrosion of mild
steel and galvanized steel was SO2-dependent. Butlin et al. monitored the corrosion of steel
samples by SO2 and ozone under artificially fumigated environments, and NO2 under natural
conditions. Annual average SO2 concentrations ranged from 2.1 jtg/m3 in a rural area to 60
ptg/m3 in on of the SCVfuniigated locations. Annual average NO2 concentrations ranged
from 1.5 to 61.8 ptg/m3. The study concluded that corrosion of the steel samples was
primarily dependent on the long-term SO2 concentration and was only minimally affected by
nitrogen oxides.
b. Effects on Paint
Paints undergo natural weathering processes from exposure to environmental factors
such as sunlight, moisture, .fungi, and varying temperatures. In addition to the natural
environmental factors, studies show paniculate matter exposure may give painted surfaces a
dirty appearance (CD, Chapter 9). Several studies also suggest that particles serve as
carriers of other more corrosive pollutants, allowing the pollutants to reach the underlying
surface or serve as concentration sites for other pollutants (Cowling and Roberts, 1954).
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A number of studies have shown some correlation between paniculate matter and
damage to automobile finishes. Fochtman and Langer (1957) reported damage to automobile
finishes due to iron particles emitted from nearby industrial facilities. General Motors
conducted field tests in Jacksonville, Florida to determine the effect of various
meteorological events, the chemical composition of rain and dew, and the ambient air
composition during the event, on automotive paint finishes. Painted (basecoat/clearcoat
technology) steel panels were exposed for varying time periods, under protected and
unprotected condition. The researcher concluded that calcium sulfate formed on the painted
surface by the reaction of calcium from dust and sulfuric acid contained in rain or dew. The
damage to the paint finish increased with increasing days of exposure (Wolff et al., 1990).
Paint films permeable to water are also susceptible to penetration by acid forming
aerosols (U.S. EPA, 1995). Baedecker et al. (1991) reviewed studies dealing with solubility
and permeability of SO2 in paints and polymer films. These studies showed permeation and
absorption rates varied depending on the formulation of the paint.
Studies reported in the criteria document (Spence et al., (1975); Campbell et al.,
(1974); Haynie and Spence, (1984); Yocom and Grappone, (1976); and Yocom and Upham,
(1977)) support the conclusion that gaseous pollutants contribute to the erosion rates of
exterior paints.
c. Effects on Stone
Damage to calcareous stones (i.e., limestone, marble and carbonated cemented stone)
has been attributed to deposition of acidic particles. Moisture and salts are considered the
most important factors in building material damage (CD, Chapter 9). However, many other
factors (such as normal weathering and microorganism damage) also seem to play a part in
the deterioration of inorganic building materials. The relative importance of biological,
chemical, and physical mechanisms has not been studied to date. Thus, the link between
ambient pollutant concentrations and damage to various building stones is difficult to
quantify.
Baedecker et al. (1991) reported that 10 percent of chemical weathering of marble and
limestone was caused by wet deposition of hydrogen ions from all acid species. Dry
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deposition of SO2 between rain events caused 5 to 20 percent of the chemical erosion of
stone, and dry deposition of nitric acid was responsible for 2 to 6 percent of the erosion
(Baedecker et al. 1991).
Under high wind conditions, particulates result in slow erosion of the surfaces, similar
to sandblasting (Yocom and Upham, 1977).
d. Effects on Electronics
Exposure to ionic dust particles can contribute significantly to the corrosion rate of
electronic devices, ultimately leading to failure. Particles derived from both natural and
anthropogenic sources and ranging in size from tens of angstroms to one /xm can cause
corrosion of electronics because many are sufficiently hygroscopic and corrosive, at normal
relative humidities, to react directly with non-noble metal and passive oxides, or to form
conductive moisture films on insulating surfaces to cause electrical leakage. The effects of
particles on electronic components were first reported by telephone companies who reported
that particles high in nitrates caused corrosion, cracking, and ultimate failure of wire spring
relays (Hermance, 1966; McKinney and Hermance, 1969). More recently, Sinclare (1992)
and Frankenthal (1993) have reported that anthropogenically-derived particles penetrating into
indoor environments can contribute to the corrosion of electronics.
2. Staff Considerations Pertaining to the Effects of PM on Materials Damage
While particles, particularly in conjunction with sulfur dioxide, have been
qualitatively associated with damage to materials, there is insufficient data available to relate
such damage to specific particle levels in the ambient air. Absent better quantitative data,
the staff does not believe the Administrator should consider a separate secondary standard
based on materials damage.
3. Soiling
Soiling is the accumulation of particles on the surface of an exposed material resulting
in the degradation of its appearance. When such accumulation produces sufficient changes in
reflection from opaque surfaces and reduces light transmission through transparent materials,
the surface will become perceptibly dirty to the human observer. Soiling can be remedied by
cleaning or washing, and depending on the soiled material, repainting.
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Determination of what accumulated level of paniculate matter leads to increased
cleaning or repainting is difficult. For example, Carey (1959) found that the appearance of
soiling only occurred when the surface of paper was covered with dust specks spaced 10 to
20 diameters apart. When the contrast was strong, e.g., black on white, it was possible to
distinguish a clean surface from a surrounding dirty surface when only 0.2 percent of the
areas was covered with specks, while 0.4 percent of the surface had to be covered with
specks with a weaker color contrast.
Hancock et al. (1976) found that with maximum contrast, a 0.2 percent surface
coverage (effective area coverage; EAC) by dust can be perceived against a clean
background. A dust deposition level of 0.7 percent EAC was needed before the object was
considered unfit for use. The minimum perceivable difference between varying gradations of
shading was a change of about 0.45 percent EAC. Using the information on visually
perceived dust accumulation, Hancock et al. (1976) concluded that dustfall rates of less than
0.17 EAC/day would be tolerable to the general public. Similar studies have not been
reported for other soiling effects.
Despite the observation that airborne particles soil a wide range of man-made
materials, there is only limited information available with respect to size and composition of
the culpable particles. In general, the soiling of fabrics and vertical surfaces has been
ascribed to fine particles, particularly dark, carbonaceous materials. Soiling of horizontal
surfaces may result from deposition of a wide range of particles, including coarse mode
dusts.
An important consideration in assessing soiling potential is deposition velocity, which
is defined as flux divided by concentration. Deposition velocity is a function of particle
diameter, surface orientation and roughness, wind speed, atmospheric stability, and particle
density. As a result, soiling is expected to vary v/ith the size distribution of particles within
an ambient concentration, whether the surface is positioned horizontally or vertically, and
whether the surface is rough or smooth (CD, Chapter 9).
Theoretically, coverage of horizontal surfaces will be related to particle surface areas
and deposition velocity. Particle surface areas per unit mass decreases linearly with diameter
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(assuming spherical particles), while, under quiescent conditions, deposition velocity
increases with the square of the diameter. Under such conditions, large particles would
result in more soiling than an equivalent mass of smaller particles. Although second order
effects may enhance fine particle deposition relative to larger particles, deposition velocity
data still suggest substantially higher deposition on horizontal surfaces for particles larger
than 10 /xm than for smaller particles (U.S. EPA, 1982b).
The increasing soiling potential associated with increased particle size is mitigated by
lighter particle color, effects of rainfall, smaller transport distance from sources and
markedly lower penetration of larger particles to indoor surfaces (relative to smaller
particles). Because these conflicting factors have not been fully evaluated, it is not possible
to make clear particle size divisions with respect to soiling of horizontal surfaces.
The time interval that it takes to transform horizontal and vertical surfaces from clean
to perceptibly dirty is generally determined by particle composition and rate of deposition.
The process is influenced by the location (sheltered or unsheltered) and spatial alignment of
the material, the texture and color of the surface relative to the particles, and meteorological
variables such as moisture, temperature, and wind speed.
Haynie and Lemmons (1990) conducted a soiling study in a relatively rural
environment in Research Triangle Park, North Carolina. The study was designed to
determine how various environmental factors contribute to the rate of soiling of white painted
surfaces, which are highly sensitive to soiling by dark particles and represent a large fraction
of all man-made surfaces exposed in the environment. Hourly rainfall and wind speed, and
weekly data for dichotomous sampler measurements and TSP concentration were monitored.
Gloss and flat white paints were applied to hardboard house siding surfaces and exposed
vertically and horizontally for 16 weeks, either sheltered or unsheltered from rainfall.
Measurements, including reflectance, were taken at 2, 4, 8, and 16 weeks. Based on the
results of this study, the authors concluded that: (1) coarse mode particles initially contribute
more to soiling of both horizontal and vertical surfaces than fine mode particles; (2) coarse
mode particles, however, are more easily removed by rain than are fine mode particles; (3)
for sheltered surfaces, reflectance changes are proportional to surface coverage by particles,
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and particle accumulation is consistent with deposition theory; (4) rain interacts with particles
to contribute to soiling by dissolving or desegregating particles and leaving stains; and (5)
very long-term remedial actions are probably taken because of the accumulation of fine
rather than coarse particles (Haynie and Lemmons, 1990).
Creighton et al. (1990) reported that horizontal surfaces soiled faster than vertical
surfaces and that large particles were primarily responsible for the soiling of horizontal
surfaces not exposed to rainfall. Soiling was related to the accumulated mass of particles
from both the fine and coarse fraction.
Fine mode black smoke and motor vehicle exhaust have been associated with the
soiling of building material and facades (Tarrat and Joumard, 1990; Lanting, 1986).
Ligocki et al. (1993) studied the potential soiling of art work in five Southern
California museums. The authors concluded that a significant fraction of fine elemental
carbon and soil dust particles had penetrated to the indoor atmosphere of the museums
studied and may constitute a soiling hazard to displayed art work. The seasonally averaged
indoor/outdoor ratios for paniculate matter mass concentrations ranged from 0.16 to 0.96 for
fine particles and from 0.06 to 0.53 for coarse particles, with lower values observed for
building with sophisticated ventilation systems that include filters for particulate removal.
4. Societal Costs
a. Soiling/Property Value
The effect of particles on aesthetic quality depends in part on human perception of
pollution. The reduction of aesthetic quality may arise from the soiling of buildings or other
objects of historical or social interest from the mere dirty appearance of a neighborhood. A
number of studies have indicated that such perceptions of neighborhood degradation are
revealed indirectly through effects on the value of residential property. That is, when
residential properties similar in other respects are compared, the properties in the more
highly polluted areas typically have lower value.
Freeman (1979), reporting on 14 prope/ty value studies that used particulate matter
or dustfall as one of their pollutant measures, noted that the results generally supported the
premise that property values are affected by the full range of particle pollution. He
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cautioned, however, that direct comparison of the monetary results is not possible since the
studies cover a number of cities and use different data bases, empirical techniques, and
model specifications.
The extent to which the city-specific results represent soiling as opposed to
perceptions of the effects of particles on health and visibility is not clear. Therefore, the
results of these studies cannot provide reliable quantitative estimates of the effects of soiling
on property values (U.S. EPA, 1982b).
b. Soiling/Materials
Airborne particles soil a wide range of materials in all sectors of the economy.
Assuming that these sectors are not as well off in a dirtier state as a cleaner one, soiling will
result in an economic cost to society. While the household sector has been examined by a
number of investigators, their results have been questioned because of methodology
problems and their failure to appropriately address particle size, composition, and deposition
rates. As a result, no single study has produced a completely satisfactory estimate of soiling
costs for the household sector. It is unfortunate that little or no effort has been expended to
account for soiling costs in the commercial, manufacturing, or public sectors. Results from
MathTech, Inc. (1983) suggest that soiling costs for the manufacturing sector alone could be
significant.
In the review of effects of household soiling, the staff paper has relied principally on
Booz, Allen and Hamilton, Inc., (1970); Watson and Jaksch, (1978, 1982) [which was cited
in the CD and discussed in more detail in the 1982 criteria document]; and MathTech, Inc.,
(1983) to derive estimates of household soiling costs. For the year 1970, the estimate for
amenity loss due to exterior household soiling was estimated to range form 1 to 3.5 billion
dollars (1978 dollars). The 14 /tg/m3 reduction in U.S. annual TSP levels between 1970 and
1978 was estimated to have, resulted in an annual benefit for the year 1978 of 0.2 to 0.7
billion dollars or 14 to 50 million dollars for each jig/m3 of reduction (U.S. EPA, 1982a).
MathTech, Inc. (1983) estimated household soiling costs in the range of $88.3 million to
$1.2 billion (1980 dollars) for attaining the primary PM10 standard nationwide. Gilbert
(1985) used a household production function framework to design and estimate the short-run
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costs of soiling. The results were comparable to those reported by MathTech (1983).
Finally, McClelland et al. (1991) concluded that households were willing to pay $2.70 per
/ig/m3 change in particle level to avoid soiling effects.
Haynie (1989), using fine and coarse mode particle levels calculated from 1987 EPA
AIRS data for PMio and TSP, estimated that $1.74 billion of annual national residential
repainting costs could be attributed to soiling (using national average painting costs and
frequencies). Haynie and Lemmons (1990) estimated that the national soiling costs associated
with repainting the exterior walls of houses probably were within the range of $400 to $800
million a year in 1990. This lower estimate, as compared to Haynie (1989), reflects that
households in dirtier areas may not respond with average behavior but mitigate their behavior
by (1) accepting greater reductions in reflectance before repainting, (2) washing surfaces
rather than painting as often, or (3) selecting materials or paint colors that do not tend to
show dirt. Haynie and Lemmons (1990) extrapolated their findings for houses to all exterior
paint surfaces and produced a range from $570 to $1,140 million per year.
5. Staff Considerations Pertaining to the Effects of PM on Soiling
It is clear that, at high enough concentrations, particles become a nuisance and result
in increased cost and decreased enjoyment of the environment. The available data are
limited, however, and do not permit any definitive findings with respect to societal costs or
provide clear quantitative relationships between ambient particle loading and soiling. Absent
sufficient data, the staff concludes that there is not a sufficient basis to set a separate
secondary standard based on soiling effects alone. The recommended suite of primary
ambient air quality standards and the regional haze program should reduce the soiling and
nuisance effects associated with particle pollution. The effects associated with dustfall are
likely to be very localized and thus, more appropriately addressed at the local level.
D. Summary of Staff Conclusions and Recommendations on Secondary NAAOS
This summary of staff conclusions ariii recommendations for the PM secondary
NAAQS draws from the discussions contained in the previous sections of this Staff Paper.
The key findings are:
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November 1995 VH-22
1) Anthropogenic fine particles impair visibility nationally. The level of this impairment
varies greatly from East to West, in terms of total loadings, pollutant mix, and
resulting total light extinction. Background levels of fine particles and humidity vary
regionally as well, with the East having higher levels than the West.
2) Because of regional variations in natural background levels of fine particles, annual
average humidity, pollutant mix, and resulting total light extinction, the staff
concludes that a national secondary standard to protect visibility would not be the
most effective approach for addressing visibility impairment. Therefore, the staff
recommends that the Administrator consider establishing regional haze regulations
under section 169A of the Act.
3) The available data assessed in the CD does not provide an adequate basis to establish
a national secondary standard to protect against soiling and materials damage effects.
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PM STAFF PAPER
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Research Institute, Reno, Nevada (DRI Document No.
4204.1D1). July 12, 1995.
Watson, J.G.; Rogers, C.F.; Chow, J.C. (1995) PM,0 + PM25
Variations in Time + Space. DRI Document No. 4204.IF Report
to U.S. EPA, October 24, 1995.
Watson, W. D.; Jaksch, J. A. (1982) Air pollution: household
soiling and consumer welfare losses. J. Environ. Econ.
Manage. 9: 248-262.
Watson, W. D., Jr.; Jaksch, J. A. (1978) Household cleaning costs
and air pollution. Presented at the 71st Annual Meeting,
Air Pollution Control Association, Houston, Texas, June 25-
30. Paper No. 78-52.3.
Whitby, K.T.; Sverdrup, G.M. (1980) California aerosols: their
physical and chemical characteristics. In: Hidy, G.M. ;
Mueller, P.K.; Grosjean, D.; Appel, B.R.; Wesolowski, J.J.,
eds. The character and origins of smog aerosols: a digest
of results from the California Aerosol Characterization
Experiment (ACHEX). New York, NY: John Wiley & Sons, Inc.;
pp. 477-517. (Advances in environmental science and
technology: v. 9).
Whitby, K.T.; Charlson, R.E.; Wilson, W.E.; Stevens, R.K. (1974)
The size of suspended particle matter in air. Science
(Washington, DC) 183: 1098-1099.
Whitby, K.T.; Husar, R.B.; Liu, B.Y.H. (1972) The aerosol size
distribution of Los Angeles smog. J. Colloid. Interface
Sci. 39: 177-204.
White and Roth. Progressive Lung Injury in Pulmonary Hibrination
from Monocrotaline, In: J.O. Cantor, ed. (Handbook of Am.
Model of Pulmonary Disease, Vol. 2, Boca Raton, FL; CRC
Press, 1989).
Whittemore, A. S.; Korn, E. L. (1980) Asthma and air pollution in
the Los Angeles area. Am. J. Public Health 70: 687-696.
-------
29
Willeke, K.; Whitby, K.T. (1975) Atmospheric aerosols: size
distribution interpretation. J. Air Pollut. Control Assoc.
25: 529-534.
Wilson, W.E.; Burton, R.M.; Koutrakis, P.; Suh, H.H. (1995).
Differentiating Fine and Coarse Particles: Definitions and
Exposure Relationships Relevant to Epidemiological Studies.
Wolff, G.T.; Collins, D.C.; Rodgers, W.R.; Verma, M.H.; Wong,
C.A. (1990) Spotting of automotive finishes from the
interactions between dry deposition of crustal material and
wet deposition of sulfate. J. Air Waste Manage. Assoc. 40:
1638-1648.
Wyzga, R. E.; Lipfert, F. W. (1995) Ozone and daily mortality:
the ramifications of uncertainties and interactions and some
initial regression results. Ozone conference: accepted.
Yocom, J.E.; Grappone, N. (1976) Effects of power plant emissions
on materials. Palo Alto, CA: Electric Power Research
Institute: report no. EPRI/EC-139. Available from NTIS,
Springfield, VA; PB-257 539.
Yocom, J.E.; Upham, J.B. (1977) Effects of economic materials
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air pollution. 3rd ed. New York, NY: Academic Press, Inc.;
pp. 93-94.
-------
APPENDIX A
Considerations in Selecting Particle Size Cut Point
for Fine Particles
-------
External Review Draft A-l Do Not Quote or Cite
November 1995
Appendix A. Considerations in Selecting Particle Size Cut Point for Fine Particles
An important decision relating to the choice of indicator is the choice of measurement
which in a sense serves as an operational definition of fine particles. The CD concludes that
the minimum of mass between the fine and coarse modes lies between 1 and 3 jam, and that
the scientific data support a cut point to delineate fine particles in this range. Because of the
overlap of fine and coarse particles in this intermodal region, specific cut points are only an
approximation of fine particles. Thus, the decision within this range is largely a policy
judgement. Staff recommend the three primary factors to consider in selecting a cut point are
consistency with health data, potential for intrusion of mass from the other mode, and
availability of monitoring technology. The main policy choice centers on two options:
PM2 5 and PMj. Although most fine particle (accumulation mode) mass is below l.Oum,
some hygroscopic particles in conditions of high relative humidity may gain water and grow
above this size.
From a public health perspective, PlvL) 5 captures all of the potential agents of concern
in the fine fraction. For example, Plv^ 5 captures most sulfates, acids, fine particle metals,
organics, and ultrafme particles and accounts for most of surface area, and particle number.
Although the CD outlines some conditions (e.g., relative humidity near 100 percent) under
which it is possible that hygroscpic particles may grow above 2.5^m, PIv^ 5 is still better
able to capture them than PMi.
PMo 5 has been used directly in many health studies as described in the CD and
Chapter V above (see Table V-5). Associations have been reported between exposures to
PM2 5 and mortality, hospital admissions, cough, upper respiratory infection, lower
respirator}' infection, and asthma status, and pulmonary function changes (although not all of
these associations are statistically significant).
PM"> c measurement technologies are widely available and have been in routine use in
the field since the early 1980s. For example, the EPA AIRS database contains PM^ 5 data
from the Inhalable Particle Network (1982-1984), the IMPROVE network (1989-present), and
NESCAUM network (1988- present). In addition, the California Air Resource Board (CARB)
dichotomous sampler network has been collecting PM^ 5 data routinely since 1980, and many
-------
External Review Draft A-2 Do Not Quote or Cite
November 1995
other special studies using PN^ 5 have been conducted across the country. Furthermore,
dichotomous samplers allow the coincident measurement of PMi Q and PlVk c, increasing the
certainty of comparability between the two measurements.
PMj, on the other hand, has not been used in health studies primarily due to lack of
available monitoring data. Comparisons between PMj and other measurements that were used
in the health studies (e.g., PM^Q) are also not widely available due to lack of available PMj
monitoring data. Furthermore, PMj may not capture as much of the hygroscopic substances
such as sulfates. Health studies report statistically significant associations between sulfate
measurements and endpoints including increased mortality and hospital admissions.
PMi sampling technologies have been developed and some limited validated data are
available from locations such as Phoenix, Arizona. However, the PMi samplers have not
been widely field-tested to date.
Proponents of the PMj option are concerned that the intrusion of particles generated
by grinding or crushing (i.e., coarse mode particles) into the daily PM9 c measurement could
£*» *J
create spurious NAAQS exceedances. Given the lack of PMj data currently available, it is
difficult to determine how much intrusion might occur or what areas might be affected during
the implementation of the PM NAAQS. The available data show that typically only 5-15
percent (on the order of 1 to 5 ug/m ) of the PN^ 5 mass is attributable to soil-type sources
even in dusty areas such as San Joaquin Valley, California, and Phoenix, Arizona. However,
this percentage may increase during events such as high winds.
The staff judges that hi typical urban areas, the potential for this type of intrusion may
be smaller, but without sufficient data these determinations remain very uncertain. A sharper
inlet for the Federal Reference Method may help to minimize the intrusion of coarse mode
particles into the PM2 5 measurement. Although intrusion of coarse mode particles into daily
PM9 5 measurements is not anticipated to be significant in most situations, if in light of more
data a problem is identified, this issue might be better addressed on a case-by-case in the
monitoring and implementation programs.
Finally, the staff concludes that PM2 5 measurements are more appropriate than some
of the measurements historically used in the epidemiological studies (e.g., BS, CoH) although
-------
External Review Draft A-3 Do Not Quote or Cite
November 1995
these measurements have been useful in advancing the state of scientific knowledge of particle
effects. British Smoke (BS) reading varies more with darkness of particles (i.e., carbon
content) than with mass, making associations with mass highly site- and time-specific. Using
a similar principle to BS, the principle of COH is that visible light is transmitted through (or
reflected from as in the case of BS) a section of filter paper before and after ambient air is
drawn through it. Thus, COH associations with mass are also highly site- and time-specific.
The BS method emphasizes control of primary elemental carbon emissions; however,
elemental carbon is a minor contributor to fine and total mass in current U.S. atmospheres.
Furthermore, lack of consistent relationships between BS reflectance and PM mass
measurements diminishes one of the major advantages: BS is not related to the available
quantitative health data from U.S. cities with as much certainty as the PVU 5 mass
measurements although BS is used in many other countries.
Thus, because of the consistency with health data, small potential for intrusion, and
availability of monitoring technology and existing air quality database, the staff judges that
the PM2 5 measurement is more appropriate for regulatory purposes than PMj, or historical
measurements such as BS or COH.
-------
APPENDIX B
Chemical Composition Data for Participate Matter
-------
PM2.5 COMPOSITION (24-h AVG)
EASTERN U.S.
Units g ug/m3
D
T1
I
O
O
Z
O
H
O
C
O
H
m
O
»
n
H— «
H
tn
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
TI
V
Zn
1
Smoky Mtns
9/20-26/78
12
12
24.00
222
1.10
0.30
12.00
<0.054
<0.003
0.018
0.016
<0.010
0.003
0.028
0.040
0.097
3.744
0.001
0.038
<0.006
-------
PM2.5 COMPOSITION (24-h AVG) WESTERN U.S.
Tl
H
6
o
"Z
o
H
O
C
O
H
m
n
>— i
H
tn
Units as ug/m3
Ref
Site
Dates
Hours
Our
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
SI
Sn
Sr
Ti
V
Zn
8(a)
Res.Tr.Pk
1980
24
3
28.77
0.073
0.002
0.007
0.035
0.016
0.120
0.148
0.003
0.001
0.042
0.106
2.835
0.002
0.350
0.018
9(g)
Los Angeles
Summer'87
4,5 and 7
11 days
41.10
8.27
2.37
4.34
9.41
0.035
0.022
0.015
0.013
0.022
0.093
0.022
0.063
0.099
0.041
0.024
0.016
0.202
0.005
0.060
0.038
2.832
0.013
0.052
0.019
0.005
0.006
0.090
9(g)
Los Angeles
Fall'87
4 and 6
6 days
90.20
18.46
7.28
22.64
4.38
0.250
0.015
0.043
0.065
0.335
0.453
0.025
0.273
0.557
1 0.217
0.075
0.043
0.466
0.007
0.046
0.185
1.998
0.011
0.520
0.028
0.060
0.007
0.298
10f.)
San Joaquln Valley
6'88-6'89
24
~35
29.89
4.87
3.24
8.17
3.00
0.152
0.012
0.010
0.096
<0.007
0.094
0.003
0.096
0.180
0.188
0.006
0.016
0.007
0.029
0.001
1.242
<0.002
0.001
0.460
<0.015
0.002
0.017
0.015
0.078
110)
Phoenix
10/13/89-1/17/90
6 h, 2x/day
~ 100 days
29.37
10.10
7.47
3.60
1.33
0.130
.<0.020
<0.106
0.011
0.170
<0.018
0.365
0.003
0.015
0.216
0.207
0.023
<0.006
0.003
<0.051
0.039
<0.0025
0.437
<0.033
<0.002
0.430
<0.028
<0.030
<0.016
0.056
5(d)
Boise
12/86-3/87
7am-7pm-7a
12
35.70
12.70
1.70
0.102
0.002
0.014
0.026
0.122
0.001
0.011
0.022
0.145
0.002
0.002
0.045
0.603
0.001
0.069
i
0.001
0.019
12(0
Nevada
11/86-1/87
00-2400
24
24
56.92
19.97
15.17
2.43
1.67
0.275
0.001
0.013
0.033
0.215
0.145
0.002
0.010
0.310
0.280
0.015
0.006
0.041
0.115
0.001
0.765
0.000
0.860
0.004
0.043
0.009
0.033
8(a)
TarrantCA
1980
24
6
57.05
0.177
0.102
0.455
0.002
0.047
0.316
0.186
0.032
0.003
0.619
2.578
0.583
0.010
0.095
8(a)
Five Points C
1980
24
3
31.80
0.239
0.015
0.150
0.004
0.001
0.024
0.216
0.244
0.005
0.025
0.007
0.087
1.129
0.001
0.656
0.005
0.006
0.016
8(a)
Riverside CA
1980
24
4
35.18
0.036
0.037
0.301
0.009
0.040
0.127
0.120
0.007
0.007
0.376
1.653
0.001
0.234
0.003
0.029
References are listed In Table 1 Appendix. Associated notes are explained In Table 1.
Values for this size fraction are calculated from the average measured values reported for the other two size fractions.
w
I
-------
PM2.5 COMPOSITION (24-h AVG)
CENTRAL U.S.
Unite » ug/m3
Ret
Site
Dates
Hours
Dur
Number
Mass
! OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
C!
Cr
Cu
Fe
K
' Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
8(a)
San Jose CA
1980
24
6
56. 26
0.123
0.001
0.188
0.089
0.050
0.003
0.043
0.148
0.248
0.006
0.006
0.013
0.891
0.852
0.292
0.002
0.061
8(a)
Honolulu
1980
24
1
21.10
1.127
0.017
1.024
0.518
0.004
0.018
0.726
0.371
0.020
0.002
0.002
0.071
0.313
2.363
0.063
0.001
0.011
8(a)
Winnemucca
1980
24
5
9.6T
0.361
0.006
0.243
0.026
0.231
0.149
0.003
0.001
0.042
0.358
0.914
0.009
0.011
8(a)
Portland
1980
24
4
37.15
0.581
0.012
0.093
0.154
0.021
0.009
0.072
0.270
0.218
0.052
0.027
0.017
0.422
1.944
0.001
0.377
0.005
0.014
0.081
8(a)
Seattle
1980
24
1
10.70
0.002
0.006
0.019
0.037
0.002
0.024
0.098
0.080
0.004
0.006
0.006
0.215
0.831
0.001
0.092
0.059
5(d)
Albuquerque
12/84-3/85
7am-7pm-7am
12
20.60
13.20
2.10
0.077
0.085
0.059
0.036
0.045
0.074
0.000
0.237
0.507
0.076
0.007
13
Denver
1/11-30/82
6f\m-6pm-6a
12
~26
26.73
7.11
2.15
2,22
2.06
0.394
<0.002
0.031
0.103
0.047
0.006
0.052
<0.009
0.010
0.079
0.079
0.011
0.003
0.043
0.326
<0.003
0.709
0.277
,<0.003
<0.027
0.046
14(m)
Urban Denver
11/87-1/88
9am-4pm-9am
7&17
~136
19.67
7.25
4.41
3.96
1.55
0.037
0.018
0.056
0.005
0.141
0.003
0.017
0.111
0.077
0.012
0.002
0.075
0.642
0.004
0.001
0.272
0.006
0.001
0.009
0.031
14(aa) 15
Non-urban Denver Chicago
11/87-1/88 7/94
9am-4pm-9am 0800-0800
78,17 24
"150 16
10.35 13.57
5.39
1.31
0.046
<0.003
< 0.091
0.004
0.045
<0.029
0.011
<0.005
0.011
0.089
0.061
0.012
0.005
<0.002
0.022
<0.001
0.008
0.027
1.321
<0.042
<0.001
0.074
<0.049
<0.029
<0.009
0.052
H
tn
References are listed in Table 1 Appendix. Associated notes are explained in Table 1.
* Values for this size fraction are calculated from the average measured values reported for the other two size fractions.
-------
PM2.5 COMPOSITION (24-h AVG)
CENTRAL U.S.
O
O
2
O
H
O
d
o
H
m
o
H-l
H
m
Units = ug/m3
Ref
Site
Dates
Hours
Our
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
16
Houston
9/10-19/80
12
20
38.60
5.68
1.42
0.59
14.61
0.123
<0.005
0.048
0.055
0.155
<0.003
0.032
<0.005
0.028
0.162
0.119
0.014
<0.38
0.004
0.028
0.465
<0.002
4.834
0.006
<0.002
0.210
<0.005
<0.002
<0.014
<0.008
0.084
6,7
Harriman
5/80-5/81
0000-0000
24
256
20.80
8.10
36.1
0.038
0.150
0.021
0.120
0.017
BQL
0.180
2.500
0.002
0.120
BQL
17 6,7
Harriman Kingston
9/85-8/86 5/80-6/81
0000-0000
24 24
330 169
21.00 24.60
8.70
36.1
0.044
0.120
BQL
0.097
0.010
BQL
0.194
2.400
0.002
0.200
BQL
6,7
Portage
3/79-5/81
0000-0000
24
271
11.00
6.81
10.5
0.011
0.045
0.027
0.049
0.003
BQL
0.061
1.400
0.001
0.075
BQL
6,7
Topeka
8/79-5/81
0000-0000
24
286
12.50
6.05
11.6
0.045
0.250
0.031
0.090
0.004
BQL
0.163
1.100
0.000
0.190
i
BQL
8(a)
El Paso
1980
24
10
27.16
0.155
0.025
0.070
0.332
0.001
0.036
0.134
0.127
0.004
0.001
0.481
0.823
0.002
0.436
0.003
0.055
8(a)
Inglenook
1980
24
8
32.03
0.082
0.001
0.040
0.326
0.003
0.002
0.032
0.281
0.408
0.037
0.001
0.008
0.309
2.655
0.001
0.685
0.133
8(a)
Braldwood
1980
24
1
28.20
0.089
0.003
0.084
0.024
0.071
0.052
0.001
0.001
0.041
2.060
0.001
0.220
0.011
8(a)
Kansas City KS
1980
24
8
25.66
0.091
0.003
0.027
0.519
0.004
0.032
0.189
0.311
0.006
0.002
0.013
0.180
1.816
0.001
0.434
0.004
0.034
References are listed in Table 1 Appendix
* Values for this size fraction are calculated
Associated notes are explained in Table 1.
from the average measured values reported for the other two size fractions.
w
-------
PM2.5 COMPOSITION (24-h AVG)
CENTRAL U.S.
Units « ug/m3
o
H
O
C
O
H
o
h~<
H
m
Ref
Site
Dates
Houre
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
*Ba
Br
Ca
Cd
8(a)
Minneapolis
1980
24
6
15.50
0.004
0.047
0.103
Cl |
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
SI
Sn
Sr
Tl
V
Zn
0.001
0.035
0.087
0.092
0.005
0.001
0.308
0.907
0.001
0.169
0.045
8(a)
Kansas City MO
1980
24
3
16.77
0.007
0.064
0.213
0.002
0.021
0.140
0.142
0.006
0.001
0.369
0.763
0.177
0.046
8(a)
Akron
1980
24
7
36.09
0.046
0.012
0.039
0.110
0.010
0.037
0.609
0.268
0.085
0.006
0.059
0.412
3.419
0.008
0.522
0.009
0.150
8(a)
Cincinnati
1980
24
2
29.80
0.062
0.013
0.024
0.062
0.003
0.024
0.174
0.136
0.011
0.004
0.043
0.343
2.876
0.005
0.328
0.003
0.053
8(a)
Buffalo
1980
24
14
38.75
0.192
0.009
0.003
0.218
0.002
0.026
0.671
0.310
0.033
0.008
0.060
0.359
3.706
0.005
0.241
0.001
0.078
8(a)
Dallas
1980
24
4
28.93
0.111
0.033
0.223
0.691
0.005
0.043
0.248
0.125
0.015
0.002
0.018
1.066
1.514
0.442
0.007
0.002
0.054
8(a)
St Louis
1980
24
5
23.06
0.119
0.003
0.025
0.090
0.018
0.076
0.126
0.002
0.002
0.020
0277
2.333
0.002
0.170
i
0.023
18(k)
St Louis
8-9/76
6-12
34.00
0.203
0.002
0.020
0.132
0.132
0.004
0.087
0.006
0.029
0.275
0.261
0.036
0.004
0.001
0.688
0.000
4.655
0.006
0.004
0.458
0.009
0.002
0.112
0.002
0.101
6,7 17
St Louis St Louis
9/79-6/81 9/85-8/86
0000-0000
24 24
306 311
19.00 17.70
8.10 8.00
10.3 9.7
0.078
0.101
0.052
0.190
0.021
0.003
0.327
2.100
0.002
0.160
BQL
6.7
Steubenville
4/79-4/81
0000-0000
24
499
29.60
12.80
25.2
0.042
0.097
0.092
0.590
0.029
0.005
0.216
4.700
0.005
0.290
0.011
References are listed In Table 1 Appendix,
Values for this size fraction are calculated
Associated notes are explained In Table 1.
from the average measured values reported for the other two size fractions.
-------
PM10 COMPOSITION (24-hr AVG)
EASTERN U.S.
•n
H
6
o
z
o
H
O
d
o
H
m
n
N-H
3
Units a ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
SI
Sn
Sr
Tl
V
Zn
1
-------
PM10 COMPOSITION (24-hr AVG)
WESTERN U.S.
Units * ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
C!
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
8(a.q)
Res.Tr.Pk
1980
24
3
36.53
0.679
0.002
0.010
0.121
0.002
0.026
0.302
0.216
0.006
0.001
0.042
0.119
3.058
0.002
1.737
0.021
0.025
9(9)
Los Angeles
Summer'87
4,5 and 7
1 1 days
67.40
11.61
3.19
9.47
11.28
0.758
0.007
0.070
0.016
0.585
1.119
0.023
0.022
0.836
0.237
0.335
0.033
1,632
0.005
0.187
0.084
3.353
0.008
2.040
0.018
0.077
0.005
0.114
9(g)
Los Angeles
Fall'87
4 and 6
6 days
98. 7u
23.35
8.49
27.50
5.39
0.847
0.019
0.127
0.072
1.190
0.880
0.042
0.178
2.192
0.460
0.287
0.063
0.518
0.005
0.099
0.251
2.262
0.010
2.162
0.024
0.165
0.009
0.293
10fl)
San Joaquln Valley
6'8&-6'89
24
~35
74.05
10.59
5.62
10.55
3.62
3.570
0.051
0.015
1.057
0.487
0.010
0.087
1.633
0.820
0.037
0.010
0.059
0.061
0.004
1.463
0.001
8.037
0.014
0.147
0.014
0.094
110)* 5(d)
Phoenix Boise
10/13/89-1/17/90 12/86-3/87
7am-7pm-7a
6h.2x/day 12
~ 100 days
62.45
14.56
8.30
4.46
2.34
2.67
BQL
0.01
0.01
2.10
BQL
0.56
0.01
0.04
1.47
0.88
BQL
0.05
BQL
BQL
0.01
0.05
0.06
BQL
0.62
BQL
BQL
7.44
BQL
0.01
0.14 '
BQL
0.09
12(0 B(a,q)*
Nevada Tarrant CA
11/86-1/87 1980
00-2400
24 24
24 6
100.90
2.407
0.149
4.543
0.007
0.077
1.257
0.441
0.067
0.006
0.002
0.786
2.888
5.791
0.093
0.147
8(a,q)*
Five Points CA
1980
24
3
124.37
7.317
0.019
1.786
0.026
0.007
0.037
3.275
1.437
0.055
0.037
0.155
0.105
1.422
0.001
16.657
0.277
0.013
0.032
8(a,q)*
Riverside CA
1980
24
4
106.26
3.549
0.065
5.082
0.173
0.005
0.061
2.015
1.081
0.049
0.013
0.144
0.489
2.373
0.001
7.778
0.182
0.003
0.059
References are listed
Values Tor this size
In Table 1 Appendix. Associated notes are explained In Table 1.
fraction are calculated from the average measured values reported for the other two size fractions.
-------
PM10 COMPOSITION (24-hr AVG)
CENTRAL U.S.
Units g ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
8(a.q)*
San Jose CA
1980
24
6
66.68
2.053
0.001
0.250
0.771
0.480
0.009
0.071
1.214
0.508
0.027
0.014
0.045
1.119
1.109
5.506
0.086
0.002
0.105
8(a,q)*
Honolulu
1980
24
1
46.90
2.992
0.023
1.981
1.456
0.009
0.025
1.384
0.665
0.034
0.005
0.002
0.093
0.571
6.129
0.130
0.001
0.019
8(a,q)*
Winnemucca
1980
24
5
65.42
6.925
0.010
2.177
0.176
0.006
0.043
1.995
1 1.200
0.044
0.003
0.063
0.573
12.817
0.173
0.026
8(a,q)*
Portland
1980
24
4
117.55
6.932
0.014
0.121
1.459
0.197
0.019
0.109
2.059
0.805
0.108
0.036
0.028
0.537
2.371
0.001
12.505
0.191
0.018
0.119
8(a,q)*
Seattle
1980
24
1 .
36.00
2.296
0.008
0.033
0.585
0.228
0.005
0.041
1.001
0.231
0.022
0.007
0.006
0.292
0.952
0.001
4.424
0.091
0.093
8(a.q)* 13(q)*
Albuquerque Denver
12/84-3/85 1/11-30/82
7am-7pm-7am 6am-6pm-6am
12 12
~26
56.46
7.11
2.15
2.22
2.45
3.294
<0.004
0.089
0.127
0.705
0.018
1.287
<0.018
0.018
1.033
0.727
0.031
0.008
0.155
0.424
0.005
0.709
<0.004
<0.004
7.737
<0.004
; 0.009
0.09
<0.004
0.085
14(m) 14(aa) 15(3)*
Urban Denver Non-urban Denver Chicago
11/87-1/88 11/87-1/88 7/94
9am-4pm-9am 9am-4pm-9am 0800-0800
7417 7&17 24
~136 ~150 16
28.54
5.39
1.31
5.46
0.269
<0.0043
<0.130
0.011
0.761
<0.041
0.047
<0.0073
0.017
0.432
0.161
0.118
0.013
<0.0041
0.022
<0.0018
0.035
0.032
1.363
<0.059
<0.0017
0.813
<0.070
0.019
<0.013
0.090
References are listed
Values for this size
in Table 1 Appendix. Associated notes are explained in Table 1.
fraction are calculated from the average measured values reported for the other two size fractions.
-------
D
O
2
O
H
O
c
O
H
m
o
?o
n
PM10 COMPOSITION (24-hr AVG)
CENTRAL U.S.
Units » ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
SI
Sn
Sr
TI
V
Zn
16(q)*
Houston
9/10-19/80
12
20
63.40
8.78
1.42
2.22
15.52
1.216
<0.015
0.139
0.091
2.935
<0.012
0.398
0.007
0.046
0.766
0.289
0.035
<1.49
0.008
0.128
0.589
<0.006
4.83
0.006
<0.003
3.200
0.036
<0.045
0.142
6,7(P.q) 17*
Harriman Harriman
5/80-5/81 9/85-8/86
0000-0000
24 24
256 330
32.50 30.00
11.14 8.70
36.1
0.052
1.800
0.050
0.690
0.038
0.001
0.237
2.500
0.002
2.000
ND
6J(p.q)
Kingston
5/80-6/81
0000-0000
24
169
35.40
13.63
0.056
0.960
0.018
0.360
0.027
ND
0.234
2.400
0.002
1.900
ND
6,7(p.q)
Portage
3/79-5/81
0000-0000
24
271
18.20
7.29
0.014
0.380
0.083
0.230
0.009
0.001
0.074
1.500
0.001
0.980
ND
6.7(P,q)
Topeka
8/79-5/81
0000-0000
24
286
26.40
6.60
0.055
2.400
0.031
0.580
0.020
0.001
0.203
1.200
0.000
2.500
ND
8(a,q)*
El Paso
1980
24
10
76.21
2.903
0.037
0.103
3.964
0.043
0.004
0.083
0.946
0.623
0.027
0.002
0.672
1.072
0.003
5.813
0.080
0.112
8(a,q)*
Inglenook
1980
24
8
72.45
2.508
0.001
0.061
2.924
0.003
0.006
0.059
1.474
0.717
0.07B
0.003
0.030
0.388
2.969
0.001
6.997
0.116
0.188
8(a,q)*
Braidwood
1980
24
1
56.90
2.020
0.002
0.006
1.490
0.002
0.044
0.727
0.355
0.018
0.002
0.014
0.054
2.632
0.002 '
5.987
0.083
0.023
8(a,q)*
Kansas City KS
1980
24
8
70.33
2.144
0.003
0.036
4.371
0.010
0.048
0.989
0.660
0.026
0.005
0.013
0.237
2.031
0.001
4.976
0.076
0.060
References are listed In Table 1 Appendix. Associated notes are explained In Table 1.
Values tor this size fraction are calculated from the average measured values reported for the other two size fractions.
w
I
-------
PM10 COMPOSITION (24-hr AVG)
CENTRAL U.S.
Units m ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Tl
V
Zn
8(a,q)«
Minneapolis
1980
24
6
46.35
2.191
0.005
0.069
1.674
0.293
0.003
0.057
0.831
0.402
0.031
0.002
0.406
1.131
0.001
4.848
0.062
0.072
B(a,q)«
Kansas City MO
1980
24
3
58.43
2.284
0.010
0.093
3.967
0.530
0.006
0.036
1.119
0.503
0.031
0.003
0.478
1.043
4.986
0.074
0.086
8(a,q)*
Akron
1980
24
7
70.90
2.555
0.015
0.064
1.541
0.572
0.024
0,055
2.249
0.592
0.129
0.011
0.059
0.509
3.870
0.008
5.531
0.116
0.219
8(a,q)*
Cincinnati
1980
24
2
62.95
2.972
0.013
0.041
1.374
0,103
0.005
0.038
1.057
0.499
0.032
0.007
0.080
0.442
3.265
0.005
6.961
0.099
0.201
8(a,q)*
Buffalo
1980
24
14
83.32
3,000
0.009
0.015
2.768
0.728
0.017
0.048
2.711
0.516
0.111
0.017
0.060
0.467
4.471
0.005
2.916
0.051
0.001
0.121
8(a,q)*
Dallas
1980
24
4
61.55
1.405
0.039
0.274
4.127
0.029
0.010
0.066
0.968
0.335
0.035
0.004
0.018
1.318
1.754
3.652
0.058
0.002
0.084
8(a,q)*
St. Louis
1980
24
5
56.82
3.956
0.004
0.046
1.874
0.053
0.001
0.032
0.663
0.417
0.019
0.004
0.020
0.372
2.612
0.002
4.638
i
0.058
0.044
18(x)*
St. Louis
8-9/76
6-12
62.00
1.412
0.003
0.054
0.179
2.949
0.005
0.344
0.015
0.043
1.493
0.653
0.071
0.009
0.099
0.877
0.002
5.188
0.007
0.005
4.928
0.010
0.009
0.587
0.006
0.175
6,7(p,q) 17*
SL Louis St Louis
9/79-6/81 9/85-8/86
0000-0000
24 24
306 311
31.40 27.60
11.14 8.00
9.7
0.099
1.600
0.145
0.770
0.040
0.005
0.415
2.300
0.002
2.100
ND
6,7(p,q)
Steubenville
4/794/81
0000-0000
24
499
46.50
17.60
0.052
1.120
0.303
2.200
0.068
0.008
0.259
5.500
0.005
2.300
0.013
o
o
z
o
H
o
c
o
H
m
o
?o
O
*—I
H
m
References are listed
Values for this size
in Table 1 Appendix. Associated notes are explained in Table 1.
fraction are calculated from the average measured values reported for the other two size fractions.
-------
O
O
Z
O
H
O
G
O
O
a
COARSE COMPOSITION (24-hr AVG) EASTERN U.S.
Units = ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
AS
A3
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
1(0)
Smoky Mtns
9/20-26/78
12
12
5.60
<0.300
<0.001
0.005
0.322
<0.012
<0.005
0.118
0.108
<0.002
0.014
<0.560
<0.0006
0.580
0.018
<0.004
1(0)
Shenandoah
7/23-5/08/80
12
28
7.40
078
0.311
<0.002
0.003
0.304
0.179
0.006
0.158
0.129
<0.006
<0.003
0.009
<0.711
<0.001
0.813
0.017
0.006
2(b)
Camden
7/14-8/13 '82
6am-6pm-6am
12
50
11.40
<3.00
0.42
0.57
<0.90
0.550
0.015
0.360
<0.006
0.069
<0.009
0.490
0.151
0.011
0.004
0.054
0.230
0.181
<0.0015
1.610
<0.009
0.002
0.065
0.007
0.030
3(ab) 4(c) 5(d) 5(d)
Philadelphia Deep Creek Raleigh Roanoke
7/25-8/14/94 8/83 1/85-3/85 10/88-2/89
4x daily 7am-7pm-7a 7am-7pm-7am
24 6 12 12
21 98
8.42
0.325
0.003
0.421
0.047
0.014
0.352
0.100
0.104
0.006
0.136
0.002
0.027
0.013
BQL
BQL
0.933
0.030
BQL
0.052
6,7(o,p)*
Watertown
5/79-6/81
0000-0000
24
354
9.30
2.44
0.022
0.209
0.305
0.276
0,006
0.076
0.200
1.000
8(a.o)
Hartford
1980
24
2
27.85
1.875
0.046
0.864
0.302
0.008
0.026
1.070
0.310
0.021
0.005
0.033
0.171
0.428
4.517
0.094
0.008
0.054
8(a,o)
Boston
1980
24
1
105.60
3.458
0.001
0.025
1.069
0.301
0.004
0.023
1.612
0.533
0.029
0.022
0.016
0.177
0.502
6.760
0.154
0.008
0.054
References are listed In Table 1 Appendix. Associated notes are explained In Table 1.
Values for this size fraction are calculated from the average measured values reported for the other two size fractions.
-------
COARSE COMPOSITION (24-hr AVG)
WESTERN U.S.
Units « ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Tl
V
Zn
8(a,o)
Res.Tr.PK
1980
24
3
8.17
a
0.606
0.003
0.086
0.002
0.010
0.182
0.068
0.003
0.013
0.223
1.387
0.021
0.007
9(9)*
Los Angeles
Summer'87
4,5 and 7
11 days
26.30
3.34
0.82
5.13
1.87
0.723
SQL
0.055
0.003
0.563
1.026
0.002
BQL
0.737
0.196
0.311
0.017
1.431
BQL
0.127
0.046
0.520
BQL
1.988
BQL
0.072
BQL
0.024
9(9)*
Los Angeles
Fall'87
4 and 6
6 days
8.50
4.89
1.21
4.86
1.01
0.597
0.004
0.084
0.006
0.854
0.426
0.017
BQL
1.635
0.243
0.212
0.021
0.052
BQL
0.053
0.066
0.264
BQL
1.642
BQL
0.106
0.003
BQL
10«*
San Joaquin Valley
6'88-6'89
24
~35
44.17
5.71
2.38
2.38
0.62
3.418
0.000
0.040
0.006
0.961
0.393
0.007
BQL
1.453
0.632
0.000
0.031
0.000
BQL
0.052
0.032
0.222
0.000
7.577
0.012
0.130
BQL
0.016
11(j) 5(d)
Phoenix Boise
10/13/89-1/17/90 12/86-3/87
7am-7pm-7a
6h. 2x/day 12
~ 100 days
33.09
4.46
0.84
0.86
0.37
2.539
<0.002
<0.077
0.002
1.929
<0.016
0.194
0.008
0.021
1.259
0.669
0.032
<0.005
0.003
0.038
0.022
0.003
0.178
<0.030
< 0.002
7.013
<0.026
0.014 ,
0.121
<0.014
0.034
12(f) 8(a,o)
Nevada Tarrant CA
11/86-1/87 1980
00-2400
24 24
24 6
43.85
2.230
0.047
4.088
0.005
0.030
0.941
0.255
0.035
0.003
0.002
0.167
0.310
5.208
0.083
0.052
8(a,o)
Five Points CA
1980
24
3
92.57
7.078
0.004
1.636
0.022
0.006
0.013
3.059
1.193
0.050
0.012
0.148
0.018
0.293
16.001
0.272
0.007
0.016
8(a,o)
Riverside CA
1980
24
4
71.03
3.513
0.028
4.781
0.164
0.005
0.021
1.888
0.961
0.042
0.006
0.144
0.113
0.720
7.544
0.182
0.030
References are listed In Table 1 Appendix. Associated notes are explained In Table 1.
* Values for this size fraction are calculated from the average measured values reported for the other two size fractions.
-------
COARSE COMPOSITION (24-hr AVG)
CENTRAL U.S.
Unto = ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Ni
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
8(a,o)
San Jose CA
1980
24
6
30.40
1.930
0.062
0.682
0.430
0.006
0.028
1.066
0.260
0.021
0.008
0.032
0.228
0.257
5.214
0.086
0.044
8(a.o)
Honolulu
1980
24
1
25.60
1.865
0.006
0.957
0.938
0.005
0.007
0.6581
0.294
0.014
0.003
0.022
0.258
3.766
0.067
0.008
8(a,o)
Wlnnemucca
1980
24
5
55.74
6.564
0.004
1.934
0.176
0.006
0.017
1.764
1.051
0.041
0.002
0.021
0.215
11.903
0.164
0.015
8(a.o)
Portland
1980
24
4
80.36
6.351
0.002
0.028
1.305
0.176
0.010
0.037
1.789
0.587
0.056
0.009
0.011
0.115
0.427
12.128
0.186
0.004
0.038
8(a,o)
Seattle
1980
24
1
25.30
2.294
0.002
0.014
0.548
0.228
0.003
0.017
0.903
0.151
0.018
0.001
0.077
0.121
4.332
0.091
0.034
5(d) 13(o)
Albuquerque Denver
12/84-3/85 1/11-30/82
7am-7pm-7am 6am-6pm-6a
12 12
~26
35.73
0.39
2.900
0.058
0.024
0.658
0.012
1.235
<0.009
0.008
0.954
0.648
0.021
0.005
0.113
0.099
0.005
<0.48
7.460
0.009
0.090
0.039
14(m) 14(ab) 15(s)
Urban Denver Non-urban Denver Chicago
1 1 /87-1 /88 11 /87-1 /88 7/94
9am-4pm-9am 9am-4pm-9am 0800-0800
7&17 78.17 24
~136 ~150 16
14.97
0.223
<0.0013
<0.038
0.007
0.716
<0.012
0.036
<0.0024
0.006
0.344
0.101
0.106
0.008
<0.0017
<0.017
<0.0007
0.027
0.005
0.043
<0.017
<0.0006
0.739
<0.021
0.019
<0.004
0.038
c
o
"Z
o
H
O
c
o
H
m
n
H
m
References are listed
Values for this size
in Table 1 Appendix Associated notes are explained in Table 1.
fraction are calculated from the average measured values reported for the other two size fractions.
-------
COARSE COMPOSITION (24-hr AVG)
CENTRAL U.S.
O
o
z
o
H
O
H
n
h— H
H
m
Units g ug/m3
Ref
Site
Dates
Hours
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
Cl
Cr
Cu
Fe
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Ti
V
Zn
16(o)
Houston
9/10-19/80
12
20
24.80
3.10
1.63
0.91
1.093
<0.006
0.091
0.036
2.780
<0.006
0.366
0.007
0.018
0.604
0.170
0.021
<0.74
0.004
<0.1
0.124
<0.003
<1.29
<0.009
2.990
<0.009
<0.008
0.036
<0.03
0.058
6,7(o.p)*
Harrlman
5/80-5/81
0000-0000
24
256
11.70
3.04
0.014
1.650
0.029
0.570
1
0.021
0.001
0.057
BQL
1.880
17 6,7(o,p)*
Harriman Kingston
9/85-8/86 5/80-6/81
0000-0000
24 24
330 169
9.00 10.80
0.012
0.840
0.018
0.263
0.018
BQL
0.040
BQL
1.700
6,7(o,p)*
Portage
3/79-5/81
0000-0000
24
271
7.20
0.48
0.003
0.335
0.056
0.181
0.006
0.001
0.013
BQL
0.905
6,7(o,p)*
Topeka
8/79-5/81
0000-0000
24
286
13.90
0.55
0.010
2.150
0.000
0.490
0.016
0.001
0.040
BQL
2.310
8(a,o)
El Paso
1980
24
10
49.05
2.748
0.012
0.033
3.632
0.043
0.003
0.047
0.812
0.496
0.023
0.001
0.191
0.249
0.001
5.377
i
0.077
0.057
8(a,o)
Inglenook
1980
24
8
40.43
2.426
0.021
2.598
0.004
0.027
1.193
0.309
0.041
0.002
0.022
0.079
0.314
6.312
0.116
0.055
8(a,o)
Braldwood
1980
24
1
28.70
1.931
0.002
0.003
1.406
0.002
0.020
0.656
0.303
0.017
0.001
0.014
0.013
0.572
0.001
5.767 '
0.083
0.012
8(a,o)
Kansas City KS
1980
24
8
41.67
2.284
0.003
0.029
3.754
0.530
0.004
0.015
0.979
0.361
0.025
0.002
0.109
0.280
4.809
0.074
0.040
w
I
References are listed
* Values for this size
In Table 1 Appendix. Associated notes are explained In Table 1.
fraction are calculated from the average measured values reported for the other two size fractions.
-------
O
O
z
O
O
C
O
H
m
o
?a
o
m
COARSE COMPOSITION (24-hr AVG)
CENTRAL U.S.
Units =; ug/m3
Ret
Site
Dates
Houra
Dur
Number
Mass
OC
EC
Nitrate
Sulfate
Acidity
Al
As
Ba
Br
Ca
Cd
C!
Cr
Cu
8(a,o)
Minneapolis
1980
24
6
3o.es
2.191
0.001
0.022
1.571
0.293
0.002
0.022
Fe 0.744
K
Mg
Mn
Mo
Na
Nl
P
Pb
Rb
S
Sb
Se
Si
Sn
Sr
Tl
V
Zn
0.310
0.026
0.001
0.098
0.224
4.679
0.062
0.027
8(a,o)
Kansas City MO
1980
24
3
4l.6>
2.284
0.003
0.029
3.754
0.530
0.004
0.015
0.979
0.361
0.025
0.002
0.109
0.280
4.809
0.074
0.040
8(a,o)
Akron
1980
i
24
7
34.81
2.509
0.003
0.025
1.431
0.572
0.014
0.018
1.640
0.324
0.044
0.005
0.097
0.451
5.009
0.107
0.069
8(a.o)
Cincinnati
1980
24
2
33.15
2.910
0.017
1.312
0.103
0.002
0.014
0.883
0.363
0.021
0.003
0.037
0.099
0.389
6.633
0.096
0.148
8(a,o)
Buffalo
1980
24
14
44.57
2.808
0.012
2.550
0.728
0.015
0.022
2.040
0.206
0.078
0.009
0.108
0.765
2.675
0.051
0.043
8(a,o)
Dallas
1980
24
4
32.63
1.294
0.006
0.051
3.436
0.029
0.005
0.023
0.720
0.210
0.020
0.002
0.252
0.240
3.210
0.051
0.030
8(a,o)
St. Louis
1980
24
5
33.76
3.837
0.001
0.021
1.784
0.053
0.001
0.014
0.587
0.291
0.017
0.002
0.095
0.279
4.468
0.058
0.021
18(k.r)
St. Louis
8-9/76
6-12
28.06
1.209
0.001
0.034
0.047
2.817
0,001
0.257
0.009
0.014
1.218
0.392
0.035
0.005
0.098
0.189
0.002
0.533
0.001
0.001
4.470
0.001
0.007
0.475
0.004
0.074
6.7(o,p)* 17
St Louis St Louis
9/79-6/81 9/85-8/86
0000-0000
24 24
306 311
12.46 9.§6
3.04
0.021
1.499
0.093
0.580
0.019
0.002
0.088
0.200
1.940
BQL
6.7
-------
B-16
List of References
1. Stevens, R.K., Dzubay, T.G., Lewis, C.W., and Shaw, R.W. (1984). Source apportionment
methods applied to the determination of the origin of ambient aerosols that affect visibility in
forested areas. Atmos. Environ. IS 261.
2. Dzubay, T.G. and Stevens, R.K. (1988). A composite receptor model applied to Philadelphia
aerosol. Environ. Sci. Techn. 22 46-
3. Unpublished data from J. Pinto, U.S. EPA, Research Triangle Park, NC (1995>.
4. Vossler, T.L., Lewis, C.W., Stevens, R.K., Dzubay, T.G., Gordon, G.E., Tuncel,
S.G.,Russworm, G.M., and Keeler, G.J. (1989). Composition and origin of summertime air
pollutants at Deep Creek Lake, Maryland. Atmos. Environ. 211535.
5. Stevens, R.K., Hoffman, A.J., Baugh, J.D., Lewis, C.W., Zweidinger, R.B., Cupitt, L.T.,
Kellogg, R.B. and Simonson, J.H. (1995). A comparison of air quality measurements in
Roanoke, Va, and other integrated air cancer project monitoring locations. In: Measurement of
Toxic and Related Air Pollutants. Proceedings of the 1993 U.S. EPA/A&WMA International
Symposium. A&WMA, Pittsburgh, PA, p!85.
6. Spengler, J.D. and Thurston, G.D. (1983). Mass and elemental composition of fine and coarse
particles in six US cities. JAPCA 221162.
7. Dockery, D.W., Pope, C.A., Xu, X., Spengler, J.D., Ware, J.H., Fay, M.E., Ferris, E.G. and
Speizer, F.E. (1993). An association between air pollution and mortality in six U.S. cities. New
Eng. J. Medicine 222 1753.
8. Davis, B.L. Johnson, L.R., Stevens, R.K., Courtney, WJ. and Safriet, D.W. (1984). The quartz
content and elemental composition of aerosols from selected sites of the EPA inhalable paniculate
network. Atmos. Environ. 18 771.
9. Chow, J.C., Watson, J.G., Fujita, E.M., Lu, Z., Lawson, D.R. and Ashbaugh, L.L. (1994).
Temporal and spatial variations of PM2.S and PM10 aerosol in the Southern California Air
Quality Study. Aerosol Sci. and Tech. 212061.
10. Chow, J.C., Watson, J.G., Lowenthal, D.H., Solomon, P.A., Magliano, K.L. Ziman, S.D. and
Richards, L.W. (1993). PM10 and PM2.5 compositions in California's San Joaquin Valley.
Aerosol Sci & Tech. 1£ 105.
11. Unpublished data from the Desert Research Institute (1995).
12. Chow, J.C., Watson, J.G., Pritchett, L., Lowenthal, D.H., Frazier, C., Neuroth, G. and Evans
K. (1990). Wintertime visibility in Phoenix, Arizona. Paper 90-66.6 in Proceedings of the 83rd
National Meeting of the Air & Waste Management Association, Pittsburgh, PA, 24-29 June,
1990.
13. Lewis, C.W., Baumgardner, R.E., Stevens, R.K., and Russworm, G.M. (1986). Receptor
modeling study of Denver winter haze. Environ. Sci. Techn. 2Q 1126.
DRAFT-DO NOT QUOTE OR CITE
-------
B-17
14. Watson, J.G., Chow, J.C., Richards, L.W., Neff, W.D., Andersen, S.R., Dietrich, D.L. Houck,
I.E. and Olmez, I. (1988). The 1987-88 metro Denver brown cloud study, vol 3: data
interpretation. Desert Research Institute. Document No. 8810 1F3.
15. Unpublished data (1995).
16. Johnson, D.L., Davis, B.L., Dzubay, T.G., Hasan, H., Crutcher, E.R., Courtney, W.J.,
Jaklevic, J.M., Thompson, A.C., and Hopke, P.K. (1984). Chemical and physical analyses of
Houston aerosol for interlaboratory comparison of source apportionment procedures. Atmos.
Environ. 1£, 1539.
17. Dockery, D.W., Schwartz, J. and Spengler, J.D. (1992). Air pollution and daily mortality:
associations with particulates and acid aerosols. Environ. Research 52 362.
18. Dzubay, T.G. (1980). Chemical elements balance method applied to dichotomous sampler data.
In: Annals of the New York Academy of Sciences 338 126.
19. Stevens, R.K. (1985). Sampling and analysis methods for use in source apportionment studies
to determine impact of wood burning on fine particle mass. Environment International H 271.
20. Mukerjee, S., Stevens, R.K., Vescio, N., Lumpkin, T.A., Fox, D.L., Shy, C. and Kellogg, R.B.
(1993). A methodology to apportion ambient air measurements to investigate potential effects on
air quality near waste incinerators. In: Proceedings of the 1993 Incineration Conference,
Knoxville, TN. 527.
21. Koutrakis, P. and Spengler, J.D. (1987). Source apportionment of ambient particles in
SteubenvDle, OH using specific rotation factor analysis. Atmos. Environ. 2JL 1511.
22. Chow, J.C., Watson, J.G., Ono, D.M. and Mathai, C.V. (1993). PM10 standards and
nontraditional paniculate source controls: a summary of the A&WMA/EPA international specialty
conference. Air & Waste 43 74.
23. Solomon, P.A. and Moyers, J.L. (1986). A chemical characterization of wintertime haze in
Phoenix, Arizona. Atmos. Environ. 2_Q 207.
24. Ellenson, W.D., Schwab, M., Egler, K.A., Shadwick, D. and Willis, R.D. (1994). Draft
technical report for the pilot project of Lower Rio Grande Valley environmental study. ManTech
Environmental Technology, Inc. Submitted to the U.S. EPA.
25. Chow, J.C., Watson, J.G., Frazier, C.A., Egami, R.T., Goodrich, A. and Ralph, C. (1988).
Spatial and temporal source contributions to PM10 and PM2.5 in Reno, NV. In: Transactions:
PM10 Implementation of Standards, an APCA/EPA international specialty conference. Air
Pollution Control Association, 439.
26. Pope, C.A., Schwartz, J. and Ransom, M.R. (1992). Daily mortality and PM10 Pollution in Utah
Valley. Archives of Environ. Health 47 211.
27. Fairley, D. (1990). The relationship of daily mortality to suspended particulates in Santa Clara
county 1980-1986. Environ. Health Perspectives £9j 159.
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-------
B-18
28. Chow, J.C., Watson, J.G., Lowenthal, D.H., Solomon, P.A., Magliano, K.L. Ziman, S.D. and
Richards, L.W. (1992). PM10 source apportionment in California's San Joaqin Valley. Atmos.
Environ. 26A 3335.
29. Chow, J.C., Fairley, D., Watson, J.G., De Mandel, RM Fujita, E., Lowenthal, D.H., Lu, Z.,
Frazier, C.A., Long, G. and Cordova, J. (1994). Source apportionment of wintertime PM10 at
San Jose, CA. J. Environ Engineers, in press.
30. Watson, J.G., Chow, J.C., Lu, Z., Fujita, E.M., Lowenthal, D.H., Lawson, D.R. and
Ashbaugh, L.L. (1994). Chemical mass balance source apportionment of PM10 during the
Southern California Air Quality Study. Atmos. Environ. 12 2061.
31. Wolff, G.T., Ruthkosky, M.S., Stroup, D. adn Korsog, P.E. (1991). A characterization of the
principal PM10 species in Claremont (summer) and Long Beach (fall) during SCAQS. Atmos.
Environ. 25A 2173.
32. Ashbaugh, L.L., Watson, J.G. and Chow, J. (1989). Estimating fluxes from California's dry
deposition monitoring data. Paper 89-65.3 in: Proceedings of the 82nd Annual Meeting of the
Air & Waste Management Association, Anaheim, CA.
33. Chow, J.C., Watson, J.G., Solomon, P.A., Thuillier, R.H., Magliano, K.L. Ziman, S.D.,
Blumenthal, D.L. and Richards, L.W. (1994). Planning for SJVAQS/AUSPEX Paniculate matter
and visibility sampling and analysis. In: Planning and Managing Regional Air Quality, ed. by
Paul Solomon. CRC Press, Inc.
34. Schwartz, J. (1994). Air pollution and hospital admissions for the elderly in Birmingham,
Alabama. Am. J. Epidemiology. 139 589.
35. Schwartz, J. and Dockery, D.W. (1992). Increased mortality in Philadelphia associated with daily
air pollution concentrations. Am. Rev. Respir. Dis. 145 600.
36. Suh, H.H., Koutrakis, P. and Spengler, J.D. (1993). Validation of personal exposure models for
sulfate and aerosol strong acidity. J. Air Waste Manage. Assoc. 4J 845.
37. Conner, T.L., Miller, J.M., Willis, R.D,, Kellogg, R.B. and Dann, T.F. (1993). Source
apportionment of fine and coarse particles in Southern Ontario, Canada. In: Proceedings of the
86th Annual Meeting of the Air & Waste Management Association, Denver, CO. Paper 93-TP-
58.05.
38. Kim, B.M., Zeldin, M. and Liu, C. (1992). Source apportionment study for state implementation
plan development in the Coachella Valley. In: PM10 Standards and nontraditional paniculate
source controls. Chow and Ono, Eds., Air & Waste Management Association, Pittsburgh, PA,
979.
39. Houck, J.E., Rau] J.A., Body, S. and Chow, J.C. (1992). Source apportionment - Pocatello,
Idaho PM10 nonattainment area. Ibid, 219.
/
40. Chow, J.C., Watson, J.G., Lowenthal, D.H., Frazier, C.A., Hinsvark, B.A., Pritchett, L.C. and
Neuroth, G.R. (1992). Wintertime PM10 and PM2.5 chemical compositions and source
contributions in Tuscon, Arizona. Ibid, 231.
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B-19
41. Vermette, S.J., Williams, A.L. and Landsberger, S. (1992). PM10 source apportionment using
local surface dust profiles: examples from Chicago. Ibid, 262.
42. Thanukos, L.C., Miller, T., Mathai, C.V., Reinholt, D. and Bennett, J. (1992). Intercomparison
of PM10 samplers and source apportionment of ambient PM10 concentrations in Rillito, Arizona.
Ibid, 244.
43. Skidmore, L.W., Chow, J.C. and Tucker, T.T. (1992). PM10 air quality assessment for the
Jefferson County, Ohio air quality control region. Ibid, 1016.
DRAFT-DO NOT QUOTE OR CITE
-------
APPENDIX C
Summary of PM2 5 Air Quality Databases
and Model for Predicting PM2 5
-------
External Review Draft C-l Do Not Quote or Cite
November 1995
Appendix C. PM2 5 Databases and Models for Predicting PM2 5 from PM10 Values
PM2.5 Databases
Most of the air quality analyses used all available PMjQ and PN^ 5 data (1982-1993)
from sites with both PM measurements in the AIRS, IMPROVE, NEPART and Inhalable
Particle Network (IPN) monitoring networks, and some analyses used data from the California
Air Resources Board (CARB) Dichot and Southern California Air Basin (SCAB) Intensive
Monitoring Network databases. Table C-l describes the concurrent PMjQ and PM2 5
databases. See SAI February 1995 report for more details.
For the peak-to-mean analyses, the combined data from the AIRS, IMPROVE, IPN,
CARB Dichot and SCAB Intensive Monitoring Network databases were used. NEPART data
were not used because of frequent cases with PM2 ^/PMjQ ratios above 1 (due to the use of
different measuring instruments).
Predicting Daily PM2 c Values
Because there are more PMjQ data than fine particle data, some efforts were made to
predict PM2 c concentrations from PMjQ values. However, variation monitoring techniques
and variation in the coarse fraction can complicate the ability to predict daily values,
especially in areas with relatively large coarse fractions. Predictions of annual PM2 5 values
are more reliable than estimates of daily PM2 5 values.
In view of the difficulties hi predicting daily PM2 5 values from PMjQ mass alone,
alternative approaches to the ratio estimators were used to provide better estimates of PM2 5
based on PMin and other available data such as region, season, and windspeed.
-------
IMPROVE'
NFS
Class f areas
56
since 10/89
rural
data in-house
I
NESCAUM
(NEPART),
NESCAUM
Class I areas
since 9/88
NE, rural
only PM2 5 is described in
reference
AIRS
Mostly Northeastern
Urban sites
68,
(8 rural)
since '83
mostly NE,
urban
IPN
EPA
All regions, but
most in northeast
36,
(6 rural)
1/82- 1/84
mostly NE,
urban
dlchots
CARS Dichot
Network
CARB
California sites
routine since
1/80
W, mostly
urban?
o
NJ
SJVAQS
DRI
San Joaquin Valley,
CA
6
6/88 - 6/89
SW,urban
& rural
3 urban, 3 rural
seasonal data summary in-
house
SNAPS-II
DRI
Reno, NV
2/87 - 3/87
SW, urban
data (graph) In-house (JAPCA
1990)
Phoenix PM10
DRI
Phoenix,, AZ
8
9/89-1/90
SW, urban
data summary In-house
Phoenix Urban
Haze
DRI
Phoenix,'A2
9/89- 1/90
SW, urban
6-hr samples
(mornlng/afteroon); data
summary in-house
Tucson PMt0
DRI
Tucson, AZ
9/89-1/90
SW, urban
data summary In-house
Tucson Urban
Haze
fJRI
Tucson, AZ
9/89 • 1/90
SW, urban
6-hr samples
(morning/afternoon)
to
n
«T
SCAB Intensive
Monitoring
SCAQMD
Downtown Los
Angeles, CA
1/88- 12/86
SW, urban
data In-house
-------
fcftjOY " ""
#h>'M < ' -
Neighborhood-
Scale Rubidoux
Oregon AQSN
Jefferson
County SIP
PREVENT
Shenandoah
Visibility
MOHAVE
AUSPEX
CADMP
Acid Aerosol
Forest Response
Puget Sound Air
Toxics
ma*?* '
W*"
-------
External Review Draft C-4 Do Not Quote or Cite
November 1995
By significantly augmenting the database of PM9 5 concentrations, these regression
predictions could be used to provide more complete information on the impact of proposed
alternative PM9 c NAAQS formulations. The applicability of these results would depend
4*t »?
upon the strength of the regression model (predictive accuracy).
For the regression modeling the 1988-1993 AIRS PM database was combined with
wind speed data (daily maximum and daily mean) for the nearest monitor, and AIRS daily
maximum hourly ozone data (for the nearest monitor within 20 miles).
The models included regressions on selected measured factors and variables such as
season, region, wind speed, and daily maximum hourly ozone; however, the predictions of
daily PM7 r values still has uncertainties as represented by a low R squared correlation
jLi • _J
statistic (R = 0.4) and by high mean squared errors of the predicted ratio (0.025) and PN^ 5
concentration.
The best model was selected using a stepwise regression procedure to avoid including
terms that would increase the complexity of the model without significantly improving the
model accuracy. This model expresses the mean ratio as the sum of terms for season, land
use, region, log daily maximum hourly ozone concentration, log daily maximum wind speed,
log daily mean wind speed, some of their two-factor interactions and quadratic terms,
together with a multiple of PMjQ. (An interaction measures the extent to which the effect of
one variable varies with the level of another variable. For example, the inclusion of a
season/region interaction term means that the model assumes that the mean ratio for a season
is different for different regions.)
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External Review Draft
November 1995
C-5
Do Not Quote or Cite
The final model had a R-squared statistic of 0.4. The "typical" error, as defined by the
root mean square error divided by the mean measured value, is about 30 percent for the ratio
and about 40 percent for the predicted PN^ 5. Table C-2 gives more information about the
regression models, including a list of the independent variables. For more details about this
table and about the regressions, see SAI, 1995.
TABLE C-2. Summary of GLM ratio predictions for 1988-1993 using 3 regression
models.
Model
Effects
1
Range of
Predicted
Ratios
Mean Square Error
Predicted Predicted
R-Square Ratio
PM
2 5
1. Full
2. Best
3. PM
Only
S,R,L,0,P,W,M,SR,
SL,SO,SW,SM,RL,RO,
RW,RM,LO,LW,LM,
OO,OW,OM,WW,WM,
MM
S,R,L,O,W,M,SR,SL,
SO,RL,RO,RW,RM,
LO,MM,OO,P
S,R,L,SR,LR,SL
0.125 to
1.005
0.402 0.0254 63.20
0.164 to
0.997
0.241 to
0.785
0.399 0.0254 63.01
0.345 0.0259 69.43
1 S = Season; R = Region; L = Land use; P = PMjQ-, O = Log Ozone; W = Log
Maximum Wind Speed; M = Log Mean Wind Speed.
All predictions are based on 4,158 observations, of which 2,221 had
PM1Q > 30 /xg/m3.
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External Review Draft
November 1995
C-6
Do Not Quote or Cite
Table C-3. Regression Coefficients
Description
Intercept
11
ri
r2
r3
r4
61
62
83
M
W
O
MM
00
P
rl*sl
r2*Bl
r3*El
r4*6l
rl«s2
r2*s2
r3*B2
r4*B2
rl*s3
r2*e3
r3*63
rl*0
r2*O
r3*0
r4*O
rl*M
r2*M
r3*M
r4*M
ll*O
61*0
62*0
B3*O
Il*r3
rl*W
r2*W
r3*w
r4*W
11*61
11*62
11*63
Coefficient
1.3959325348
0.3073145307
-0.3776503620
-0.1340208501
-0.1666333810
-0.0279404757
-0.1074828313
0.0008228475
0.0378687052
0.0077850304
-0.0571402112
-0.3013312495
-0.0166049496
0.0272285221
-0.0005619142
-0.0063374696
-0.0234241617
-0.0022432622
-0.0039536140
-0.0034235951
0.0106803520
0.0030315657
0.0013630935
-0.0316804924
0.0050697115
-0.0041470165
0.0448202236
-0.0014492506
0.0457880844
0.0063878655
-0.0162975221
-0.0566163387
0.0015303057
-0.0048482228
-0.0839335316
0.0328830035
0.0006064914
0.0025819148
0.0243145834
0.0962484064
0.0682528572
-0.0026358922
-0.0120560988
0.0304714189
-0.0087578574
0.0130235897
Std. Error
0.1474182834
0.0956879182
0.1309241123
0.0539672399
0.0402760651
0.0229316883
0.0378706642
0.0228386788
0.0229151628
0.0246859620
0.0247969456
0.0597227364
0.0076897974
0.0074196893
0.0001437664
0.0108643150
0.0060784225
0.0036520019
0.0025380381
0.0072239755
0.0037837339
0.0024723039
0.0016068555
0.0134740214
0.0051831044
0.0033092445
0.0247292661
0.0105907134
0.0075674780
0.0043171802
0.0401053217
0.0187467621
0.0125849727
0.0096187141
0.0230356244
0.0086496791
0.0052878957
0.0054471383
0.0082318869
0.0428591060
0.0222493632
0.0157960596
0.0108329495
0.0147528462
0.0089204190
0.0082105759
P = PMjO' O = log (daily maximum hourly ozone),
W = log (daily maximum wind speed),
M = log (daily mean wind speed) rl-r4, sl-s3,
11 are coded region, season, and land-use variable
-------
APPENDIX D
Strengths and Limitations
of Experimental Human and Animal Studies
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External Review Draft j)o Not Quote or Cite
November 1995 D-l
Appendix D
STRENGTHS AND LIMITATIONS OF CONTROLLED HUMAN AND ANIMAL
STUDIES
As discussed above, the adverse effects of particulate matter exposure have been
shown to be consistent between historical and more recent studies. The effects can be severe
and tend to be concentrated in sensitive sub-populations who have pre-existing conditions or
characteristics that tend to make them vulnerable to respiratory insult (the very young and
old, asthmatics, COPD patients, patients with pneumonia etc). The additional risk of
reported mortality and morbidity from particulate matter exposure is relatively small in terms
of the whole population. Therefore, large numbers of people must be exposed before effects
can be discerned in studies. The question arises as to how to elucidate the mechanism of
action of particulate matter in humans. What are the considerations that must be taken into
account when an analysis of the body of human clinical data and experimental animal work is
done in order to infer a plausible mechanism for particulate matter effects?
1. Numbers of Individuals Affected
An issue of primary concern is that of statistical power. The nature of the effect
described in epidemiological work is consistent, and serious, but occurring in a relatively
small fraction of the total population (1 in a million increased risk for daily mortality).
Therefore, theoretically a relatively large number of animals would be needed to mimic the
frequency of response at similar doses. The use of a similar number of animals to mimic the
frequency of response to ambient air concentrations of particles which have been associated
with effect in humans is impractical. Therefore, in many experimental paradigms, relatively
large concentrations are often given investigate the response from a limited number of
animals. However, the questionable relevancy and sensitivity of such paradigms limits their
use in the determination of the mechanism of action of relatively low changes in
concentrations of inhaled particulate matter.
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External Review Draft Do Not Quote or Cite
November 1995 D-2
2. Heterogeneity of Human Population
The human population for which the effects are most demonstrable are a sub-
population from a genetically heterogenous group. Furthermore, consistency of response is
highly variable among the population at risk (e.g., a relatively small group of asthmatics
have aggravation of symptoms and not all patients with pneumonia or COPD die as a result
of an increase in inhaled particle concentration). The CD suggests that for clinical studies
involving asthmatics, differences among subjects may explain in part the differing results
between laboratories who study effects of acid aerosols. As an example of differential
susceptibility to a respiratory insult, a minority of individuals (3-5%) who are exposed to
etiologic agents responsible for hypersensitivity pneumonitis (allergic alveolitis) will develop
disease. Determinants of susceptibility for that disease have been described as both the
genetic constitution of the individual and the presence of preexisting lung disease. Similar
factors probably play a role in susceptibility to inhaled paniculate matter effects.
By contrast experimental animals are bred as much as possible to be homogenous
genetically so as to give great consistency in response. They are also usually studied in their
prime in regard to age and general health. Presence of disease is generally considered to be
a confounding factor to be stringently controlled in most animal paradigms. As stated above,
those segments of the general population most affected from PM,0 exposure are the sick, the
very young, and the old. Therefore the sensitivity of studies using relatively small numbers
of healthy, genetically homogenous, laboratory animals who are in their prime is diminished
in exploring mechanism of paniculate matter effects.
3. Heterogeneity of PM10 Composition
Another key element helps to frame the discussion of the relevance of human clinical
studies and experimental animal work to establish a mechanism of action of paniculate matter
in humans. That is the issue of heterogeneity of both the composition of and exposure to
paniculate matter. Paniculate matter is a broad class of physically and chemically diverse
substances (as described in Chapter IV). The PM,0 fraction is composed of two distinct sub-
fraction of particle: fine and coarse particles. PM10 samplers collect all of the fine particles
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External Review Draft DO Not Quote or Cite
November 1995 D-3
and a portion of the coarse ones. There is a fundamental uncertainty regarding which
components or properties of particulate matter is essential to the observed effects in humans.
Coarse particles are typically composed of re-suspended dusts from fields and streets
and may contain metal oxides of silica, aluminum, magnesium, titanium, and iron. Coal and
oil fly ash, calcium carbonate, sodium chloride, sea salt, small pollen, mold spores, and
plant parts may also be present. Fine particles are generally composed of sulfate, nitrate,
hydrogen ion, elemental carbon, organic compounds, biogenic organic compounds such as
terpenes, and metals such as iron, lead, cadmium, vanadium, nickel, copper, and zinc.
Some materials which are more typically found in the coarse fraction, may be also found the
fine fraction. Similarly, some materials typically found in the fine fraction may also be in
the coarse fraction due to particle growth in conditions of high relative humidity (e.g.,
sulfates). Additionally, the properties of PM,0 vary greatly from place to place because of
differences in source mixes and atmospheric conditions.
Thus unlike a typical experimental paradigm, where the agent to be studied is isolated
and the effects of exposure described in well controlled studies, the heterogeneity of the PMj0
entity forces a different experimental approach. Typically constituents of the fraction are
tested individually to see if effects similar to those observed in humans are reproduced.
Consequently, animal studies are further weakened in regard to ability to establish a
mechanism of action of particulate matter and to either refute or validate epidemiological
observation of effect in humans.
4. Dosimetric Heterogeneity
Finally, as discussed above in section V.A.I., dosimetric comparisons between
laboratory animals and humans, show that there are significant differences in the respiratory
architecture and ventilation of the two which adds additional complication to comparisons of
experimental and observed data. Ventilation differences coupled with differences in upper
airway respiratory tract structure and size, branching pattern, and structure of the lower
respiratory tract occur between species as well as between healthy versus diseased states.
These differences may result in significantly different patterns of airflow affecting particle
deposition patterns in the respiratory tract (CD, Section 13). Additionally, inter-species
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External Review Draft Do Not Quote or Cite
November 1995 D-4
variability in regard to cell morphology, numbers, types, distribution, and functional
capabilities between animal and human respiratory tracks, leads to differences in clearance of
deposited particles which may in turn affect the potential for toxicity. (CD, Section 13).
Consequently the difficulty of using experimental animal data to investigate particulate matter
effects is further defined.
5. Lack of Distinct Disease Pathology
The background levels of cardiopulmonary disease as the cause of death for the
general population is very high. Given that COPD and heart diseases are frequent causes of
death, it is difficult to discern those who die from the additional effects of particulate matter
from those already dying from such diseases and to do autopsy to identify a specific
pathology associated with particulate matter caused mortality. Even in historical studies
involving higher levels resulting in more pronounced effect it is hard to get an adequate
characterization of pathology related to particulate matter effects. Thus without such a
characterization of the pathology of particulate matter induced mortality, development and
validation of appropriate models to study such effects are more difficult.
6. Lack of Appropriate Equivalents to Epidemiological Endpoints
Animal lexicological equivalents of such epidemiological endpoints as hospital
admissions and emergency room visits as an indication of morbidity cannot be obtained.
Although mortality can be recreated in a laboratory setting, the relevance of mechanism is
currently an issue. In addition, there is question as to what the most appropriate measure of
particulate matter is in regard to its toxicity. Specifically is it the inhalable mass which is
the most relevant metric of the toxic quantity of particulate matter or is it the number of
particles which reaches specific targets? Particles may have low inherent toxicity at one size,
yet greater potency at another (CD, Section 11). A recent study by Chen et al. (1995)
confirmed that the number of particles in the exposure atmosphere not just total mass
concentration is an important factor in biological responses following acidic sulfate inhalation
(CD, Section 11). Specifically, ultrafine particles with a diameter of 20 /xm have an
approximately 6 order of magnitude increased number than a 2.5 /*m diameter particle of the
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External Review Draft Do Not Quote or Cite
November 1995 D-5
same mass concentration (CD, Section 11). Comparisons of particle number and size are
shown in Table 11-1 of the CD.
In addition to considerations of dose (inhalability and appropriate metric), the nature
of the response to particles and correlations of the appropriate response to susceptible
population are yet to be resolved. Thus, identification of the dosimeter which induces
mortality and morbidity has not been elucidated with consequent difficulty interpretation and
design of controlled animal and human studies.
-------
APPENDIX E
Epidemiological Evidence of Short-term Exposure Mortality Effects
-------
> TABLE 12-4. SUMMARIES OF PUBLISHED PM10-ACUTE MORTALITY
3. EFFECTS STUDIES BASED ON VARIOUS PM MEASURES
VO
Ui
Health Outcome Synthesis Study
Total Mortality Ostro (1993)
Dockery and Pope
(1994)
to
i
^ Respiratory Mortality Dockery and Pope
(1994)
O
j> Cardiovascular Mortality Dockery and Pope
Jjj (1994)
D'
O
z
O
H
O
d
o
H
W
0
Location
London UK
Steubenville OH
Philadelphia PA
Santa Clara CA
St. Louis MO
Kingston TN
Birmingham AL
Utah Valley UT
Philadelphia PA
Detroit MI
Steubenville OH
Santa Clara CA
Birmingham AL
Utah Valley UT
Philadelphia PA
Santa Clara CA
Birmingham AL
Utah Valley UT
Philadelphia PA
Santa Clara CA
Original PM
Measurement
BS
TSP
TSP
COH
PM10
PM10
PM,0 (3d)
PM10 (5d)
TSP (2d)
TSP
TSP
COH
PM10 (3d)
PM10 (5d)
TSP (2d)
COH
PM10 (3d)
PM10 (5d)
TSP (2d)
COH
Mean
Equivalent PM10
80
61
42
37
28
30
48
47
40
48
61
35
48
47
40
35
48
47
40
35
Percent Change
Per 10 fig/m3
PM10 Equivalent
0.3
0.6
1.2
1.1
1.5
1.6
1.0
1.5
1.2
1.0
0.7
0.8
1.5
3.7
3.3
3.5
1.6
1.8
1.7
0.8
95 Percent
Confidence Interval
(0.29, 0.31)
(0.44, 0.84)
(0.96, 1.44)
(0.73, 1.51)
(0.1,2.9)
(-1.3.4.6)
(0.2, 1.5)
(0.9,2.1)
(0.7, 1.7)
(0.5, 1.6)
(0.4, 1.0)
(0.2, 1.5)
(-5.8, 9.4)
(0.7, 6.7)
(0.1, 6.6)
(1.5,5.6)
(-1.5, 3.7)
(0.4, 3.3)
(1.0,2.4)
(0.1, 1.6)
n
HH
3
-------
TABLE 12-3. SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
KM (mc.in = 25;
SD = 11)
Total, respiratory, and cardiovascular mortality in
Los Angeles County during 1970 to 1979 related to
O3, CO, SO2, NO2, HC, daily max. temperature,
relative humidity, and KM (a paniculate matter
metric of optical reflectance by particles, related to
the ambient carbon concentration). Low pass filter
used to eliminate short-wave, so that only long-
wave associations are studied.
Frequency domain analyses indicated significant
short- and long-wave associations with KM. The
filtered (i.e., long-wave) data analysis indicated that
air pollution (including KM) was significantly
associated with seasonal variations in LA mortality.
Shumway et al.
(1988)
K>
-U
OC
o
o
z
o
H
O
G
O
H
tn
o
JO
n
^^
H
tn
TSP (OECD Method)
(Lyons, France: 3 year
mean = 87 ,ug/m3}
(Marseilles, France
3 y mean = 126
BS
(mean = 90.1 jig/m3)
(24-h avg. daily max.
709 ;tg/m3)
Daily total, respiratory, and cardiac mortality for
persons 5:65 years of age tested for associations
with S02 and TSP during 1974 to 1976 in Lyons
and Marseilles, France. Temperature also
considered in analyses.
Daily total mortality analyzed for associations with
BS, SO2, and H2SO4 in London, England, during
1963 to 1972 winters. Mean daily temperature and
relative humidity also considered.
No significant mortality associations found with TSP,
while SO2 was reportedly associated with total
elderly deaths in both cities. Seasonally addressed
by analyzing deviations from 3-year average of
31-day running means of variables. However, lags
of temperature not considered and probable seasonal
differences in winter/summer temperature-mortality
relationship not addressed.
PM, SO2, and H2S04 all indicated as having
significant associations with mortality (0, 1 day lag).
Temperature also correlated (negatively) with
mortality, but with a 2-day lag. Seasonally
addressed by studying only winters and by applying a
high-pass filter to the series and analyzing residuals.
Derriennic et al.
(1989)
Thurston et al.
(1989)
-------
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
COH (monthly mean
range = 9 to 12)
BS
Daily total, respiratory, cancer, and circulatory
associations with daily COH in Santa Clara
County, CA, during 1980 to 1982 and 1984 to
1986 winters. Daily mean temperature and
relative humidity at 4 PM also considered.
Daily total mortality in Athens, Greece, and
surrounding boroughs during 1975 to 1987
related to BS, SO2, NO2, O3, and CO2 using
multiple regression.
An association found between COH and increased
mortality, even after making adjustments for
temperature, relative humidity, year, and
seasonality.
During winter months 1983 to 1987, the daily
number of deaths was positively and statistically
significantly associated with all pollutants, but the
association was strongest with BS.
Fairley (1990)
Katsouyanni et al.
(1990a)
to
BS (annual mean range
= 51.6to73.3/ig/m3)
(maximum daily value
= 790 jig/m3)
For the period 1975 to 1982 in Athens, Greece,
199 days with high SO2 (> 150 iigtm*) were
each matched on remperarure, year, season, day
of week, and holidays with two low SO2 days.
Mortality by-cause comparisons made between
groups by analysis of variance by randomized
blocks. BS correlated with SO2 at r = 0.73, but
not directly employed in the analysis.
Mortality was generally higher on high SO2 days,
with the difference being most pronounced for
respiratory conditions. BS levels for each group
not provided, and BS-SO2 confounding not
addressed, limiting interpretability of results.
Katsouyanni et al.
(1990b)
-------
XJ
a.
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
KM
(mean = 25;
SO -• 11)
Shumway et al. (1988) 1970 to 1979 Los Angeles
mortality dataset analyzed using a high-pass filter
to allow investigation of short-wave (acute)
associations with environmental variables (by
removing seasonality effects). Environmental
variables considered in regression analyses
included temperature, relative humidity,
extinction coefficient, carbonaceous paniculate
matter (KM), SO2> NO2, CO, and O3.
Analyses demonstrated significant associations
between short-term variations in total mortality and
pollution, after controlling for temperature. Day-
of-week effects found not to affect the
relationships. The results demonstrated significant
mortality associations with O3 lagged 1 day, and
with temperature, NO2, CO, and KM. The latter
three pollutants were highly correlated with each
other, making it impossible to separately estimate
paniculate matter associations with mortality.
Kinney and Ozkaynak
(1991)
N> TSP
tl* (mean = 87 ng/m3)
(24-h avg. range:
46 to 137 /ig/m3,
5th to 95th percentiles)
Total deaths in Detroit, MI, 1973 to 1982
analyzed using Poisson methods. Environmental
variables considered included TSP, SO2, O3,
temperature, and dew point. Seasonality
controlled via multiple dummy weather and time
variables.
Significant associations reported between TSP and
mortality in autoregressive Poisson models (RR of
100 /ig/m3 TSP = 1.06). However, most TSP
data estimated from visibility, which is best
correlated with the fine aerosol (and especially
sulfate) portion of the TSP. Thus, results suggest
a fine particle association.
Schwartz (1991)
TSP
(mean = 77 /ig/m3)
(max. -- 380 jig/m3)
(5th to 95th percentiles
37 to 132
Total and cause specific daily mortality in
Philadelphia, PA during 1973 to 1980 related to
daily TSP and SO2 (n «2,700 days). No other
pollutants considered in the analysis. Poisson
regression models, using GEE methods, included
controls for year, season, temperature, and
humidity. Autocorrelation addressed via
autoregressive terms in model.
Strongest associations found with pollution on the
same and prior days. Total mortality (mean =
48/day) estimated to increase 7% (95% C.I. =
4 to 10%) for a 100 jig/m3 increase in TSP.
Cause-specific effects of TSP were larger (as %).
SO2 associations were non-significant in
simultaneous models with TSP, but correlations of
their coefficients not reported
Schwartz and Dockery
(1992a)
-------
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
to
O
O
'Z
G
O
H
W
TSP
(mean = 69 /tg/m3)
(5th to 95th percentiles
32 to 120 /tg/m3)
TSP
(mean = 111
(24-h avg. range:
36 to 209 ng/m3,
10th to 90th percentiles)
TSP
(mean = 113 /ig/m3)
(10th to 90th percentiles
38 to 212 /ig/m3)
Age and cause-specific daily mortality in
Philadelphia, PA during 1973 and 1990 related
to daily TSP, SO2, and O3. Other environmental
variables included were: temperature,
barometric pressure, humidity, and precipitation.
Various models employed, including poisson and
autoregessive. Prefiltering methods also applied
to remove long-waves in data.
Daily total mortality in Steubenville, OH,
between 1974 to 1984 related to TSP, SO2,
temperature, and dew point. Poisson regression
employed, because of very low death counts/day
(mean = 3.1). Regressions controlled for
season by including dummy variables for winter
and spring, and autoregrcssive methods also used
to address any remaining autocorrelation.
Daily mortality in Steubenville, OH during 1974
to 1984 related to TSP, SO2, temperature, and
dew point (to allow comparisons of results with
Schwartz and Dockery, 1992b). Poisson method
employed. Analyses done overall and by-season.
TSP effect found only in winter season. TSP
never significant in by-cause analyses of those
< 15 or ^65 years of age. TSP effects
weakened by the addition of other pollutants
(TSP-SO2 r = 0.57). However, the inclusion of
barometric pressure and precipitation in these
models may have acted as surrogates for PM,
potentially confounding results. Correlations
between TSP and these variables not presented.
In regressions controlling for season and
weather, previous day's TSP was a significant
predictor of daily mortality. SO2 was less
significant in regressions, becoming
nonsignificant when entered simultaneous with
TSP. Auto-regressive models gave similar
results.
In single pollutant models, the TSP coefficient
was the same as Schwartz and Dockery (1992b),
but TSP effects were found to be attenuated by
S02 inclusion in the model. S02 was also
attenuated by the addition of TSP. It is
concluded that TSP and SO2 effects cannot be
separated in this dataset. Intel-correlations
among these variables not presented.
Li and Roth (1995)
Schwartz and Dockery
(1992b)
Moolgavkar et al.
(1995)
n
-------
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
RS
(mean =
90. 1 ;
-------
vo
vo
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICULATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
TSP
(mean = 52 jug/m3;
SD = 19.6
Daily total and cause-specific mortality in Cincinnati,
OH, (mean total = 21/day) during 1977 to 1982
related to TSP, temperature, and dew point. Poisson
model employed with dummy variables for each month
and for eight (unspecified) categories of temperature
and dew point. Linear and quadratic time trend terms
also included. Spline and nonparametric models also
applied. Autocorrelation not directly addressed.
TSP was significantly associated with increased risk of total
mortality. The relative risk was higher for the elderly and
for those dying of pneumonia and cardiovascular disease.
However, the analysis failed to consider other pollutants,
and there remains the potential for within-month, long-wave
confoundings.
Schwartz
(1994a)
U)
TSP
(mean =
375 fig/m3)
(maximum
1,003
PM)0
(mean = 47
(24 h max.
365 ,ig/m3)
(5 day max.
297 ,zg/m3)
jtg/m3)
Daily deaths during 1989 in two residential areas in
Beijing, China, (mean total deaths = 21.6/day) related
to TSP and S02 using Poisson methods. Controlling
indicator variables for quintiles of temperature and
humidity, as well as for Sunday also included.
Long-wave confounding and autocorrelation not
directly addressed. However, season-specific results
presented.
Total, respiratory, and cardiovascular mortality in
Utah County, UT, during 1985 to 1989 related to
5-day moving average PM)0, temperature, and
humidity. Time trend and a random year terms also
included in autoregressive Poisson models employed.
Seasonally not directly addressed in this basic model,
but the addition of four seasonal dummy variables
changed results little.
Significant mortality associations found for In (S02) and In Xu et al.
(TSP). Associations were strongest for chronic respiratory (1994)
diseases. In simultaneous regressions, SO2 was significant,
but not TSP. However, the two pollutants were highly
correlated with each other (r = 0.6), as well as with
temperature. In season-specific analyses, both pollutants
were significant in summer, but only SO2 in winter.
A significant positive association between total non- Pope et al.
accidental mortality and PM,0 was observed, the strongest (1992)
association being with the 5-day moving average of PM10.
The association was largest for respiratory disease, the next
largest for cardiovascular, and the lowest for all other.
Association noted below 150 jig/m3 PM10. The possible
influence of other pollutants discussed, but not directly
addressed.
-------
D.
\o
TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
PM
10
St. Louis, MO:
(mean = 28 ^g/m3)
(24 hr max. = 97 /tg/m3)
Kingston/Harriman, TN
(mean = 30 /ig/m3)
(24 h max. = 67
Total mortality in St. Louis, MO, and
Kingston/Harriman, TN (and surrounding
counties), during September 1985 to August 1986
related to PM)0> PM2 5, SO2, N02, O3, H + ,
temperature, dew point, and season using auto-
regressive Poisson models.
Statistically significant daily mortality associations
found with PM10 and PM2 5 in St. Louis, but not
with other pollutants. In Kingston/Harriman, PM10
and PM2 5 approached significance, while other
pollutants did not. Seasonality was reduced by
season indicator, variables, but within season long
wave cycles not directly addressed.
Dockery et al.
(1992)
PM10
(mean = 48 /*g/m3)
(24 h max. = 163 A 150
employed addressed seasonal long wave influences /ig/m3. However, the possible role of other
by the inclusion of 24 sine and cosine terms having pollutants not evaluated.
periods ranging from 1 mo to 2 years.
Autoregressive linear models also applied.
D
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m
PMIO
(mean = 40
(24 h max. = 96
Total, cardiovascular, cancer, and respiratory
mortality in Toronto, Canada, during 1972 to 1990
related to PM10, TSP, SO4, CO, O3, temperature,
and relative humidity. Nineteen-day moving
average filtered data used in OLS regressions.
Sixty-three hundred and three PM10 values
estimated based on TSP, S04, COH, visibility
(Bex() and temperature data, using model developed
from 200 PM,0 sampling days during the period.
Significant associations found between all pollutants
considered and mortality, after controlling for
weather and long wave influences. However, it was
not possible to separate the PM10 association from
other paniculate measures considered. Simultaneous
PM and ozone regressions gave significant
coefficients for each, but intercorrelations among the
pollutants not presented.
Ozkaynak et al.
(1994)
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TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
PM
10
(mean = 58 /*g/m3)
(24 h max. =
177 i/m3)
Total mortality in Los Angeles, CA, during 1985 to 1990
related to PM,0, O3, CO, temperature, and relative
humidity. Poisson models employed addressed seasonal
long-wave influences by including multiple sine and cosine
terms ranging from 1 mo to 2 years in periodicity. OLS
and long linear models also tested. Winter and summer
analyzed separately also.
Association between PMj0 and mortality found to be
only mildly sensitive to modeling method. CO also
individually significant. The addition of either CO or
03 lowered the significance of PM10 in model
somewhat, but the PM10 coefficient was not as
affected, indicating minimal effects on the PM10
association by other pollutants in this case.
Kinney et
al. (1995)
to
PM10
(mean = 38
(24 h max.
128 /zg/m3)
Total mortality in Los Angeles, CA and Chicago, IL
during 1985 through 1990 related to PM10, O3, and
temperature. Analysis focused on importance of monitor
choice to modeling results. Poisson models used
addressed seasonal long wave influences by including
multiple sine/cosine terms ranging from 1 mo to 2 years
in periodicity.
Average of multiple sites' PM10 found to be
significantly associated with mortality in each city after
controlling for season, temperature and ozone. Other
pollutants and relative humidity not yet considered.
Individual sites' PM10 varied from non-significant to
strongly significant. Also, dividing the data by season
diminished the significance of the multi-site average
PM10 in mortality regressions. Both site selection and
sample size concluded to influence results.
Ito et al.
(1995)
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VO
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TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
to
PMIO
(mean = 115
(24 h max.
367 /ig/nv,)
PM10
(mean = 82.4 /ig/m3)
(24 h avg. SE =
38.9 fig/m3)
Total, respiratory, and cardiovascular daily deaths/day
(means = 55, 8, and 18, respectively) in Santiago, Chili
during 1989 through 1991 related to PM10, O3, SO2, NO2,
temperature and humidity. Seasonal influences addressed
by various methods, including seasonal stratification, the
inclusion of sine/cosine terms for 2.4, 3, 4, 6, and 12
month periodicities, prefiltering, and the use of a
nonparametric fit of temperature. Log of PM10 modeled
using OLS with first order autoregressive terms.
Respiratory mortality among children < 5 years old
(mean = 3/day) in Sao Paulo, Brazil during May 1990
through April 1991 related to PM10, SO2, NOX, O3, CO,
temperature, humidity, and day of week. Season
addressed by including seasonal and monthly dummy
variables in regressions. Mortality data adjusted for non-
normality via a square root transformation.
Significant association found between PMto and daily Ostro et al.
mortality, even after addressing potential confounders (1995a)
(e.g., weather), other pollutants, lag structure, and
outliers. Strongest associations found for respiratory
deaths. S02 and NO2 also significantly associated
individually, but only PM10 remained significant
when all were added simultaneously to the
regression. Correlations of the coefficients not
reported.
Significant association found between respiratory Saldiva et al.
deaths and NOX, but no other pollutants. No such (1994)
association found for non-respiratory deaths.
However, auto-correlation not addressed. Also,
inter-correlations of the pollutant coefficients not
reported (but NOX - PM10 correlation = 0.68)
PM
0
O
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m
10
Total mortality among the elderly (^65 years old)
(mean = 82.4 /ig/m3) (mean = 63/day) in Sao Paulo, Brazil during May 1990
(24 h avg. SE =
38.9 /lg/m3)
through April 1991 related to two day avg. of PM10, S02,
NOX, O3, and CO, and to temperature, humidity, and day
of week. Season addressed by including seasonal and
monthly dummy variables. Temperature addressed using
three discrete dummy variables.
Significant associations found between total elderly Saldiva et al.
deaths and all pollutants considered. In a (1994)
simultaneous regression, PM10 was the only pollutant
which remained significant. The PM10 coefficient
actually increased in this regression, suggesting
interpollutant interactions. Correlations of the
pollutant coefficients not provided.
o
I— <
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I— I
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TABLE 12-3 (cont'd). SUMMARIES OF RECENTLY PUBLISHED EPIDEMIOLOGICAL STUDIES
RELATING HUMAN MORTALITY TO AMBIENT LEVELS OF PARTICIPATE MATTER
PM Measure
(Concentrations)
Study Description
Results and Comments
Reference
PM10 (Cook County
median = 37 /xg/m3;
max = 365 /*g/m3)
(Salt Lake County
median = 35 /*g/m3;
max = 487 jig/m3)
Total, respiratory, circulatory, and cancer mortality in
Cook County, 1985 to 1990. Elderly, total by race and
sex also evaluated. Poisson regression with seasonal
adjustments, meteorological variables, and pollen tested.
In Salt Lake Count, total and elderly mortality. One daily
station in Cook County and two daily monitoring stations
in Salt Lake County, plus multiple -day stations.
Average and single site PMi0 were significant
predictions of PM,0 in Cook County for total,
elderly, cancer, and elderly white mortality, marginal
for respiratory, circulatory, and elderly black.
Significant Fall and Spring mortality in Cook
County, not Summer or Winter. No significant
effects in Salt Lake County. No copollutants.
Styer et al.
(1995)
to
PM10 (variable by
month and year)
Reanalysis of Utah County mortality, 1985 to 1992,
broken down by year, season cause and place of death.
PM10 was entered as a dichotomous variable, less or
greater than 50 ^g/m3. No adjustment for copollutants or
for weather in Poisson regression, except for daily
minimum temperature. Poisson regression, not GEE.
Variations in RR did not appear to be associated with Lyon et al.
high or low PM10 days. High RR for cancer deaths, (1995)
age < 60, at home. Highest RR in spring.
Increased RR for sudden infant death syndrome.
Patterns appear noncausal.
-------
APPENDIX F
Miscellaneous Tables of Effects Information
-------
TABLE 11-2. CONTROLLED HUMAN EXPOSURES TO ACID AEROSOLS AND OTHER PARTICLES
l~»
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*— t
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0
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Ref. Subjects Exposures' MMAD2 GSD3
Anderson et 15 healthy 1): air
al. (1992) 15 asthmatic 2): H^C^ • 100 /ig/m3 1.0 2
18 to 45 years 3): carbon black
»200>ig/nr'
4): acid-coated carbon
with » 100 pg/m3 H2SO4
Aris et al. 19 asthmatic Mouthpiece study:
(1990) 20 to 40 years HMSA3 0 to 1000 /iM + ft j
H2SO4 50 fM vs H2SO4 50
/iM
Chamber study: ^
HMSA 1 mM + HjSC^
5 mM vs H2SO4 5 mM
Aris et al. 10 healthy HNOj 500 fig/m3 or H2O, or =6
( 1 99 1 a) nonsmokers 2 1 air followed by ozone 0.2
to 31 years ppm
ozone sensitive
Aris et al. 18 asthmatics Mouthpiece study:
( 1 99 1 b) 23 to 37 years HjSO, v» NaCI. 0.4 vs « 6
• 3000 fig/m3 with varying
particle size, osmolarity,
relative humidity
Chamber study: H2SO4 vs
NaCI, 960 to 1400 fig/m3 fi
with varying water content
Duration Exercise Temp RH4 Symptoms Lung Function Other Effects
'C %
60 min. VF = 50 22 50 Healthy subjects Largest No change in
L/min more decrements in airway
symptomatic in FVC with air responsiveness
air. exposure.
100 Won 100 HMSA did not No effects on
cycle increase SRaw6
symptoms in
comparison with
, h .25 H'S°< al0ne'
2h 50 min of 22 100 No effects of No direct effects No change in
each h fog exposure of fog exposures, airway
40 L/min Greatest responsiveness
decrements when
ozone preceded
„ ,_ by air.
22 50 '
No effects Increases in SRaw
. , . .... . . with low RH
16 mm With & .. .
... . conditions; no
without „. .- „ . .
• 24 <10vs pollutant-related
exercise. *"L
100 effects
100 Won
1 h cycle =27
Comments
Smoking
status of
subjects not
stated.
Fog may
have
reduced
ozone
effects on
lung
function.
Postulated
that effects
seen in other
studies due
to secretions
or effects on
larynx
-------
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TABLE 11-2 (CONT'D). CONTROLLED HUMAN EXPOSURES TO ACID AEROSOLS AND OTHER PARTICLES
Rrf Subjects
Avol ei al ?1 healthy
(liSS;!) 2\ asthmatic
18 to •)? years
Avol et al. 22 healthy
(!088b) 27. asthmatic
18 to 45 years
Avol et al. 32 asthmatics
(1000) 3 to 16 years
Balmes et 12 asthmatics
al. (1088) responsive to
hypcosmolar
saline aerosol
25 to 41 years
Temp
Exposures1 MMAD2 GSD3 Duration Exercise 'C
Air 0.85to 2.4 to Ih 10 min X 3 21
HjSO4: 0.91 2.5 47 to
Healthy: 363. 40 L/min
1128. 1578
Asthmatic: 396,
999. 1.460
rt'm,
H2O 9.7 to 10.7 1 h 10 min X 3 9
HjSO4: 41 to 46
Healthy: 647. L/min
1.100,2,193
pg/nr1
Asthmatic: 516,
1,085,2,034
Mg/mj
Air 40 min 30 min rest, 21
HjSO446. 127, 0.5 1.9 10 min
and 134 /jg/nr1 exercise
20L/min;m2
Mouthpiece, At rest =23
5.900to
yj.lOOptaf:
NaCl 30 mOsm
HjSO430mOsm -5 to 6 1.5
HNOj 30 mOsm
HjSO4+HN0330
fflOsin
H2SO4 300 mOsm
RH4 Symptoms Lung Function Other Effects
50 Healthy: Slight Healthy: No
increase in cough with effects on hing
highest function or
concentrations. airway reactivity.
Asthma: dose-related Asthma: 1FEV,
increase in lower 0.26 L with
resp. sx. H2SO4 1.460
100 Dose-related increase Healthy: No No effects on
in lower resp. sx. in effects on lung airway
both groups. function. responsiveness
Asthma: tpeak
flow 16% at
2.034 fig/m1
H2S04 .
48 No pollutant effect No pollutant
effect.
One subject
increased SRaw
14.2% with acid
exposure.
Concentration of
acid aerosol
required to
increase SRaw by
100% lower than
forNaCl. No
difference
between acid
species.
Comments
Half the subjects
received acidic
gargle; no
difference in
effects.
Did not
reproduce
findings of
Koeniget al..
1983.
Exposures did
not mimic
environmental
conditions. No
mitigation by
oral ammonia.
-------
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TABLE tl-2 (CONTD). CONTROLLED HUMAN EXPOSURES TO ACID AEROSOLS AND OTHER PARTICLES
Ref. Subjects
Culpctal. 16 healthy
(1995) 20 to 3° yrs
Fine ct al. 8 asthmatics
(19876) 22to29yrs
Fine et al. 10 asthmatics
(1987a) 22 to 34 yrs
Framptonet 12 healthy
al. (1992) 20to39yrs
Frampton et 30 healthy
al. (1995) 30 asthmatics
20 to 42 yrs
Green el al. 24 healthy
(1989) 18 to 35 yrs
Temp
Exposures1 MMAD2 GSD3 Duration Exercise 'C
N»CllOOO/ig/m3 0.9 1.9 2h IOminX4 22
H2SO4 =40 L/min
l.OOOMg/m3
Mouthpiece: 5.3 to 6.2 1.6 to At rest
Buffered and 1-8
unbuffered HC1
•nd
-------
p TABLE 11-2 (CONT'D). CONTROLLED HUMAN EXPOSURES TO ACID AEROSOLS AND OTHER PARTICLES
o
O"
— • H.inlev et
5* al (1'W;)
i—
^O
Koenig ct
3\ (I9R9)
Koenig et
al (1902)
H- *
I
t— *
Koenig ct
al (1 093)
rE
3
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Subjects Exposures'
22 asthmatics Mouthpiece:
12 H) 19 yrs 5): Air;
H2SO470, 130fig/m3
2): Air;
H2SO4 70 pg/m3
with and without lemonade
9 asthmatics with Mouthpiece:
exercise-induced Air;
hrnncho-spasm HjSO4 68 fig/m3:
12 to 18 yrs SOjO.l ppm;
HNOj 0.05 ppm
14 astlimatics with Mouthpiece:
exercise-induced Air;
tironcho-spasm H3SO4 35 or 70 |ug/m'
1 3 to 18 yrs
R healthy Mouthpiece:
9 asthmatic Air;
60 to 76 yrs (Nfty^SO^ «70 fig/m3;
H,SO4 -74 to 82 f
-------
TABLE 11-2 (CONT'D). CONTROLLED HUMAN EXPOSURES TO ACID AEROSOLS AND OTHER PARTICLES
Ref.
Koenig et
al. (1994)
Kulle et al.
(1986)
Laube et al.
(1993)
Linn et al.
(1989)
Linn et al.
(1994)
Subjects
28
asthmatics
12 to 19 yrs
20 healthy
20 to 35 yrs
7 healthy
20 to 31 yrs
22 healthy
19 asthmatic
18 to 48 yrs
15 healthy
30 asthmatic
18 to 50 yrs
Exposures1 MMAD2
Mouthpiece:
Air;
ozone 0.12 ppm+NOj 0.6
0.3 ppm;
ozone 0.12 ppm+NOj
0.3 ppm+HjSO4
68 fig/m •
ozone 0.12 ppm+NOj
0.3 ppm+HNOj
0.05 ppm
Air. activated carbon 517 1 .5
pglttP; SOj 0.99 ppm;
carbon 517 fig/m3 +
SO2 0.99 ppm.
Head dome:
NaCI -SOOpg/m3 10.3
H2SO4 » 500 jig/m3 10.9
H2O 20
H2S04 -2,000 /ig/m3 10
1
Air;
ozone 0.12 ppm; »0.5
H2SO4 lOOpg/m3'
ozone +H2S04
Temp
GSD3 Duration Exercise 'C RH4 Symptoms
90 min X VE 3 X 22 65 No pollutant
2 days resting effects
1.5
1.5 4h 15 minx 2, 22 60 No
35 L/min symptoms
related to
carbon
exposure
1 h 20 min 22 to 25 99 No pollutant
effects
Ih 40 to 45 «10 74 to Increased
L/min 100 total score
with larger
acid
particles.
6.5 h/dX 2 50 min X 6 21 50 Symptoms
-2 d 29 L/min unrelated to
atmosphere
Lung Function
No pollutant effects
No direct or additive
effects of carbon
exposure
No pollutant effects
No pollutant effects
IFEV, AFVCin
ozone, similar for
healthy & asthmatic
subjects. Greater fall in
FEV, for acid + ozone
than ozone alone,
marginally significant
interaction.
Other Effects
No effects on
airway
responsiveness
Trachea!
clearance
increased
(4/4 subjects).
Outer zone
clearance
increased
(6/7 subjects).
No effects on
airway
responsiveness
No effects on
airway
reactivity
Increased
airway
responsiveness
with ozone.
marginal
further
increase with
ozone + acid
Comments
6 subjects with
moderate or
severe asthma did
not complete
protocol
4 asthmatic
subjects unable to
complete
exposures because
of symptoms.
Avenge subject
lost 100 ml FEV,
with ozone, 189
ml with
ozone -(-acid
Original findings
replicated in
13 subjects
-------
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t— »
TABLE 11-2 (CONT'D). CONTROLLED/ HUMAN EXPOSURES TO
Rrf Subjects
Morrow ei si. 1? asthmatic
'IW-U ?0 tn 57 yrs
_V to ,'i! yrs
I'tcll rt ,il 15 asthmatic
(1W) 19 to 50 yrs
Yang and 30 healthy
Yang(l9i5SO4, tow NH3
Mouthpiece: Bagged
polluted air.
TSP = 202 f.g/m3
Temp
Duration Exercise 'C
2h Asthmatics: 21
10 min X 4
COPD: 7 min
X 1
30 min 10 min
VF3X
resting
?0 min At res!
ACID AEROSOLS AND OTHER PARTICLES
RH4 Symptoms Lung Function
30 No pollutant Asthmatics:
effects. iFEV, slightly
greater after acid
than after NaCI.
COPD: No
effects.
20 to 25 Greater fall in
FEV, with low
NH3(l9%)than
with high NH3
(8%).
Healthy subjects:
no change
Asthmatics:
IFEV, «756
Other Effects
Increased airway
responsiveness
in asthmatics
reported; no
allowance for
change in
airway caliber
Commeno
No control
exposure
'Exposures in environmental chamber unless otherwise stated.
2Mass median aerodynamic diameter. In some studies expressed as volume median diameter; see test.
'Geometric standard deviation.
4Relative humidity.
'Hydroxyme thane sulfonic acid.
'Specific airways resistance.
-------
TABLE 5-2. POSSIBLE RESPONSES TO PARTICLE DEPOSITION IN THE RESPIRATORY TRACT
Principal
Region of Deposition
fxtralhorAcfc (ET)
Tracheobronchial (TD)
Potential Mechanisms
Chemical and mechanical irritation/stimulation of receptors by
deposited material
Slowed, stopped Mucocillary clearance by wood dust
(Schleslnqer and Llppmann. 1970)
Enhanced deposition at larynx (Sehlesinger and Llppmann, 1976)
Chemical and mechanical irritation/stimulation resulting In
bronchoconstrlction (Wlddlcombe et aK, 1962; Made). 1973) by:
."Inert" dusts (granulated charcoal, coal dust, carbon dust,
calcium carbonate, carbon impregnated plastic, iron
hydroxide; Widdtcombe et al., 1962; Dubols and Dautrebande,
1958; Andersen et aK ,1979; Constantine et al., 1959)
.Resuspended urban dust (crustal materials, sulfates,
volatiles; Toyama, 1964)
.Coarse organic dusts, aeroallergens (grain dusts, pollens,
mold, etc. e.g.i Dosman. 1980)
.Fine acid aerosols (sulfuric acid, ammonium btsulfate;
Utell et aKt 1981)
.ConmunTFy air pollution with moderately high PH (Lebowttz
ct al., 1974)
.Ffne particles in combination with pollutant gases (SO.;
Koentg et aJL, 1981; HcJilton et aj_., 1976) '
Enhanced sensitivity to subsequent bronchoconstrie live
agents by sulfuric acid (Utell et a_K. 1981)
Altered clearance rates, Increased mucous production by
deposited material (cigarette smoke, sulfuric acid, dusts)
(Llppmann et aK, 1981; Camner et, aK, 1973)
Direct damage to tissues by acid aerosols
Increased deposition at bronchial bifurcations (Bell and
Frledlander, 1973), slower clearance (Hildlng. 1957)
Interaction of carcinogens and ambient particles
Potential Consequences/Observations
Symptomatic Effects:
-Oryness In nose, mouth, and throat (polymerized dust
containing carbon black, Andersen et a_K, 1979)
-Sneezing, rhinitis (pollen), (MIcheT et aK, 1977)
Nasal cancer (wood workers. NAS,1977a,p. 15M)
Laryngeal cancer (cigarette smoke, NAi, 1977a, p. 150)
Reduced respiratory function
Enhanced breathing difficulties or other acute aggravation
of heart and lung disease, including:
-Asthma (Smith and Paulus, 1971)
-Bronchitis (Lawther et a_K. 1970)
-Emphysema and cardiovascular disease (Martin and
< Bradley. 1960)
-Influenza (sodium nitrate, Utell ejl aK, 1980)
Enhanced deposition of fine and coarse particles
(Albert et aK. 1973)
As above
Possible promotion of bronchitis by repeated exposure
to sulfuric acid (Llppmann et a_K, 1981)
-Increased bronchitis prevalence In people exposed to
community air pollution (Holland et al., 1969;
Holland and Reid, 1965)
-Increased bronchitis prevalence In workers exposed
to coal dust, other dusts (Morgan, 1978)
Bronchial lesions (Alarie et^aj,., 1975)
S1te
-------
TABLE 5-2. POSSIBLE RESPONSES TO PARTICLE DEPOSITION IN THE RESPIRATORY TRACT
(CONTINUED)
Principal
Region of Deposition
Pulmonary (Alveolar, AL)
Thoracic, not specific
to TB, AL
Potential Mechanisms
Decreased oxygen transport and probable increased resistance
of blood flow through pulmonary capillaries
Death of macrophages resulting in release of proteolytlc
enzymes that damage alveolar tissues, by silica, other
coarse dusts (Zlskind et aj_., 1976)
Damage to macrophages, other host defense mechanisms by
surface coating of toxic materials (Camner et al., 1974a;
Aranyi et al., 1979) ~~ ~
Damage to tissues by acid aerosols
Combined effect of exposure and slow clearance of particles
(Pratt and K11 burn. 1971)
Possible effects on host mechanisms (clearance, Immunology)
promoting Infection
Successive measurements of respiratory function suggest
damage to the lung during childhood may be produced by
infection (Speizer et ah, 1980)
Absorption of systemic toxicants (e.g. pesticides, trace
elements, carcinogens) resulting in extra-respfratory
effects. Absorption efficiency greatest for alveolar
deposition
Potential Conseouencpt/nh
Aggravation of cardio-pulmonary disease associated
Increased susceptibility to infection
~taeS"5i TtalUy 1" Jnfected m1ce "posed
to Cd, Ni. Hn aerosols (Gardner 1981-
Graham etai., 1978; AdUns eta. {979 1Mtn
-Loss of alveolar surface areriVwhvse™" ?„ ^ *
exposed to H2S04 (Hyde et al!t 1978) ' °9S
Accumulation of pigment In lungs from inhaled
particulate matter (Pratt and Kilburn. 1971;
Sweet et al_., 1978)
Possible role of community air pollution In
emphysema (Ishikawa e_t a^., 1969)
Increased lower respiratory tract infection in
children with increased BS+SO exposure (Donnl
and Waller. 1966; Lunn et al..; 1967)
Increased influenza rates ("Dust"; Kalpazanov
CC pl.t 19/D)
Persistent changes In airways In those children
with higher Infection rates previously exposed
to particulate matter (Colley et al., 1973;
Klernan et al., 1976)
effects of
Gastro-intestinal cancer (Winklestein and Kantor,
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TABLE 5-3. SENSITIVE POPULATION SUBGROUPS
Subgroup
Individuals with
chronic
obstructive
pulmonary diseases
. Bronchitis
. 6ronch1ectas1s
. Emphysema
Individuals with
cardiovascular
disease
Individuals with
Influenza
Asthmatics
Clderly
Children
Smokers
touth or oronasal
breathers
Population Estimates
7,800,000 (DHEU, 1973)
16,100,000 (DOC, 1980)
Unknown
6,000,000 (DHEW, 1973)
24.658.000
>65 years old
(DOC, 1980)
46,300.000
>14 years old
(DOC, 1980)
50,000,000 {DHEW, 1977)
15X of population
(Nllnlmaa et al., 1981;
Salbene et al., 1978)
Rationale (or Criteria)
-Mucus hypersecretlbn and blocked
airways may predispose Individuals to
bronc'hospasm
-Enlarged airspaces Increase blood
flow resistance through the pulmonary
papillary network. Increasing cardiac
stress
-Enhanced sensitivity to difficulties
in breathing
-Increased sensitivity of respiratory
epithelium (Utell et, a_K, 1980)
-Hyperreactlve airways (Boushey et al.,
19801 .
-Reduced lung elasticity (Cotes, 1979)
-Immunologlcally deficient
-Immunologlcal Immaturity .Imolles
diminished protection (Elsen, 1976)
-Childhood respiratory Infection might
prevent the .lungs from reaching their
full size at maturity (Bouhuys, 1977;
Spelzer et al., 1980)
-Ch11dren~Tlk~?1y to spend a greater
amount of. time outdoors and to be
more active. Probably higher venti-
lation rates and thus, Increased
Inhalation of pollutants.
-Urban lung cancer In smokers greater
(Doll, 1978)
-Combinations of PM and carcinogens
may enhance response
-Increased tracheobronchlal. deposition
(Albert et al., 1973)
-Increased particle penetration (CD,
p. 11-20)
Observational/Associations Supporting Increased Sensitivity
Many of the deaths and Illnesses during and after air pollu-
tion episodes were among people with pre-existing obstructive
diseases (Ministry of Health, 1954; Martin, 1964;
Lawther §!§]_., 1970; Martin and Bradley, 1960)
Many deaths and hospital Izatlons during pollution episodes
among cardiovascular patients (Ministry of Health, U.K.,
1954; Martin, 1964)
Influenza patients were more sensitive to NaNO, during their
period of sickness (Utell et al., 1980). J
Highest mortality during Influenza epidemic on days with
highest PM. (Martin and Bradlev. 19601.
Su If uric acid enhanced response to bronchoconstrlctlve agent
In asthmatics, not In normals (Utell et al., 1981)
-Many of the deaths and Illnesses during air pollution
episodes were among elderly (Ministry of Health,
1954; Martin and Bradley. 1960: Greenburg et al.. 1962).
-Increased acute respiratory disease with high particles,
SOX (Lebowltz et al., 1972; Douglas and Waller, 1966)
-Effects of acute respiratory disease acquired during child-
hood persisted until adolescence or young adulthood
(Colley eial., 1973; Klernan et al., 1976).
-Frequency of respiratory symptoms and diseases greater In
smokers exposed to same occupational or community pollution
as non-smokers (Lambert and Reid, 1970: '"'iSH, 1976).
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