| 6.3 |
Comparison
with Other Studies
Many
epidemiological studies have been reported documenting
health effects of major air pollutants at concentrations
below existing guidelines and standards (Brunekreef
et al., 1995). Earlier studies, mostly in the United
States, were conducted independently. More recent work
in Europe was designed according to a standardized protocol
(APHEA protocol). This approach provides a basis for
comparison between different countries. However, it
should be cautioned that a direct comparison of numerical
risk estimates is not appropriate, due to the following:
differences in the primary datasets (types and levels
of air pollutants, numbers of hospital admissions, sub-sets
of disease codes used), and specific modelling assumptions
and procedures. The following summarizes key findings
in time series studies of acute health effects of various
air pollutants.
In
the United States, the role of particulates has been
the primary focus of research in recent years. Significant
adverse effects of particulates on health outcomes,
measured by daily mortality and hospital admissions
for respiratory and cardiovascular diseases have been
reported in ecological studies (Dockery et al., 1994;
Samet et al., 1996; Schwartz, 1996; Schwartz et al.,
1992; Schwartz et al., 1995). Independent analyses using
the same source of data (Philadelphia data) over a longer
time period have led to different conclusions (Moolgavkar,
Luebeck, Thomas & Anderson, 1995). This highlights
the dependence of the study results on the nature and
characteristics of the dataset used.
In
Europe, within the APHEA study, positive and significant
associations between particulates and respiratory mortality
or hospital admissions due to respiratory diseases have
been reported in France, Greece, Italy and Spain (Zmirou
et al., 1996; Dab et al., 1996; Touloumi, Samoli &
Katsouyanni, 1996; Vigotti, Rossi, Bisanti, Zanobetti
& Schwartz, 1996; Sunyer, Castellsague, Saez, Tobias
& Anto, 1996), but not in Britain, Slovak Republic,
Finland and The Netherlands (Ponce de Leon, Anderson,
Bland, Strachan & Bower, 1996; Bacharova et al.,
1996; Ponka & Virtanen, 1996a; Schouten, Vonk &
de Graaf, 1996).
The
magnitude and statistical significance of the associations
between air pollutants other than particulates and measures
of health outcome also varied between studies. For ozone,
significant positive associations with hospital admissions
for respiratory diseases were reported in Britain (Ponce
de Leon et al., 1996) and with hospital admissions for
asthma and ischaemic heart diseases in Finland. (Ponka
et al., 1996b; Ponka et al., 1996a) For SO2, significant
associations with total mortality were reported in Germany
(Spix et al., 1996), with mortality and hospital admissions
for respiratory diseases in Italy (Vigotti et al., 1996),
with respiratory and/or cardiovascular mortality in
France (Zmirou et al., 1996; Dab et al., 1996), with
total and cardiovascular mortality in Poland (Wojtyniak
& Piekarski, 1996), and with total, respiratory
and cardiovascular mortality in Spain (Sunyer et al.,
1996).
For
NO2, most participants of the APHEA project reported
no significant associations with health outcomes. Positive
associations with elderly mortality and cardiovascular
mortality in Spain and with asthma in France (Paris)
were the only exceptions (Sunyer et al., 1996; Dab et
al., 1996). Indoor exposure to NO2 has not been shown
to be associated with respiratory illnesses in children
in a cohort study by Samet (1993).
No
significant health effects were found for SO2 and TSP
in the Slovak Republic in Eastern Europe (Bacharova
et al., 1996). Inconsistent and conflicting results
were reported in Polish cities (Wojtyniak et al., 1996).
Significant but negative associations have also been
reported, e.g., SO2 and NO2 in Amsterdam where levels
of air pollutants were relatively low (Schouten, Vonk
& de Graaf, 1996).
In
this study, we have demonstrated consistent and significant
positive association between concentrations of all four
air pollutants (NO2, SO2, RSP and O3) with hospital
admissions for respiratory diseases in general and asthma
in particular. All air pollutants except SO2 were also
associated with respiratory mortalities. In the Interim
Report, a simple Poisson regression model was used,
without correction for serial correlation and overdispersion.
Using the logistic regression model (Williams' Method)
in this Report, the results were broadly similar. Compared
to the simple Poisson model, slightly higher RR for
the respective pollutants were found, but the confidence
intervals of the RR were broader. Samet et al. (1995)
used the "iteratively weighted and filtered least-squares
model" by Zeger to correct for serial correlation and
overdispersion. When comparing this with the simple
Poisson model, he found that the estimated regression
coefficients were insensitive to such corrections. The
standard error derived from the simple Poisson model
was under-estimated by 10% - 30% (and hence the statistical
significance was over-estimated) when no serial correlation
and overdispersion was assumed. Our estimates using
Williams' model, compared with the simple Poisson model
(adopted in the Interim Report), concurred with these
findings by Samet et al. (1995). This means that, even
accounting for overdispersion, our findings of significant
associations between air pollutants and health effects
are likely to be true.
One
possible reason for our demonstration of highly significant
findings is that the daily mean numbers of hospital
admissions for respiratory and cardiovascular diseases
were much higher than in other cities (about 7 times
that in Milan, almost twice that in Paris, 30% higher
than in London). However, compared to many studies,
our time-series period was relatively short.
In
respect of the magnitude of the relative risks, our
findings (RR=1.39) for O3 were much higher than that
for The Netherlands (RR for O38 hr max lag2 = 1.043
in summer) (Schouten et al., 1996). For SO2, our findings
(RR = 1.13 and 1.25 for respiratory diseases admissions
and asthma respectively) were also higher than in Italy,
(RR=1.04, 1.05 for age groups 64 and 15-64 respectively
for respiratory diseases admissions) and in France,
(RR = 1.042 and 1.175 for respiratory diseases admissions
and asthma respectively) (Vigotti et al., 1996; Dab
et al., 1996). For RSP and NO2, our results were also
higher than risk estimates presented in the APHEA and
United States studies. One possible reason for our findings
of higher risks for all pollutants is that, contrary
to most Western cities, a significant proportion of
the population in Hong Kong live in close proximity
to the sources of emission of air pollutants, such as
along motor highways, busy roads and near industrial
premises. As mentioned earlier, one must caution against
a direct, numerical comparison of risk estimates between
individual studies due to variations in the study design,
data quality, modelling, the range of parameter levels
(e.g., air pollutant levels and meteorological variables)
and the choice of lag in the model.
As
with studies elsewhere, inconsistencies were found in
our case, where a marginally significant reduction in
risk of acute myocardial infarction (AMI) was observed
for RSP and O3. While there is no pathophysiologic basis
for this finding, the mean number of daily hospital
admissions for AMI was only four, compared to 101 daily
admissions for cardiovascular diseases. Hence, statistical
instability cannot be ruled out.
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| 6.4 |
Single
Pollutant versus Multiple Pollutant Models
The
issue of single pollutant versus multiple pollutant
models poses one of the most difficult problems for
environmental epidemiologists. In a multiple pollutant
model, one can theoretically assess the effect of one
pollutant given the presence (or adjusting the effect)
of the other pollutants. However, collinearity between
air pollutants is considerable, as exemplified in the
high correlation coefficient (0.79) between NO2 and
RSP in our 1994 - 1995 data. This implies that the use
of a multiple pollutant model may render the results
statistically unstable. Schwartz (1996) commented that
the inclusion of several collinear pollutants in the
same model risked letting the "noise" choose which pollutants
were significant. To study the independent effects of
the pollutants, he chose a location (Tucson, Arizona)
where the PM10 levels were poorly correlated with O3
and SO2 (Schwartz, 1997). Earlier air pollution research,
which focused on single pollutants, were "largely driven
by the regulatory imperative" (Moolgavkar et al, 1997).
However, there are shortcomings in the use of the single
pollutant model. First, it is not possible to identify
a particular pollutant as the principal cause of the
measured effect. Second, one cannot examine the combined
effects of more than one pollutant, given that they
individually do exert some health effect in animal and
human studies. Lastly, the partial b are usually overestimated
compared to the multiple pollutant model. Moolgavkar
emphasized that "the focus (of research) must shift
from individual pollutants to the consideration of air
pollution as a complex mixture" (Moolgavkar et al, 1997).
The approach recommended in the APHEA protocol, is to
fit the regression model into different strata (e.g.,
centiles) of levels of air pollutants. Another method
is to use factor analysis, a statistical technique in
which air pollutants can be grouped into a number of
factors according to their correlations with one another.
In
this study, we applied Ridge regression (a method which
dealt with the collinearity problem) but found the results
were comparable to those without using this method.
This comparability of results indicates the stability
of our multiple pollutant model. Another indication
of model stability is the finding that the RRs were
broadly in the same direction (but smaller in magnitude)
as those in the single pollutant model. One important
advantage of the multiple pollutant model is the ability
to study interactions between pollutants.
The
synergistic effect between O3 and NO2 might be explained
by the fact that both were oxidizing pollutants and
thus potentiated the effect of each other. By contrast,
the antagonistic interaction of RSP with O3 could be
due to the chemically reducing properties of RSP which
partially neutralised the damaging effect of the highly
reactive and oxidizing agent O3.
Age
group-specific analysis showed that infants and children
below the age of five and those aged 65 and above were
at higher risks compared to the other (5-64 years) age
group. While SO2 appeared to affect the elderlies selectively
(they were probably more susceptible), the RR was not
significant among infants and children, who might be
less exposed to this predominantly outdoor pollutant.
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