I

PARTICULATE MATTER

Marian Fierro

3/3/2000

TABLE OF CONTENTS

Page

I. Introduction 1
II. Definition 2
III. Standard 4
IV. Physical Properties and Physiological Effects 4
V. Health Effects 7
VI. Conclusions 14
VII. Reference 18

I. INTRODUCTION
Particulate Matter (PM) is one of the six criteria pollutants, and the most important in terms of adverse
effects on human health. The marked increase in mortality that occurred during air pollution episodes

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in the small town of Donora, Pennsylvania, in 1948 (20 deaths) and the London fog of 1952 (4000
deaths), provides evidence of the impact that this pollutant has on human health. Since this date,
many epidemiological studies of PM health effects have been completed. These studies showed that
particulate matter, especially particles that are smaller than 10 microns (PM10), are likely to cause
adverse health effects including increasing morbidity and mortality in susceptible individuals. These
results influenced governments to establish strategies to control air pollution. Air quality guidelines
and standards were developed in an attempt to reduce adverse impacts on human health and the
environment. The US National Ambient Air Quality Standards (NAAQS) established in 1971 included
a the first standard for Total Suspended Particulate Matter (TSP). In 1987, the TSP standard was
replaced with PM10 standard (150mg/m3 24-h average and 50mg/m3 averaged annually), and in
1997, a standard for particles less than 2.5 micrometers in diameter (PM2.5) was established
(65mg/m3 24-h and 16mg/m3 annual). Despite the significant improvements made in air quality over
the last three decades, PM continues to exert a public health impact.

II. DEFINITION
Particulate matter (PM) is the term used for a mixture of solid particles and liquid droplets suspended
in the air. These particles originate from a variety of sources, such as power plants, industrial
processes, and diesel trucks, and they are formed in the atmosphere by transformation of gaseous
emissions. Their chemical and physical compositions depending of location, time of year, and
weather.(Figure 1). Particulate matter is composed of both coarse and fine particles.
Coarse particles (PM10) have an aerodynamic diameter between 2.5µ m and 10µ m. They are formed
by mechanical disruption (e.g. crushing, grinding, abrasion of surfaces); evaporation of sprays, and
suspension of dust. PM10 is composed of aluminosilicate and other oxides of crustal elements, and
major sources including fugitive dust from roads, industry, agriculture, construction and demolition,
and fly ash from fossil fuel combustion. The lifetime of PM10 is from minutes to hours, and its travel
distance varies from <1km to 10 km.
Fine particles have an aerodynamic diameter less than 2.5µ m (PM2.5). They differ from PM10 in origin
and chemistry (Table 1). These particles are formed from gas and condensation of high-temperature
vapors during combustion, and they are composed of various combinations of sulfate compounds,
nitrate compounds, carbon compounds, ammonium, hydrogen ion, organic compounds, metals (Pb,
Cd, V, Ni, Cu, Zn, Mn, and Fe), and particle bound water. The major sources of PM2.5 are fossil fuel
combustion, vegetation burning, and the smelting and processing of metals. Their lifetime is from days
to weeks and travel distance ranges from 100s to >1000s km.. In addition, fine particles are
associated with decreased visibility ( haze) impairment in many cities of the U.S

Table 1. Comparisons of fine and coarse particle matter

Fine Particle Coarse Particle

Formed from Gases Large solids/droplets

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Formed by Chemical reaction; nucleation; Mechanical disruption (e.g.

condensation, coagulation; crushing, grinding, abrasion of
evaporation of fog and cloud surfaces); evaporation of sprays;
droplets in which gases have suspension of dusts
dissolved and reacted
Composed of Sulfate (SO42 ¯); Nitrate (NO¯3); Resuspended dust (e.g. soil dust,
ammonium (NH4+ ); hydrogen ion street dust); coal and oil fly ash;
metal oxides of crustal elements
(H+ ); elemental carbon; organic
(Si, Al, Ti, Fe); CaCO3, NaCl, sea
compounds (e.g. PAHs, PNAs);
salt; pollen, mould spores;
metals (Pb, Cd, V, Ni, Cu, Zn, Mn,
plant/animal fragments; tyrewear
Fe); particle bound water
debris
Solubility Largely soluble, Hygroscopic and Largely insoluble and
deliquescent non-hygroscopic
Sources Combustion of coal, oil, gasoline, Resuspension of industrial dust
diesel, wood; atmospheric and soil tracked onto roads;
transformation products of NOx, suspension from disturbed soil
SO2 and organic compounds (e.g. farming, mining, unpaved
including biogenic species (e.g. roads); biological sources;
terpenes); high temperature construction and demolition; coal
processes, smelters, steel mills, and oil combustion; ocean spray
etc.
Lifetimes Days to weeks Minutes to Hours

Travel distance 100s to 1000s of kilometers <1 to 10s of kilometers

Source: EPA (1996)

III. PARTICULATE MATTER STANDARDS

In 1971, the United States Environmental Protection Agency (EPA) established the first PM National
Ambient Air Quality Standard. The original PM standard was Total Suspended Particulate (TSP). This
standard was replaced in 1987 with particulate matter less than 10 µ m in aerodynamic diameter
(PM10) and specified an annual average concentration of 50µ g/m3 and a 24-h maximum of 150µ
g/m3, based on the highest value over 3-year period. In 1997, after reviewing scientific studies, the
EPA concluded that particles with aerodynamic diameter less than 2.5µ m (PM 2.5) had a greater
association with mortality and morbidity rates than PM10. On this bases, the EPA established an
annual PM2.5 standard level of 15µ g/m3,, and a 24-h PM2.5 standard level of 65µ g/m. Also, the EPA
established the Pollutant Standard Index (PSI) as an air pollution alert system to communicate to the
general public information about the health risks of PM and other pollutants.

IV. PHYSICAL PROPERTIES AND PHYSIOLOGICAL EFFECTS

The capacity of particulate matter to produce adverse health effects in humans depends on its

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deposition in the respiratory tract. Particle size, shape, and density affect deposition rates. The most
important characteristics influencing the deposition of particles in the respiratory system are size and
aerodynamic properties. The aerodynamic diameter of a particle is the diameter of a unit density
sphere having the same settling velocity as the particle in question, whatever its size, shape or
density. Particles between 2.5 and 10µ m in aerodynamic diameter correspond to the inhalable
particles capable to be deposited, in the upper respiratory tract. Particles with aerodynamic diameter
smaller than 2.5µ m (PM2.5), called fine particles, correspond to the respirable particle fraction
capable of penetrating the alveolar region of the lung. Inhaled particles come in contact with surface of
the respiratory system. These particles pass the proximal airway (throat and larynx) of the respiratory
tract, and deposit in the tracheobronchial conductive airway of the lungs (bronchial and bronchiolar
airway) or in the gas exchange region (respiratory bronchioles, alveolar ducts, and alveoli of the lung
parenchyma).
There are five mechanisms that influence particle deposition within the respiratory tract. The primary
mechanisms are gravitational settling, impaction, and Brownian diffusion. Secondary mechanisms are
electrostatic attraction and interception. These last two processes have minimal importance for
inhalation and deposition of particulate matter. Deposition by gravitational settling occurs as a result of
the influence of gravity on particles suspended in the air. The settling rate of particles is directly
proportional to particle size. This process is most important in the distal region of the bronchial airway
and in proximal portions of the gas exchange region. Another mechanism of particle deposition is
impaction. Due to inertia airborne particles do not follow changes in direction or speed of airflow and
they may impact on the wall of the airway. This mechanism occurs primarily in the throat and larynx
with particles larger than 3µ m and increases with increasing particle size. Brownian diffusion involves
collision between gas molecules and micrometer-sized particles, which push the particle in an
irregular manner. It depends on the diffusive or thermodynamic diameter of the airborne particle rather
than on the aerodynamic diameter. Due to this, Brownian diffusion increases with decreasing particle
size. This mechanism is predominant in the gas exchange alveolar region of the lung for particles
smaller than 0.5µ m.
There are other factors that also influence particle deposition, including mode of breathing (oral
breathing permit the passage of particles greater than 10µ m to the lung), physical activity (exercise),
age, lung diseases (chronic obstructive lung disease), and ambient conditions (increase in
temperature or the presence of other pollutants).
The ability of the lung trying to protect itself against inhaled particles, clearance, will determine the
adverse health effects of particulate matter. There are two clearance mechanisms: the mucociliary
system and the alveolar macrophages. Particles deposited in the ciliated region of the
tracheobronchial airway, rise on the mucociliary ladder to be expelled by coughing or swallowing.
Particles deposited on the terminal bronchioles are cleared by lung macrophages. An early cellular
response to an acute particulate exposure is damage to epithelial cells of respiratory tract, which also
produce many different types of inflammatory mediators. The local pulmonary inflammation induced
by PM10 could impact on the cardiovascular system via the local production of procoagulant factors in
the lung or as a result of the effects of mediators released from the lungs which act on the liver, to
increase the levels of procoagulant factors which could promote myocardial infarction.

V. HEALTH EFFECTS
Several epidemiological studies have linked both PM10 and specially PM2.5 with significant health
problems, including: premature mortality, chronic respiratory disease, respiratory emergency room

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visits and hospital admissions, aggravated asthma, acute respiratory symptoms, and decreased lung
function. Like the other criteria pollutants, the elderly, whose physiological reserves decline with age
and who have higher prevalence of cardiorespiratory conditions, and children, whose respiratory
systems’ are still developing and who spend more time outdoors, are most at risk from exposure to
particulate matter. Also, individuals with preexisting heart or lung disease and asthmatics are sensitive
to PM effects. Fine particulate pollution (PM2.5), is of specific concern because it contains a high
proportion of various toxic metals and acids, and aerodynamically it can penetrate deeper into the
respiratory tract.
PREMATURE MORTALITY
Historically, the association between PM10 and mortality has been manifested in many air pollution
episodes such as those which occurred in Belgium (1930), Pennsylvania (1948), London (1952), New
York (1953), and London (1962), where the number of deaths attributed to air pollution was 63, 20,
4000, 200 and 700, respectively. Several studies have demonstrated the relationship between low
concentrations of PM10 and PM2.5 and increase in daily mortality. A study conducted by Pope, et al.,
1996, demonstrated the association between PM10 air pollution and cardiopulmonary and lung cancer
mortality. The relationship was stronger for PM2.5 than PM10. PM2.5 was associated with a 36%
increase in death from lung cancer and 26% in cardiopulmonary deaths, the risk being higher for
people over the age of 65. PM10 was not associated with lung cancer death (3,8,9,18,19). In addition,
another study conducted by Ostro demonstrated the association between PM10 levels with Sudden
Infant Disease Syndrome (SIDS) (34).
CHRONIC RESPIRATORY DISEASE
Epidemiological studies have showed the relationship between PM10 exposure and an increase in
bronchitis, chronic cough, and respiratory symptoms in persons with COPD (1,23,36).
RESPIRATORY AND HOSPITAL ADMISSION
In a number of studies, investigators have observed an increased incidence of respiratory diseases in
association with PM10 air pollution. For example, in a study conducted in the United Kingdom, an
association between emergency hospital admissions for respiratory and cardiovascular disease and
PM10 was found (2). Another study conducted in Seattle, Washington, demonstrated association with
emergency room visits for asthmatics and PM10 air pollution (27). Also, PM10 was associated with an
increase in hospital admission of the elderly for COPD and asthma and lower respiratory tract
infections including bronchitis and pneumonia (2,4,28). In addition, a study conducted in Canada by
Burnett et al., in 1980, found that increases of 10mg/m3 in PM10 and PM2.5 were associated with 1.9%
and 3.3% respective increases in respiratory and cardiac hospital admission. The relationship was
strongest between PM2.5 and cardiac disease (5,7,8,14).

AGGRAVATED ASTHMA
Persons with asthma, especially children, are more susceptible to PM air pollution. Recent studies
have associated PM10 at low concentrations with an increase in bronchodilator and asthma
medication use (27,36). The relationship between PM10 air pollution and asthma is stronger than for
PM2.5 (6).

RESPIRATORY SYMPTOMS

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A series of analyses adults and children demonstrated an association between exposure to PM and
respiratory symptoms severe to restrict their activities. Respirable particulate matter from combustion
sources (PM2.5) was associated with increased respiratory symptoms, including cough, wheeze and
shortness of breath (12,16,24). In two studies in Utah Valley, upper and lower respiratory symptoms
increased with PM10 concentrations (20,22,23). PM2.5 levels and H+ were associated with moderate
to severe cough and shortness of breath (14).
CHANGE IN LUNG FUNCTION
An association between PM10 air pollution and pulmonary function reduction was reported in several
epidemiological studies. In a study conducted in Utah Valley in 1989, Pope et al., found a relationship
between elevated PM10 levels and reduction in lung function as measured by peak expiratory flow
(PEF) (20, 22,23).
According to the NAAQS and the AQI, PM10 levels of 150µ g/m³ increase the likelihood of respiratory
symptoms and aggravation of lung disease. However, numerous studies have showed that PM10
health effects can be observed with PM10 levels below give values, although the PSI does not
describe health effects or offer cautionary statements at these levels (Table 3 and 4).

PM10 NAAQS RANGES AND HEALTH EFFECTS

NAAQS: 0.0 TO 54µ g/m³ 24-H AIR QUALITY CATEGORY: GOOD

The PSI does not describe specific health effects and cautionary statements for these PM10 concentrations.
However, numerous studies have demonstrated an association between PM10 exposure at 10µ g/m³ and
increased daily mortality for cardiorespiratory diseases. The risk is higher in individuals over 65 years
old of age (3,10,13,17,18,19). Another study conducted in the U.S. demonstrated that for each 10µ g/m³
rise in PM10 postneonatal general mortality, sudden infant death syndrome and postneonatal respiratory
mortality increased 4%, 12%, and 20% respectively (34). Other studies observed a relationship between
PM10 exposure at 20µ m/m³ and changes in PEFR in children with chronic symptoms or asthmatics
(16,24); between PM10 levels of 30µ g/m³ and increased total mortality (4.6%), decreased peak expiratory
flow (PEF) and increased symptoms and medication use in asthmatic children (7,10,27,34,35); and
between PM10 levels of 40µ g/³ an increased cardiovascular mortality in individuals under 65 years old
and mortality by Sudden Infant Death Syndrome (19,34). In addition, several epidemiological studies
observed with PM10 levels of 50µ g/m³ an increase in respiratory diseases such as pneumonia, chronic
obstructive pulmonary disease (COPD), and asthma. Also, a reduction in pulmonary function, an increase
in hospital admission, and increased cardiorespiratory mortality were found at these PM10
concentrations.

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NAAQS: 55 TO 154µ g/m³ 24-H AIR QUALITY CATEGORY: MODERATE

In the EPA PSI no health effects are described in this range. However, in a study conducted in Coachella
Valley, California, at PM10 levels of 57µ g/m³, deaths due to cardiovascular and respiratory diseases
increased in individuals older than 50 (18). Another study conducted in Coachella associated PM10 levels
of 87µ g/m³ with an increase in hospital admissions of children with respiratory disease (36). Health
effects are aggravated with concentrations approaching 100µ g/m³. Schwartz et al quoted that 100µ g/m³
PM10 concentrations increased the relative risk (1.07, 95% CI: 1.02, 1.12) for ischemic heart disease
admissions (2). Other studies have shown a relationship between 100µ g/m³ PM10 and hospital admissions
for respiratory diseases including pneumonia, COPD and asthma in all ages. Children report cough,
wheeze and asthma medication use. Also, smokers with mild to moderate COPD demonstrated a decline
in FEV1 and PEF (2,3,7,18,19,21,27,28,30,33). PM10 exposure to 100µ g/m³ is also associated with a 16%
increase in deaths per day, primarily respiratory death and cardiovascular death (7,21,26). In a study
conducted in Utah Valley, elevated PM10 levels (150µ g/m³) were associated with a statistically significant
reduction in lung function measured by reduction in peak expiratory flow (PEF) and increased symptoms
of respiratory disease (20,22,23). In addition, another study found PM10 association with a 26% increase
in upper respiratory symptoms; a 50% increase in lower respiratory symptoms and 217% increase in the
use of asthma medication and bronchodilator. (27).

NAAQS: 155 TO 254µ g/m³ 24-H AIR QUALITY CATEGORY: UNHEALTHY

FOR SENSITIVE GROUP
In this range, in a study conducted in Mexico demonstrated a relationship between PM10 exposure to
166µ g/m³ and cough and difficulty breathing in children (25). In another study, Pope et al found an
association between 195µ g/m³ PM10, reduction in EF, and an increase in symptoms of respiratory disease
and asthma medication use (20,22).
NAAQS: 255 TO 354µ g/m³ 24-H AIR QUALITY CATEGORY: UNHEALTHY

No information available.
NAAQS: 355 TO 424µ g/m³ 24-H AIR QUALITY CATEGORY: VERY UNHEALTHY

No information available.

PM2.5 NAAQS RANGES AND HEALTH EFFECTS

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NAAQS: 0.0 TO 15.4µ g/m³ 24-H AIR QUALITY CATEGORY: GOOD

According to the NAAQS, at PM2.5 levels from 0.0 to 15.4 no health effects are expected. However,
the Six U.S. Cities study found a relationship between exposure to PM2.5 at 11µ g/m³ and daily
mortality. A study conducted in Canada indicated that an increase of 10µ g/m³ in PM2.5 was
associated with an 3.3% increase in respiratory and cardiac hospital admission (5).
NAAQS: 15.5 TO 65.4µ g/m³ 24-H AIR QUALITY CATEGORY: MODERATE

In contrast with PM10, in this range the PSI includes a PM2.5 health effect cautionary statement where
it mentions the possibility of aggravation of heart or lung disease among persons with
cardiopulmonary disease and the elderly. A few epidemiological studies found that PM2.5 exposure
from 18µ g/m³ to 30µ g/m³ increased daily mortality due to cardiorespiratory mortality in the elderly
and persons with cardiovascular and respiratory disease. (7,8,9,14). In addition, other studies
demonstrated a relationship between 45µ g/m³ and increased hospital admission and chronic
bronchitis (3,7).

NAAQS: 65.5 TO 100.4µ g/m³ 24-H AIR QUALITY CATEGORY: UNHEALTH

FOR SENSITIVE GROUP MPDERATE

No information available
NAAQS: 100.5 TO 150.4µ g/m³ 24-H AIR QUALITY CATEGORY: UNHEALTHY
No information available
NAAQS: 150 TO 250.4µ g/m³ 24-H AIR QUALITY CATEGORY: VERY
UNHEALTHY

No information available
NAAQS: 250.5 TO 500.4µ g/m³ 24-H AIR QUALITY CATEGORY: HAZARDOUS

No information available

VI. CONCLUSION

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Extensive epidemiological evidence demonstrated that increases in ambient particulates

concentrations are associated with increases in total mortality from respiratory and cardiac diseases,
increases in hospitalizations and emergency room visits for respiratory and cardiac diseases,
increases in daily respiratory symptoms and decreases in pulmonary function. Sensitive groups
including the elderly, children and individuals with cardiopulmonary diseases such as asthma and
COPD, are at greater risk of developing adverse health effects from particulate exposure. Several
recently published health studies indicate that increases in cardiorespiratory mortality and morbidity
can be expected with particle levels below the particulate matter standard.

Numerous epidemiological studies have mentioned that the relationship between PM2.5 and adverse
health effects is stronger than PM10. Fine particulate pollution is of specific concern because it
contains a higher proportion of various toxic metals and acid species, and aerodynamically it can
penetrate deeper into the respiratory tract. However, the number of studies that demonstrating PM10
adverse health effects is greater than PM2.5.

VII. Reference:
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Concentrations of PM10 and Development of Respiratory Symptoms in Nonsmoking Population.
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Association between Summertime Ambient Air Pollution and Hospital for Cardiorespiratory
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Daily Mortality in Rotterdam, the Netherlands. Arch Environ Health 1997; 52(6): 455-463.
12. Koren H. Association between Criteria Air Pollutants and Asthma. Environ Health Perpec 1995;
103(6): 235-242.
13. Hong YC, Lemm JH, Ha EH, Christiani D. PM10 Exposure, Gaseous Pollutants, and Daily
Mortality in Inchon, South Korea. Environ Health Perspec 1999; 107(11): 873-878.
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Environ Health 1993; 48(5): 336-42.
18. Ostro B, Hurley S, Lipsett M. Air Pollution and Daily Mortality in the Coachella Valley, California:
A Study of PM10 Dominated by Coarse Particles.
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J Epidemiol 1991; 135(1): 12-19.
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Epidemiol 1993; 139(6): 589-598.
29. Schwartz J. Air Pollution and Hospital Admissions for the Elderly in Detroit, Michigan. Am J
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7(1): 20-27.

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32. Simpson R, et al. Associations between Outdoor Air Pollution and Daily Mortality in Brisbane,
Australia. Arch Environ health 1997; 52(6): 442-447.
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Epidemiol 1996; 7(3): 225-230.
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Particulate Air Pollution in the United States. Environ Health Perspec 1997; 105(6): 608-612.
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38. www.epa.gov/ttn/oarpg/naaqsfin/pmfact.html

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