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DAVID V. BATES
Department of Health Care and Epidemiology, Mather Building, 5804 Fairview Crescent,
University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3
Received S e p t e m b e r 29, 1991
INTRODUCTION
This communication has been prompted by the observation that authors of
papers relating air pollution to adverse health effects very rarely discuss the
interrelationships between health indices or examine their own finding in relation
to other related indices. This comment applies to papers written by the present
author as much as to the others. In the recent literature, there are at least 11
different indices of adverse health effects--as the Emperor said to Mozart, "there
are too many notes."
I have taken 44 papers on this topic published, with two exceptions, since 1980.
These have been selected to describe the range of health outcomes studied. My
intention is to examine the necessary, or possible, interrelationships between
different indices. I do not intend to critique individual papers from the point of
view of their internal strength, nor, initially, to try to distinguish between different
combinations of pollutants; this question is discussed at the end.
Episodic Data
These include, during episodes of increased pollution:
---increased respiratory mortality
---increased hospital respiratory admissions
--increased hospital respiratory emergency visits
--increased physician visits or ambulance use
--decreases in FEV 1 or PEFR
- - s y m p t o m variation
--changes in various indices of ill-health such as school or work absences or
"reduced activity days."
336
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All rights of reproduction in any form reserved.
ADVERSE E F F E C T S OF AIR P O L L U T I O N 337
Long-Term Data
In addition to the above observations, there is a series of nonepisodic or long-
term data:
--increased mortality from respiratory disease in regions of higher pollution
--changing mortality from respiratory disease in same region as pollutant levels
change
--increased prevalence of symptoms or of respiratory disease indicators in
regions of higher pollution
--cross-sectional FEV~ differences between regions with different pollution.
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ADVERSE E F F E C T S OF AIR P O L L U T I O N 339
The recent analyses of the respiratory consequences of air pollution in Utah are
unique. Air monitoring has shown that in this location, oscillations occur in PM10
levels without any significant SO2, NO2, or acid aerosol H2SO 4 accompaniments.
About 40% of the particles originate from a single source. An initial report related
hospital admissions for respiratory disease to the PM10 levels (Pope, 1989); this
was confirmed in a later analysis (Pope, 1991). A third report indicated an excess
of respiratory mortality in the impacted region (Archer, 1990), and a fourth (Pope,
1991) has shown that PM10 levels are associated with reductions in PEFR in
normal children and increased symptoms and medication use in a panel of adult
asthmatics in the area of concern. Thus in one location, without exposure to
multiple pollutants, four different adverse health indices have been found to be
associated with variations in the PM10 levels below the present U.S. standard:
respiratory mortality, increased respiratory hospital admissions, reduced lung
function, and increased symptoms and medication use. This is a unique example
therefore of remarkable coherence and is particularly valuable as multiple pollut-
ants were not present. The data taken together suggest strongly that the "reap-
praisal" of the U.S. particulate standard proposed by Holland and 11 distin-
guished collaborators (1979) is now itself in urgent need of reexamination.
There are fewer studies of oxidant pollution, and so far only one of the contin-
gent findings has been met. Of the probable or possible associated findings, 5 of
13 are met. These conclusions would be dependent on accepting evidence of
higher respiratory mortality in regions of Los Angeles with higher air pollution, as
reported in a preliminary paper in 1971 by Mahoney, and of the association of
increased mortality in relation to ozone levels recently reported by Kinney and
Ozkaynak (1991), and assuming that the variation in symptoms noted by Euler et
al. (1988) is representative of the whole population.
The difficulty with devising any index of internal coherence is that this inevi-
tably requires a series of judgements of the reliability of individual findings and
observations.
DISCUSSION
Cardiovascular mortality is usually noted to increase in episodes in which re-
spiratory mortality also increases. The relationship between heart disease and
lung disease is extremely complex (Bates, 1989), but one can identify at least three
different reasons why respiratory and cardiovascular mortality might be found to
rise together in air pollution episodes:
- - A c u t e bronchitis and bronchiolitis may be misdiagnosed as pulmonary
edema.
m A i r pollutants, such as acid aerosols or ozone, might increase lung perme-
ability and precipitate pulmonary edema in people with myocardial damage and an
increased left atrial pressure.
m A c u t e bronchiolitis or pneumonia induced by air pollutants, in the presence
of preexisting heart disease, might precipitate congestive heart failure.
It is not known to what extent increased carbon monoxide in air pollution epi-
sodes might precipitate increased cardiovascular mortality (it was not being rou-
tinely measured during the London 1952 episode), but the possible relationship
ADVERSE E F F E C T S OF AIR P O L L U T I O N 341
TABLE 2
RELATIVE SIGNIFICANCEOF ADVERSE HEALTH INDICATORSOF EFFECTS OF AIR POLLUTION
Least
Changes in general indices of ill-health
Small episodic FEV 1 declines
Increased symptoms in populations in more polluted regions
Cross-sectional FEV 1 differences
Increased prevalence of respiratory diseases
Increased hospital admission rate for respiratory disease in more polluted regions
Cross-sectional respiratory mortality differences not related to episodes
Increased hospital emergency visits in association with episodic increases in pollution
Increased hospital admissions in episodes
Increased respiratory or total mortality in episodes of increased pollution
Most
that could be derived from them. We may have made some progress in this regard
since then, but most studies (of particulate pollution, for instance) do not indicate
that a convincing threshold value exists.
Difficulties in environmental epidemiology have recently been discussed by
many authors and in different conferences and symposia. Bailar (1989) recently
listed general difficulties both in assessing exposure and in indices of outcome in
such studies. Nevertheless, direct studies of the effects of environmental factors
on populations cannot be avoided and are not replaced by other data.
In assessing the "strength" of the total data in relation to a pattern of pollution
(whether or not the differential responsibilities of different constituents can be
determined), the question of coherence is central. Such coherence may exist at
three different levels: within epidemiological data (as examined in this review);
between epidemiological and animal data; and between epidemiological, con-
trolled exposure human data and animal data.
I have suggested that the coherence within epidemiological data for the pattern
of pollution that follows SO2 emissions and particulate pollution is generally
strong and therefore convincing. However, in the case of SO2, there is very little
coherence between animal exposure data and the epidemiological data; hence,
there is no basis of biological plausibility. This factor presumably underlies the
serious underestimation of the current strength of the epidemiological data evi-
dent in such reports as that recently released by NAPAP (NAPAP 1990). The
persistent association of particulate pollution with changes in mortality should
serve as a challenge to us to explain the mechanism involved more precisely than
is now possible. In the case of oxidant pollution, the coherence between animal
data and controlled clinical data is generally strong, and the coherence between
field and controlled exposure studies is satisfactory. However, the epidemiolog-
ical component is weak; that is to say that the linkage between acute effects and
long-term consequence has still to be elucidated.
Coherence cannot be formally measured (as by some t test), which is why the
tortuous process of standard-setting is so complex and interesting a task (Bates,
1988). And it is also why efforts to remove entirely the element of (nonstatistical)
judgement from it are inevitably futile. When the problem is important what is
ADVERSE EFFECTS OF AIR P O L L U T I O N 343
required is more data, collected with all the precautions that we now realize are
necessary if major confounders are to be avoided. Concordance between findings
may occur fortuitously, as in the case of data from southern Ontario, or be
planned, as in the recent studies from Utah. It is important to stress that in the
future, coherence should be a subject for active search, once one health index has
been shown to be associated with pollutants.
In 1965, Hill (Hill, 1965) set out the aspects of an association that " w e espe-
cially consider before deciding that the most likely interpretation of it is causa-
tion." A recent volume (Rothman, 1988) contained useful discussion of these in
the light of modern data. The criteria included biological plausibility, coherence,
and consistency--that is, the replication of findings in different populations.
Among these, we might now emphasize the feature of internal coherence within
the epidemiological data which has been the subject of this enquiry.
It is important to stress that epidemiological evidence stands on its own. As
Rose recently remarked (Rose, 1989):
If there has to be a choice between trusting observation or reason, it is surely safer to trust
observation; for reason is so often based on incomplete information on transfer routes, doses
and responses. The argument that what cannot be explained cannot occur is weak, for one can
never exclude the explanation that has not been considered. In estimating risks, direct obser-
vations of evident health effects should take priority over theoretical explanations.
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