Aerosol Science & Technology

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Review: Epidemiological Basis for Particulate Air

Pollution Health Standards

C. Arden Pope III

To cite this article: C. Arden Pope III (2000) Review: Epidemiological Basis for Particulate
Air Pollution Health Standards, Aerosol Science & Technology, 32:1, 4-14, DOI:
10.1080/027868200303885

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 Aerosol Science and Technology 32:4] 14 (2000 )
Q 2000 American Association for Aerosol Rese arch
Published by Taylor and Francis
0278-6826 r 00 r $12.00 q .00

Review: Epidemiological Basis for

Particulate Air Pollution Health Standards
C. Arden Pope, III
BRIGHAM YOUNG UNIVERSITY, 140 FOB, PRO VO , UTAH, USA 84602

ABSTRACT. There are now more than 150 published epidemiologic studies of
health effects of particulate air pollution and dozens of related literature reviews.
This article explores the basic inferences currently being drawn from the literature
regarding the epidemiologic evidence particulate pollution induced health effects.
Although there is not a complete consensus of opinion, most reviewers conclude
that the overall epidemiologic evidence suggests th at particulate air pollution,
especially ® ne combustion-source pollution common to many urban and industrial
environments, is an important risk factor for cardiopulmon ary disease and mortal-
ity. Most of the epidemiological effort has focused on effects of acute exposure, but
effects of chronic exposure may be more important in terms of overall public
health relevance. Some reviewers contend that long-term, repeated exposure likely
increases the risk of chronic respiratory disease and the risk of cardiorespiratory
mortality. Th ere is more general ( but still not unanimous ) agreement that short-
term exposures to particulate pollution can exacerbate existing cardiovascular and
pulmonary disease and increase the number of person s in a population who
become symptomatic, require medical attention, or die.

By the 1970s the epidemiologic link be-
tween cardiopulmonary disease and histori-
cally high concentrations of particulate and
sulfur oxide pollution had been well estab-
lished. In 1979 an extensive research review
by several prominent British scientists
(Holland et al. 1979) was published. It con-
cluded that there are signi® cant human
health effects from particulate air pollution
at high levels, but that there is not com-
pelling evidence of health effects at the low
to moderate concentrations that existed in
the U.S. and Britain by the 1970s. Other
reviewers disagreed and suggested that
there are likely important health effects
even at low to moderate concentrations
(Shy 1979; Bates 1980; Ware et al. 1981).
In the 1970s through the mid-1980s there
were a few scattered original studies that
suggested adverse he alth effects at contem-
porary pollution levels. Then, during the
relatively short time period of 1989] 1992,
results of several loosely connected epi-
demiological research efforts from the U.S.
were reported. Health effect associations at
unexpectedly low concentrations of particu-
late air pollution were observed. While
some of these studies were controversial,
the convergence of their reported conclu-
sions resulted in a critical mass of evidence
Aerosol Science and Technology
32:1 January 2000
that prompte d serious reconsideration of
the contribution of particulate air pollution
on human health and motivate d abundant
additional research (Kaiser 1997; Pope and
Dockery 1999).
Currently there are more than 150 pub-
lished epidemiologic studies of the human
health effects of particulate air pollution.
There are also dozens of publications that
have reviewed the epidemiological evidence
of he alth effects of particulate air pollu-
tion. This discussion will not attempt to
present a comprehensive review of the epi-
demiological literature on the health ef-
fects of particulate pollution as has been
done elsewhere (U.S. EPA 1996; Vedal
1997; Pope and Dockery 1999). It will focus
primarily on the basic inferences currently
being drawn from evaluations of the litera-
ture that pertain to need for particulate air
pollution he alth standards and the question
of whether or not low to moderate levels of
ambient particulate air pollution effects hu-
man he alth. The possible consensus of the
scienti® c community regarding the epi-
demiologic evidence of he alth effects of
particulate air pollution will be explored.
METHODS
Articles and reports that reviewed epidemi-
ological studies on the health effects of
particulate air pollution were identi® ed
from a general literature se arch that in-
cluded an electronic se arch of Medline. A
total of 27 reviews that were published be-
tween 1993 and mid-1998 were collected.
These reviews, however, did not represent
27 distinct and independent evaluations of
the literature. Many of the authors have
written multiple reviews, and there is sub-
stantial ``overlapping’’ of authors and coau-
thors. The reviews included 18 individual
authors plus 5 committees or agencies that
have written reviews including: The World
He alth Organization-European Region
Epidemiological Basis for PM NAAQS 5
(WHO-EURO 1995); the Committee on the
Medical Effects of Air Pollutants, U.K. De-
partment of He alth (1995); the Committee
of the Environmental and Occupational
He alth Assembly of the American Thoracic
Society (CEOHA-ATS 1996); the U.S. En-
vironmental Protection Agency (U.S. EPA
1996); and the Canadian Federal-Provincial
Working Group on Air Quality Objectives
and Guidelines (CEPA r FPAC 1998). In
this analysis, reviews were clustered accord-
ing to author groupings that represented at
least somewhat independent evaluations of
the epidemiological literature.
An evaluation of the inferences being
drawn from these reviews required a recog-
nition of broadly different study designs
that have been used and the different he alth
endpoints that have been studied. The pub-
lished epidemiologic studies of air pollution
typically fall within two broad classi® ca-
tions: 1) acute exposure studies and 2)
chronic exposure studies. The acute expo-
sure studies use short-term te mporal
changes in pollution as their source of ex-
posure variability. These studies evaluate
short-term changes in health endpoints as-
sociated with short-term changes in levels
of pollution. These studies range from sim-
ple observations of changes in health over a
single air pollution episode of one or more
days, to sophisticated statistical analyses of
daily time-series over months or years. Be-
cause these studies typically evaluate only
short-term temporal relationships (usually
1] 5 days), the observed pollution effects
are usually interpreted as he alth effects of
acute exposure. Common cardiopulmonary
health outcomes that have been evaluate d
in these acute exposure studies include
mortality, hospitalizations or health care
visits for respiratory and r or cardiovascular
disease, respiratory symptoms, and lung
function. Chronic exposure studies primar-
ily use spatial differences in pollution as
their source of exposure variability. Chronic
6 C. A. Pope, III
exposure studies therefore compare various
health outcomes across communities or
neighborhoods with different levels of
pollution. These studies are principally
cross-sectional in design and use longer-
term pollution data (usually 1 year or more ).
These studies are often interpreted as eval-
uating chronic and r or cumulative effects
of exposure. Common cardiopulmonary
health outcomes that have been evaluated
in the chronic exposure studies include
mortality, lung cancer, respiratory disease,
and lung function.
In this analysis, the reviews for each
grouping of authors were evaluate d and a
judgment was made regarding whether or
not the reviewers directly made or implied
the inference of a non-spurious association
between particulate air pollution and the
health endpoint being considered. Because
an appraisal of the strength of the overall
epidemiological evidence of he alth effects
of particulate air pollution requires an eval-
uation of consistency and coherency (Bates
1992), an evaluation was made regarding
whether or not the reviewers make an argu-
ment for consistency and coherency. Also,
a qualitative judgment was made regarding
the overall epidemiological evidence of
particulate he alth effects implied by the
different reviews and the existence of re-
maining uncertainties and concerns.
RESULTS
Inferences Regarding Short-Term Exposure
Table 1 presents a summary of the infer-
ences that seem to be implied by approxi-
mately 16 individual reviewers or groupings
of reviewers. All of these reviewers ad-
dressed the potential relationships between
day-to-day changes in mortality and short-
term exposure to particulate air pollution.
Currently there are more than 30 published
Aerosol Science and Technology
32:1 January 2000
acute exposure, population-base d mortality
studies. Reviews ranged from very detailed
and rigorous reanalysis of a few daily time-
series mortality studies (Samet et al. 1995)
to more comprehensive reviews with little
or no re analysis (Pope and Dockery 1999).
Although all of the reviewers agree that the
biological mechanisms are poorly under-
stood, there seems to be general agreement
that at extremely high levels ambient par-
ticualte air pollution may be an important
risk factor for increased cardiopulmonary
disease and early mortality.
Recent daily time-series mortality stud-
ies, based on relatively advance d regression
modeling, have also observed changes in
daily de ath counts associate d with short-
term changes in particulate air pollution
even at relatively low or moderate levels of
air pollution. Studies that provided a break-
down of mortality by broad cause-of-death
categories observed that particulate air pol-
lution generally had the largest effect on
respiratory and cardiovascular disease mor-
tality. These studies did not observe a par-
ticulate pollution threshold. The relative
risk of mortality increased monotonically
with particulate concentrations } usually in
a ne ar linear fashion. Some reviewers have
suggested that the absence of a threshold
may be due to a possible artifact of mea-
surement errors (Lipfert and Wyzga 1995;
Lipfert 1997). Also, these studies often ob-
served a lead-lag relationship between air
pollution and mortality. The results sug-
gested that the increased mortality oc-
curred concurrently or within 1] 5 days fol-
lowing an increase in air pollution. Because
various me asurements of particulate pollu-
tion were used in the different studies, and
because various modeling strategies were
used, precise comparisons of effect esti-
mates across all the studies were dif® cult.
However, changes in daily mortality associ-
ated with particulate air pollution were typ-
 TABLE 1. Summary of inferences from selected reviews of the health effects of low to moderate levels of particulate air pollution.

Inferences Regarding Inferences Regarding Overall epi. Are there

Short-Term Exposure Long-Term Exposure
Evidence of Remaining
Resp Lung Symp Lung PM Health Uncertainties
Authors and year of publication Mort Hosp Symp Func Mort Dis Func Consistency? Coherency? Effects and Concerns?

Bates 1995, 1996 yes yes yes yes yes yes yes yes yes probable yes
Brunekreef et al. 1995 yes yes yes yes na na na yes yes probable yes
Dockery and Pope 1994, 1996, 1997 yes yes yes yes yes yes yes yes yes probable yes
Pope and Dockery 1996, 1999
Pope et al. 1995a, 1995b
Gamble and Lewis 1996 no no no no no naa na no no weak r yes
Gamble 1998 discount
Lipfert 1994, 1997 ? ? ? ? ? ? ? ? ? possible r yes
Lipfert and Wyzga 1995 question
Moolgavkar and Luebeck 1996 ? na na na no na na no no weak r yes
discount
Ostro 1993 yes na na na yes na na yes yes probable yes
Samet et al. 1995 yes na na na na na na yes na possible yes
Schwartz 1994, 1997 yes yes na na na na na yes yes probable yes
Thurston 1996 yes na na na na na na ? na probable yes
Vedal 1997 yes yes yes yes ? ? ? ? yes probable r yes
question
WHO-EURO 1995 yes yes yes yes yes yes yes yes yes probable yes
U.K. Department of He alth 1995 yes yes yes yes yes ? ? yes yes probable yes
CEOHA-ATS 1996 yes yes yes yes yes yes yes yes yes probable yes
U.S. EPA 1996 yes yes yes yes yes yes yes yes yes probable yes
CEPA r FPAC 1998 yes yes yes yes yes yes yes yes yes probable yes
a
na indicates ``not addressed’’ enough in the review to make a judgement about inference.

7
8 C. A. Pope, III
ically estimated at approximately 0.5] 1.5%
per 10 m g r m 3 increase in PM 10 concentra-
tions.
Daily counts of hospital admissions can
be analyzed in the same way that daily
counts of mortality have been assessed.
More than 30 daily time-series studies have
reported associations between particulate
air pollution and various respiratory hospi-
talization or related he alth care endpoints.
Most of these studies have evaluate d asso-
ciations between respiratory hospital ad-
missions and air pollution. Several studies
have also analyzed emergency department
visits for asthma, chronic obstructive pul-
monary disease, and other respiratory
ailments and observed associations with
particulate air pollution. More recent stud-
ies have observed associations between par-
ticulate air pollution and hospitalizations
for cardiovascular disease.
Daily diaries have been used to record
respiratory or other symptoms and evaluate
acute changes in respiratory he alth. There
have been more than 15 published studies
that have similarly evaluated associations
between daily respiratory symptoms and
particulate air pollution. While many of
these studies focused on asthmatics and
exacerbation of asthma, others followed
nonasthmatic s and evaluated changes in
acute respiratory health status more gener-
ally. Reported symptoms were often aggre -
gated into upper respiratory symptoms
(including such symptoms as runny or stuffy
nose, sinusitis, sore throat, wet cough, he ad
cold, hay fever, and burning or red eyes)
and lower respiratory symptoms (including
wheezing, dry cough, phlegm, shortness
of breath, and chest discomfort or pain).
In addition, cough, the most frequently
reported symptom, was often analyzed
separately. Small, often statistically in-
signi® cant, associations between particulate
pollution and upper respiratory symptoms
were observed. Associations with lower res-
Aerosol Science and Technology
32:1 January 2000
piratory symptom s and cough, however,
were typically larger and usually statistically
signi® cant. Exacerbation of asthma, based
on recorded asthma attacks or increased
bronchodilator use, were also associate d
with particulate air pollution.
In addition to recordings of respiratory
symptoms, measures of lung function have
been used as an objective and potentially
sensitive indicator of acute response to air
pollution. Various studies have taken re-
peated measurements of the lung function
of panels of children and r or adults. These
studies have typically reported very small,
but often statistically signi® cant, decreases
in lung function associated with elevated
levels of particulate air pollution concen-
trations. Lagged effects of up to 7 days
were observed.
As can be seen in Table 1, most of the
recent reviews seem to conclude that the
epidemiological evidence leads to infer-
ences of nonspurious associations between
short-term exposure to particulate air pol-
lution and cardiopulmonary mortality,
health care visits, respiratory symptoms, and
lung function. A few of the reviewers, how-
ever, argue that the observed associations
between daily mortality and particulate air
pollution may be due to the selection of
modeling techniques or confounding by
long-term time trends, season, weather
variables, other pollutants, or some other
unknown factor (Moolgavkar and Luebeck
1996; Lipfert and Wyzga 1995; Gamble and
Lewis 1996).
Inferences Regardin g Long-Term Exposures
As noted above, acute exposure studies
suggest that short-term exposures to ele-
vated particulate air pollution may be
associated with short-term increases in car-
diopulmonary mortality and various mea-
sures of morbidity. These acute exposure
studies provide little information about how
Aerosol Science and Technology
32:1 January 2000
much life is shortened, how pollution
effects longer-term mortality rates, or pol-
lution’s potential role in the process of
inducing chronic disease that may or may
not be life threatening. Chronic exposure
studies attempt to evaluate the effects of
low or moderate exposure that persists for
long periods of time as well as the cumula-
tive effects of repe ated exposure to ele-
vate d levels of pollution.
Several population-based , cross-sectional
mortality studies have evaluate d associa-
tions between annual mortality rates and
particulate air pollution across U.S. metro-
politan areas. Formal regression modeling
techniques to evaluate cross-sectional dif-
ferences in air pollution and mortality and
to control for other ecological (population-
based) variables have been used. In an
attempt to control for other risk factors,
population average values for demographic
variable s and other factors such as smoking
rates, education levels, income levels,
poverty rates, and housing density were of-
ten included in the regression models. The
basic conclusions from these population-
based cross-sectional studies were that
mortality rates were associate d with air pol-
lution and were most strongly associated
with ® ne or sulfate particulate matter. Al-
though population-based cross-sectional
studies suggested that air pollution con-
tributes to human mortality, these studies
had severe limitations and have been largely
discounted for several reasons. An overrid-
ing concern of these studies was that popu-
lation-based cross-sectional studies could
not directly control for individual differ-
ences in cigarette smoking and other risk
factors.
The results of a few cohort mortality
studies, however, have also been reported.
These individual-base d studies used com-
munity or citywide air pollution data to
estimate exposures and subject-speci® c
information on risk factors to adjust for
Epidemiological Basis for PM NAAQS 9
potential confounding of the air pollution
associations. Mortality, especially car-
diopulmonary mortality, was signi® cantly
associated with sulfate and r or ® ne particu-
late air pollution } even after directly
controlling for individual differences in
age, sex, cigarette smoking, and other risk
factors.
There have also been several studies that
have evaluated associations between partic-
ulate air pollution and chronic respiratory
symptoms and disease or lung function
(Pope and Dockery 1999). The effects of air
pollution on respiratory disease or symp-
toms were often estimated while adjusting
for individual differences in various other
risk factors. Statistically signi® cant associa-
tions between particulate air pollution and
various respiratory symptoms were often
observed. Chronic cough, bronchitis, and
chest illness (but not asthma) were associ-
ated with various me asure of particulate air
pollution, thus suggesting that particulate
air pollution was most consistently associ-
ated with bronchitic symptoms. These stud-
ies that evaluated the effects of air
pollution on lung function all adjuste d for
individual differences in age, race, sex,
height, and weight and controlled for smok-
ing or restricted the analysis to never-
smokers. These studies observed small
associations between decreased lung func-
tion and particulate air pollution that were
often statistically signi® cant.
Many of the recent reviews of the epi-
demiological evidence of he alth effects of
particulate air pollution did not speci® cally
or adequately address the studies de aling
with he alth effects of long-term exposures.
However, as can be seen in Table 1, most
of the reviewers that addressed the issue of
health effects of long-term exposure con-
cluded that an inference of nonspurious
associations between long-term exposure to
particulate air pollution and cardiopul-
monary he alth effects was reasonable. A
10 C. A. Pope, III
number of the reviewers, however, strongly
question (Lipfert 1997; Vedal 1997) or
heavily discount (Moolgavkar and Luebeck
1996; Gamble 1998) the evidence of effects
of long-term particulate exposures. They
note that the number of high-quality stud-
ies for long-term exposure is much less
than that for short-term exposure and also
argue that the observed associations may
be due to modeling techniques or con-
founding by other pollutants, socioeco-
nomic variables, or some other unknown
factor.
Consistency, Coherency, and Ov erall Ev idence
It is generally accepted that the overall
epidemiological evidence is enhanced if
similar adverse effects of exposure are re-
producibly observed by different investiga-
tors in different settings. That is, there
should be consistency of effects across in-
dependent analytic studies. In addition,
there should be a coherence of effects
where the effects can be observed across a
cascade of related he alth outcomes. Most,
but not all, of the reviewers make the judg-
ment that the epidemiological evidence is
reasonably consistent and coherent and that
the overall epidemiological evidence indi-
cates a probable link between particulate
air pollution and adverse effects on car-
diopulmonary he alth. However, the review-
ers generally avoid making a clearly stated
conclusive inference of causality. Yet the
issue of a causal link is not entirely avoided.
Two of the most negative reviews con-
clude that ``there is no substantive basis for
concluding that a cause] effect relationship
exists’’ (Gamble and Lewis 1996; Gamble
1998). Another review argued, however, that
``when a substantial body of epidemiologic
evidence indicates that a material to which
people are commonly exposed may be hav-
ing serious adverse he alth effects the bur-
den of proof may be deemed to have shifted
Aerosol Science and Technology
32:1 January 2000
from those who draw a causal inference, to
those who maintain no causal inference is
possible’’ (Pope et al. 1995a). This review
does not conclusively infer causality but it
further argue s that ``there is enough consis-
tency and coherency of results across a
large number of studies and a wide range
of expected outcomes, methodologies, study
areas, and researchers to merit a reassess-
ment of the importance of ® ne and r or
respirable particulate pollution on car-
diopulmonary he alth.’’ The report from the
U.K. Department of He alth (1995) also
stopped short of a direct inference of
causality but stated that ``in terms of pro-
tecting public health it would be imprudent
not to regard the demonstrated associa-
tions between daily concentrations of parti-
cles and acute effects on he alth as causal.’’
The recent report from Canada (CEPA r
PFAC 1998) notes that epidemiological
studies cannot provide precise biological
mechanisms of action but that ``a funda-
mental purpose of epidemiology is to estab-
lish a cause with enough certainty that it
will be justi® able and highly appropriate to
take action to mitigate effects on public
health. This point has clearly been re ached
with respect to particulate matter.’’
Remaining Uncertainties and Concerns
As can be seen in Table 1, the only summa-
rized issue of which there is complete una-
nimity is regarding remaining uncertainties
and concerns. All reviewers agree that there
are substantial limitations and weaknesses
of the epidemiology of particulate pollu-
tion. One of the most substantial concerns
deals with limited information about rele-
vant biological me chanisms. Biological
plausibility may be enhanced by the obser-
vation of a coherent cascade of cardiopul-
monary he alth effects and by the fact that
noncardiopulmonar y health endpoints are
not typically associated with particulate pol-
Aerosol Science and Technology
32:1 January 2000
lution, yet the epidemiological evidence is
limited on this subject. A related concern is
that the large majority of studies evaluated
only effects of short-term exposures. Long-
term, chronic exposure, however, may be
much more important in terms of overall
public health. The large number of acute
exposure studies relative to the chronic ex-
posure studies has less to do with public
health relevance than the relative ease and
low cost of conducting acute exposure stud-
ies. The studies provide little information
on the biological linkages between effects
of short-term versus long-term exposures.
Another concern relates to the limited
information regarding ambient versus per-
sonal exposures. Accurate me asures of
personal exposure to air pollutants for pop-
ulation-based studies or for studies of large
cohorts is impractical and, for some appli-
cations, unnecessary. Exposure to air pollu-
tion has typically been estimated by using
ambient air pollution data. Such an ap-
proach is useful because public policy and
pollution abatement strategies typically
( and often necessarily) focus on ambient
concentrations of air pollutants. Yet con-
cerns about exposure measurement error
and the interpretation of the studies based
on ambient pollution data remain.
A major limitation of the epidemiological
studies involves the dif® culty of disentan-
gling independent effects or potential inter-
actions between highly correlated risk
factors. This dif® culty exists largely because
alternative risk factors may be correlated
with air pollution resulting in potential con-
founding. Confounding may result when
another risk factor that is correlated with
both exposure and disease is not ade-
quately controlled for in the analysis, re-
sulting in spurious correlations. Any single
epidemiology study is highly limited in its
ability to de al with all potential con-
founders. The broader body of epidemio-
logical evidence provides some important
Epidemiological Basis for PM NAAQS 11
information. For example, cigarette smok-
ing may contribute to underlying respira-
tory disease rates in a population but
cannot be a common confounder in the
acute exposure studies for several reasons:
1) most of the lung function, respiratory
symptoms, and school absences studies were
conducted among mostly nonsmoking chil-
dren; 2) the largest association between
respiratory hospitalizations and pollution
was often with mostly nonsmoking children;
and 3) cigarette smoking does not change
day-to-day in correlation with air pollution.
Furthermore, recent cohort-based chronic
exposure studies estimated pollution effects
after analytically controlling for cigarette
smoking or restricting the analysis to never
smokers. As with cigarette smoking, socioe-
conomic status in a population does not
change day-to-day in correlation with air
pollution. Therefore, socioeconomic vari-
ables are not likely confounders in the
short-term time-series studies looking at
lung function, respiratory symptoms, school
absences, outpatient visits, and mortality.
Furthermore, recent cohort-based chronic
exposure studies controlled for various so-
cioeconomic variable s including sex, race,
and education levels.
Although daily, se asonal, or annual
changes in weather are not potential con-
founders in the chronic exposure mortality
and morbidity studies, in the acute expo-
sure studies, potential confounding due to
temporal correlations between pollution,
weather, and se asonal variable s must be
dealt with. Various approache s to control
for weather variables in the time-series
analysis have been used, and estimated pol-
lution effects have been observed for areas
with very different climates and weather
conditions.
Potential confounding by correlated
copollutants remains one of the most im-
portant concerns with the current epidemi-
ology. Two basic approache s to evaluating
12 C. A. Pope, III
the potential of confounding by copollu-
tants have been used. One approac h is to
try to analytically control for copollutants
by including them in regression models and
using statistical criteria such as signi® cance
levels or coef® cient size and stability to
evaluate the impact. When there are strong
correlations between pollutants such ana-
lytic control techniques are replete with
statistical problems. Attempts to separate
effects of a single pollutant are rarely con-
clusive for any single data set. An alterna-
tive approach to evaluate for confounding
by copollutants is to compare the estimated
particulate effects in areas with different
potential for confounding by copollutants.
If the estimated particulate effects are due
to confounding by copollutants, then esti-
mated effects would be larger in areas with
higher potential for positive confounding
by copollutants. When this approac h is used
there is little evidence of confounding by
O 3 or SO 2 (Schwartz 1997). The potential
for confounding by other me asured or un-
me asured pollutants remains unclear.
A fundamental concern about the epi-
demiological studies is their inability to fully
explore the relative he alth impacts of vari-
ous constituents of particulate pollution.
Me asures of particulate matter mass may
be serving only as proxy variable s for a
primary toxic component or characteristic
of particles, such as combustion-sourc e par-
ticles, sulfates, ultra ® ne particles, or par-
ticulate acidity. Infectious particles can
certainly have impacts on human he alth.
Airborne pollens, spores, dander, and in-
sect-related proteins can be a health prob-
lem for many, especially asthmatics. In dry
areas, dust particles at high concentrations
may have health effects. Major components
of particulate pollution in urban environ-
ments are primary and secondary particles
generated from combustion processes. Var-
ious physiologi c and toxicologic considera-
tions suggest that combustion-source
Aerosol Science and Technology
32:1 January 2000
particulate pollution may be an important
health concern. Their size is such that they
can be breathed deeply into the lungs, and
they include sulfates, nitrates, acids, transi-
tional metals, and carbon particles with
various chemicals adsorbed onto their sur-
faces. Also, indoor and personal exposure
to combustion-sourc e ® ne particles are rel-
atively well represented by central site
ambient monitors. The currently available
epidemiological data cannot reveal if the
relative importance of combustion-sourc e
particles is due to the relative small size of
these particles, their chemical composition,
or both.
Finally, with regards to public policy ac-
tions to mitigate effects on public he alth,
the epidemiological studies do not provide
speci® c concentration levels that would be
appropriate for public he alth standards or
objectives. The epidemiological studies
generally observed morbidity and mortality
effects from very low ambient levels up to
very high levels. The concentration-re -
sponse curves appear to be monotonically
increasing (often ne ar linear ) with no clear
``threshold level’’ under which there are no
effects.
CONCLUSION
Based on recently published reviews of the
epidemiological literature, it is clear that
there is not a complete consensus of opin-
ion about the human health effects of
particulate air pollution. Most reviewers,
however, generally conclude that the over-
all epidemiologic evidence suggests that
particulate air pollution, especially ® ne
combustion-sourc e pollution, common to
many urban and industrial environments is
an important risk factor for cardiopul-
monary disease and mortality. Reviewers
often note that evidence of he alth effects
due to acute or short-term exposures is
stronger than the evidence for chronic ef-
Aerosol Science and Technology
32:1 January 2000
fects due to longer-term exposure. Cer-
tainly much of the recent epidemiological
effort has focused on effects of acute expo-
sure, primarily because of the relative avail-
ability of relevant time-series data sets.
However, the effects of chronic exposure
may be more important in terms of overall
public health relevance. The evidence from
epidemiological studies of long-term expo-
sure is questioned or disputed by some
reviewers, but most conclude that long-
term, repeated exposure likely increases the
risk of chronic respiratory disease and the
risk of cardiorespiratory mortality. There is
more general (but still not unanimous)
agreement that the epidemiological studies
indicate that short-term exposures to par-
ticulate pollution can exacerbate existing
cardiovascular and pulmonary disease and
increase the number of persons in a popu-
lation who become symptomatic, require
medical attention, or die. The pattern of
cardiopulmonary he alth effects associated
with particulate air pollution that has been
observed by epidemiological studies is the
strongest evidence of the he alth effects of
this pollution. The relative consistency and
coherency of this pattern continue to be
debated. All reviewers agree that the epi-
demiological studies have important limita-
tions that stem largely from the use of
people who are living in uncontrolled envi-
ronments and who are exposed to complex
mixtures of air pollution. A more complete
understanding of the health effects of par-
ticulate air pollution will require additional
contributions from toxicology, exposure as-
sessment, and other disciplines.
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