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Executive Summary

Executive Summary

Background and objectives: Locally derived data are needed for the SAR Government and regulatory agencies to support the drafting and implementation of effective legislation for the management and control of the environment. In 1996, the Environmental Protection Department commissioned the Chinese University of Hong Kong to carry out a study on health effects of air pollution and in 1997 the University of Hong Kong to carry out a follow-up validation study. The study performed by the University of Hong Kong identified some irregularities in the way the data were selected, managed and analysed in the previous study. It also obtained effect estimates which were more comparable to the results obtained by the collaborating centres of Air Pollution on Health: a European Approach (APHEA). Finally it pointed to new directions in methodology and in modelling methods adopted by the APHEA Phase Two study which could be used in Hong Kong.

In this study, reported here, the problems of the earlier Hong Kong studies were resolved in that (i) three years of data were used to obtain better models; (ii) non-linearity effects in the pollutant and covariates were modelled using a generalized additive modelling method; and (iii) patterns in the daily variations were explained as far as possible by using more appropriate wave lengths, introducing influenza epidemics in the models and using more recently developed statistical methods to control for autocorrelation in the data.

Health outcomes: Daily counts of hospital admissions with a discharge diagnosis of respiratory disease (ICD9 460-519), chronic obstructive pulmonary disease (COPD) (490-496 excluding 493), asthma (493), cardiac disease (390-429) and ischaemic heart disease (IHD) (410-414), for all ages, as well as hospital deaths due to respiratory (460-519) and cardiovascular (390-459) diseases, for all ages, were used as the 7 major health outcomes. Among them, admissions were sub-categorised as follows: for respiratory disease, into 0-14, 15-64, 65-74 and 75+ age groups; for asthma, into 0-14 and 15-64 age groups; for cardiac disease, into 15-64, 65-74 and 75 age groups and for IHD, into 15-64, 65-74 and 75+ age groups. These categories for all ages and specific age groups formed 19 categories of health outcomes for analysis.

Summary of findings: The effects for each pollutant without adjustment for co-pollutant, on the above-mentioned 19 health outcomes and with adjustment for the most confounding co-pollutant, on the above 7 major health outcomes are summarized in this section.

NO2: NO2 was shown to have strong effects on all the 19 health outcomes under study without adjustment for co-pollutants, except on the IHD 15-64 and all ages groups. The effects on the 7 major health outcomes, with adjustment for co-pollutant and autocorrelation, were significant at the 5% level except IHD admissions and cardiovascular hospital deaths for all ages. The effects on asthma admissions and respiratory deaths for all ages were likely to be non-linear. The effects on respiratory, COPD, cardiac and IHD admissions for all ages were higher in the cool than in the warm season.

SO2: SO2 did not have an effect on most of the 19 health outcomes under study without adjustment for co-pollutant. With adjustment for co-pollutant and autocorrelation, it had an effect on COPD admissions for all ages (p=0.005). The effect on cardiac admissions for all ages was higher in the cool than in the warm season.

RSP: RSP was associated with most of the 19 health outcomes under study without adjustment for co-pollutant. With adjustment for co-pollutants and autocorrelation, it had an effect on respiratory (p=0.023) and asthma (p=0.045) admissions for all ages and the effects were likely to be non-linear. The effect on cardiac admissions for all ages was higher in the cool than in the warm season.

O3: O3 had effects on most of the 19 health outcomes under study without adjustment for co-pollutant. With adjustment for co-pollutant and autocorrelation, it had strong effects on respiratory and asthma admissions for all ages (p=0.000). The effects on COPD, cardiac and IHD admissions for all ages were stronger in the cool than in warm season.

FSP: FSP (PM2.5) had effects on most of the 19 health outcomes under study without adjustment for co-pollutant. With adjustment for co-pollutant, the effects were not significant for all of the 7 major health outcomes for all ages (p>0.192). But as the pollutant was measured in only one monitoring station and there were missing data problems, the effects need to be further investigated.

Public health implications: The results from this study showed strong short-term effects of air pollutants on hospital admissions and hospital deaths.

In the daily number of hospital admissions for all ages, there was a 4-8% increase due to respiratory disease; 5-15% increase due to chronic obstructive pulmonary disease and 11-22% increase due to asthma. There was also a 3-7% increase in admissions due to a cardiac disease. There was a 3-5% increase due to a cardiovascular disease (ICD9 390-459), which includes cardiac disease as well as cerebrovascular disease and diseases of arteries, arterioles, capillaries, veins and lymphatics. These percentage increases are all expressed as rates per 50 ug/m3 increase in the concentration of air pollutants (NO2, SO2, O3 and RSP).

In the daily number of hospital deaths for all ages, there was a 10% increase due to respiratory disease and 8% increase due to cardiovascular disease for every 50 ug/m3 increase in NO2. For other pollutants the increases were not significant and they need to be further investigated.

The results suggest that air pollution may show stronger health effects in Hong Kong than those obtained in European cities.

Conclusions: The results from this study show that short-term effects of air pollutants on health are strong. It is both feasible and worthwhile to develop further studies on the health effects of air pollution with a longer series of data, using the methodology adopted by the APHEA protocol. Territory-wide SAR mortality, based on daily mortality counts from the Census and Statistics Department, should be included as one of the main health outcomes to be studied.

1.0 Background and introduction

In 1997, the Department was offered a contract by the Environmental Protection Department (EPD) to study the short-term effects of ambient air pollution on public health using hospital admission data in Hong Kong for the period January 1995 to June 19971 and to validate the findings of another similar study on data for the period January 1994 to June 1996.2 The results revealed that, similar to other studies overseas, there were significant effects on morbidity and mortality of individual pollutants i.e. nitrogen dioxide (NO2), sulphur dioxide (SO2), respirable suspended particulates (RSP) and ozone (O3). The study performed by the Department modified the way the data were selected, managed and analysed in the previous study and obtained effect estimates which were more comparable to the results obtained by collaborating centres of Air Pollution on Health: a European approach (APHEA). In line with new directions in methodology and in modelling methods adopted by the APHEA-2 protocol,3 our report also pointed out some limitations of both of the Hong Kong studies and indicated what should be done in any future studies.

The limitations in the Hong Kong studies will be further resolved and discussed in this new phase of study. First, with three years of data, a better prediction model will be developed. Second, non-linearity effects in the pollutant(s) or covariates will be modelled using a generalized additive model (in statistical package S-Plus). Third, unexplained patterns in the daily variations will be explained as far as possible by (i) using more appropriate wave lengths for seasonality and terms for time trends, to eliminate as far as possible all unobserved confounding effects; (ii) introducing influenza epidemics in the model to control as much of the observed confounding effects as possible in addition to those due to air temperature and humidity etc; and (iii) using more recently developed statistical methods to control for any auto-correlation and/or extra-Poisson variations in the data.

2.0 Scope and objectives

The following tasks will be completed by the Department of Community Medicine.

  1. Single pollutant: A model for each health outcome is fitted with terms to account for all long-term and seasonal patterns and other possible confounding effects. Short-term daily variations are then studied and accounted for by daily variations in SO2, NO2, RSP and O3 individually, based on data from 1 January 1995 to 31 December 1997.

  2. Multiple pollutants: From each single pollutant model, the joint effects of each pollutant with other pollutants are studied by putting them in the model. Interactions and multi-collinearity among pollutants are also studied and taken account of, based on the same data as in a) above.

  3. Single pollutant PM2.5: The effect due to PM2.5 is studied in a similar way as in a) above, but using data from 1 August 1995 to 31 December 1997 when the PM2.5 concentrations are available from the EPD.

  4. Multiple pollutants with PM2.5: Study b) above but with PM2.5 instead of RSP. Compare the models with either PM2.5 or RSP in terms of stability (reliability) in effect estimates.

  5. Verification of model: The best model developed from a) to d) above is then used to obtain the predicted daily numbers of admissions for each health outcome. The observed number of admissions in the data 1 January 1998 to 30 June 1998 are compared with the predicted for verification (i.e. predictive validity) of model.

3.0 Materials and methods

3.1

Study design

The same design as in the previous report was used. It utilized routinely collected hospital admission data, air pollutant concentration data and meteorological data by the Hospital Authority, Environmental Protection Department and Observatory. Variations in the daily number of hospital admissions were studied, and their relationships with each of the pollutants were modelled to assess the effects of air pollution on health after adjustment for confounding factors.

   
3.2

Databases

In the APHEA-2 protocol there were changes in age group definitions and missing data handling methods from those in APHEA. All the changes were incorporated in this report as far as possible. In order to be more comparable with results from APHEA studies, there were also some alterations in the choice of health outcomes, in that the category of chronic obstructive pulmonary disease (ICD9 490-496) excluded asthma (ICD9 493), and cardiac diseases (ICD9 390-429) was used instead of circulatory disease (ICD9 390-459) in the admission categories.

Hospital admission data: The hospitals included for compilation of hospital admissions were the publicly funded hospitals (accounting for 90% of hospital beds in Hong Kong) with an accident & emergency department, or those which were the referral base from the accident & emergency department of another hospital or had a 24-hour outpatient department. One other hospital which was the only hospital in the most polluted district in Hong Kong was also included. All hospitals should have a computerized system for inputting and retrieval of patient data (Basic Table A1).

Information for patients admitted to the above-mentioned hospitals between 1.1.1995 and 30.6.1998, on date of admission, discharge diagnosis (in ICD9 codes) and age (and other information not required in this study) were retrieved from the databases. The number of cases by discharge diagnosis and age, grouped according to APHEA-2 protocol (hospital deaths not in APHEA-2 categories, were also included) were summarized in Table 1 below.

Table 1: Number of patients admitted between 1.1.1995 and 30.6.1998 by discharge diagnoses and age groups

Number of cases
Discharge diagnosis (ICD9 codes) Age groups 1995-1997 1998 (Jan-June)
Respiratory disease (460-519) All ages* 223,225 46,877
0-14 yrs 74,164 16,450
15-64 yrs 48,909 9,451
65-74 yrs 38,783 7,640
75+ 61,318 13,329
Chronic obstructive pulmonary disease
(490-496 excluding 493)
All ages* 53,374 9,795
Asthma (493) All ages* 27,080 4,286
0-14 yrs 14,005 2,133
15-64 yrs 8,520 1,332
Cardiac disease (390-429) All ages* 108,150 18,835
15-64 yrs 37,195 5,961
65-74 yrs 32,205 5,715
75+ 37,356 6,976
Ischaemic heart disease (410-414) All ages* 39,483 6,940
15-64 yrs 14,259 2,402
65-74 yrs 13,969 2,507
75+ 11,201 2,029
Deaths: Respiratory (460-519) All ages* 11,798 2,095
Cardiovascular (390-459) All ages* 11,202 1,779

* Including patients without information on age.

Pollution data: Hourly concentrations of air pollutants (Table 2) by monitoring stations (Table 3) were provided by the Air Services Group of the Environmental Protection Department.

Table 2: List of pollutants used in the study

Pollutant Unit
1. Nitrogen Dioxide {24-hr} (NO2) micrograms/cubic metre
2. Sulphur Dioxide {24-hr} (SO2) micrograms/cubic metre
3. Respirable Suspended Particulates {24-hr} (RSP)* micrograms/cubic metre
4. Ozone {8-hr} (O3) micrograms/cubic metre
5. Fine Suspended Particulates {24-hr} (FSP) micrograms/cubic metre

* Measured by Tapered Element Oscillating Microbalance (TEOM), an instrument for the continuous measurement of particulate matter in air.

Table 3: List of air pollution monitoring stations

Station Sampling height Above ground Date start operation
1. Central/West (C/W) 78m 18m (4th floor) 11/83
2. Kwai Chung (KC) 82m 25m (6th floor) 7/88
3. Kwun Tong (KT) 34m 25m (6th floor) 7/83
4. Sham Shui Po (SSP) 21m 17m (4th floor) 7/84
5. Shatin (ST) 27m 21m (5th floor) 7/91
6. Tai Po (TP) 31m 25m (6th floor) 2/90
7. Tsuen Wan (TW) 21m 17m (4th floor) 8/88

Two stations were excluded, one in Yuen Long (in suburban area) due to the extent of missing data and one in Mong Kok (in urban area) which provided concentrations measured on ground level.

In each station, for O3 the 8-hourly (9 am - 5 pm when O3 concentrations were highest) means were taken as daily data if there were at least 6 valid hourly data each day; and for the other pollutants the 24-hourly means were used as daily data if there were at least 18 valid hourly data. Other data were missing data. The percentages of non-missing daily data were shown in Table 4 below.

Table 4: Percentage of valid measures of air pollutants in each monitoring station

Station#
Pollutant C/W KC KT SSP ST TP TW
NO2 (24-hr average)
1995 93 92 96 89 97 97 95
1996 93 96 95 90 96 95 93
1997 91 90 87 98 93 89 85
1995-97 92 93 93 92 95 93 91
1998* 97 96 94 85 97 98 96
SO2 (24-hr average)
1995 98 97 97 93 99 - 95
1996 98 95 98 89 99 - 98
1997 92 93 93 96 94 - 82
1995-97 96 95 97 93 97 - 91
1998* 97 98 94 86 97 - 94
RSP (24-h average)
1995 85 95 79 - 87 - 94
1996 99 98 92 - 87 - 86
1997 90 92 85 - 91 - 90
1995-97 91 95 85 - 89 - 90
1998* 99 95 95 - 99 - 92
O3 (8-hr average)
1995 94 93 - - - - -
1996 92 95 - - - - -
1997 87 90 - - - - -
1995-97 91 93 - - - - -
1998* 92 96 - - - - -
FSP (24-hr average)
1995 (Aug-Dec) - - - - - - 94
1996 - - - - - - 82
1997 - - - - - - 92
1995 (Aug)-97 - - - - - - 88
1998* - - - - - - 97

* the data are available only for first half year of 1998
- not available
# Abbreviations referred to Table 3.

Daily mean concentrations representing the pollutant levels in all Hong Kong areas were obtained from non-missing data for each of the pollutants under study by means of the following steps:

  1. Estimate the annual mean concentration of each pollutant in each monitoring station and subtract this annual mean from the daily concentrations of the corresponding year. The resulting series is regard as "centered".

  2. Take the arithmetic mean over all monitoring stations of these centered series day by day.

  3. Finally add the annual mean of all stations to the series obtained in step 2. The series for each health outcome is used for the analysis.

Overall, daily means obtained using APHEA-2 method were highly correlated (Spearman's correlation coefficient above 0.99) with those obtained using the previous APHEA method (Basic Table D3).

Meteorological data: Daily means of temperature and relative humidity were obtained from the Environmental Protection Department which derived the data from the Observatory.

   
3.3

Statistical modelling

The statistical modelling methods followed the guideline recommended by the APHEA-2 protocol and are outlined as follows:

a) Poisson regression with adjustment for over-dispersion using quasi-likelihood4 approach was used to model the hospital admission counts of the health outcomes under study.
   
b)

Using Poisson regression mentioned in a) above, a core model was established to remove all the long term trends and seasonal variations by means of the following covariates:

Covariate Explanation
t (day) Daily trend
t2 Daily curvature
cos (2?kt/365.25) Seasonality
sin (2?kt/365.25) for k cycles per year to be determined by spectral analysis
Monday Monday vs Sunday
Tuesday Tuesday vs Sunday
Wednesday Wednesday vs Sunday
Thursday Thursday vs Sunday
Friday Friday vs Sunday
Saturday Saturday vs Sunday
Holiday1 Holidays
Holiday2 Day after holidays
Temperature Linear effect of temperature
Humidity Linear effect of relative humidity
Influenza
  • Dummy variable for weeks with number of influenza admissions (ICD9 487) above 75 percentile in a year

The numbers of seasonal cycles per year were obtained from spectral analysis5 instead of 1-4 cycles used in the previous study.

   
c) The residuals from fitting the core model for each health outcome, were examined for any discernible patterns, lack of normality and autocorrelation in them.
   
d) If there are no discernible patterns and lack of normality in the residuals, then potential confounding is not evident in the daily variations. Air pollutant concentrations were then fitted to obtain the air pollution effects for pollutants. Autocorrelations were taken account of for identified models.
   
e) In order to obtain an indicator of the amount (proportion) of variations in the health outcome explained, the number of admissions was tranformed by taking the logarithm and multiple regression was then applied. The value R2 was used to quantify the proportion of variations explained by the core model.
   
f) Effects were obtained per unit change in pollutant levels measured by current day and average of current day up to a previous day, called the best lag day, to be determined by AkaikeÕs Information Criterion with the minimum value. The best lag day was determined up to previous 5 days for ozone and up to previous 3 days for the other pollutants.
   
g) Interaction effect between each pollutant (in the original scale) and each of the other pollutants was checked by first dichotomizing the other pollutants using the median and multiplying each of them to obtain the interaction term, and then introducing the interaction term into the model. When there was an interaction effect, the air pollutant effect was estimated for high and low levels of the other pollutant.
   
h) Interactions between pollutant concentrations and season were checked by defining a season dummy variable with 1 for cool (January-April; November-December) and 0 for warm (May-October) season, multiplying the season dummy variable with concentrations to obtain the interaction term and fit each interaction term to the model. When there was an interaction effect, relative risks in cool and warm seasons were obtained respectively.
   
i) Effects due to copollutants were estimated by putting the other pollutants one by one in the model. Effect with adjustment for a copollutant which was associated with the maximum adjusting effect was used.
   
j)

Autocorrelations were adjusted for using Newy-West method.6 Non-linear copollutant effects were studied by means of generalised additive model.7

Non-linear dose-response relationships of pollutants were also studied using generalised additive model.

   
k) Validation of the models for 1995-97 was achieved by comparing the observed numbers of health outcomes in the first half year of 1998 with the predicted from the model developed using 1995-97 data.

 

4.0 Findings

4.1

Descriptive statistics

Summary statistics of all the health outcomes used in this study are shown in Tables 5-6 below.

Table 5: Summary statistics of daily hospital admissions (including deaths) by disease groups (1995-97)

Admission No. (days) Mean SD Min P25 Median P75 Max
Respiratory 1096 203.7 38.49 116 175 197 227 335
Asthma 1096 24.7 8.59 7 19 23 29 63
COPD 1096 48.7 12.27 22 40 48 56 94
Cardiac 1096 98.7 23.28 40 80 101 114 179
IHD 1096 35.0 10.26 8 28 35 44 76
Death:
  • Cardiovascular
  • 1096 10.2 3.77 1 8 10 13 24
  • Respiratory
  • 1096 10.8 4.06 1 8 10 13 27

    Min: Minimum; P25: 25% centile; P75: 75% centile; Max: Maximum
    Note : COPD - Chronic obstructive pulmonary disease excluding asthma
    IHD - Ischaemic heart disease

    Table 6: Summary statistics of daily hospital admissions (including deaths) by disease groups (1998 Jan-June)

    <
    Admission No. (days) Mean SD Min P25 Median P75 Max
    Respiratory 181 259.0 43.39 174 227 259 285 389
    Asthma 181 23.7 7.2 10 19 22 28 48
    COPD 181 54.1 11.86 32 45 53 62 90
    Cardiac 181 104.1 22.27 48 88 106 118 166
    IHD 181 38.3 10.52 15 31 39 45 65
    Death: