Environmental Health and Biostatistics and Computing GroupsDepartment of Community MedicineThe University of Hong Kong

Environmental Health and
Biostatistics and Computing Groups
Department of Community Medicine
The University of Hong Kong

Project Team

Dr CM Wong
(Data analysis and report writing)
Mr Stefan Ma
(Computation and statistical advice)
   
Professor AJ Hedley
(Head of Department)
Professor TH Lam
(Epidemiological advice)

CONTENTS

Executive Summary

References

Figures

Basic Tables

Operation Manual


 

Executive Summary

Background and objectives

Valuable indicators of the possible benefits of environmental management and control can be obtained by extrapolation from analysis carried out in other locations; but governments and local regulatory agencies are usually unable to draft or implement effective legislation without relevant local information to support their proposals. A study had been commissioned to the Chinese University of Hong Kong (CUHK) by the Environmental Protection Department, to evaluate the acute health effects of air pollution, using data for 1994-96 as a first attempt towards utilizing local intelligence. This study is a follow-up of the first study, aiming to validate the methods and results in the first study.

Methods

A series of daily hospital admissions and deaths in 1995, 1996 and the first half of 1997, due to respiratory and circulatory diseases, were obtained from routinely collected data and were analysed using Poisson regression with adjustment for overdispersion and long term effects of covariates

(including trend, seasonality, weekdays, holidays, after holidays, temperature and humidity). The health effects due to daily pollutant concentrations of sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3) and respirable suspended particulates (RSP) were then estimated and compared with those obtained from other similar studies.

Findings

(a) For hospital admissions

Air pollution was found to have an effect on circulatory and respiratory diseases combined and separately (relative risk, RR=1.03-1.10; p<0.084) for all ages; on circulatory admissions (RR=1.05-1.10; p<0.001) for the 65 or above age group; on respiratory admissions, the effects of which appeared to be j-shaped from the younger to the older age groups; on asthma (RR=1.10-1.16; p<0.018, except SO2); on chronic obstructive pulmonary disease (RR=1.08-1.14; p<0.0001); and on ischaemic heart disease (RR=1.04-1.09; p<0.051, except SO2 and RSP).
   
(b) For hospital deaths

Both NO2 and O3 were positively associated with circulatory and respiratory diseases combined and separately (for NO2: RR= 1.10-1.14, p<0.038; and for O3: RR=1.07-1.22, p<0.010).
   
(c) Validation and composite score

The above estimates were consistent with and in between those obtained from similar studies using the European (APHEA) approach overseas and in the CUHK. But in addition, a composite score was derived from the four pollutants and was found to provide consistent estimates for all the health outcomes under study in all ages (RR=1.04-1.11, p<0.098, except hospital deaths due to circulatory diseases).

Conclusions

Routine hospital morbidity and mortality data, air pollution and meteorological observations can be utilized to provide information for the estimation of acute health effects of air pollution. Environmental management and control should and could take into account health effects of air pollution based on locally derived information. However the processes are errors prompted (as large and complex data sets are involved) and are vulnerable to the misuse of health and other parameters and to misinterpretation of the results as it involves knowledge from several different fields. A team approach with expertise from epidemiological, environmental, statistical and computational professionals is required.

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1.0 Background and introduction

1.1 The contribution of epidemiological studies to the process of environmental management and control of health hazards is well established world-wide. Valuable indicators of possible benefits can be obtained by extrapolation from analyses carried out in other locations but, in general, governments and local regulatory agencies are unable to draft or implement effective legislation without relevant local information to support their proposals.
   
1.2 Several epidemiological studies have now shown an association between particulate air pollution and exacerbations of illness in individuals with respiratory disease and also increases in the numbers of deaths from cardiovascular and respiratory disease, particularly in the elderly. New hypotheses have been advanced to postulate mechanisms underlying these observed effects (Seaton et al 1995).1

Respirable particulates (RSP) with an aerodynamic diameter of <10 um(or particles measured as black smoke by the smoke stain method) comprise the principal pollutant associated with these findings. In addition RSP sulphate and sulphur dioxide concentrations, are reported to be associated with all causes mortality and respiratory mortality in recent studies from the USA (Pope et al 1995)2 and the UK (Anderson et al 1996)3 respectively. A recent review in the United Kingdom concludes that the associations between daily concentrations of particles and acute health effects principally reflect a causal relationship (Committee on the Medical Effects of Air Pollutants 1995).4 After a lengthy scientific review, the USEPA determined that new standard should be added for particulates less than 2.5 ? of aerodynamic in size and the welfare-base standards were also revised by making them identical to the health-based standards.5

In Hong Kong we have found that SO2, RSP and SO4 concentrations are associated with excess risks for symptoms of cough, phlegm and wheeze and also bronchial hyper-responsiveness (by histamine challenge test) in primary school children (Hedley et al 1993; Peters et al 1996; Tam et al 1994; Wong et al 1998).6,7,8,9 However in the London study the strongest association with daily mortality was for ozone. The effects of ozone and black smoke were independent of the effects of other pollutants.

Evidence on the risks associated with other pollutants is variable and less consistent. In the recent London study (Anderson et al 1996)3 the NO2 (1 hour maximum) was associated with all causes mortality and cardiovascular mortality; however a negative effect was seen for respiratory mortality. A significant positive effect on mortality was seen for SO2 and all cause mortality in the warm season period.

Several authors point to the complex between-season covariation of several pollutants, which is sometimes negative and at other times positive.
   
1.3 The published literature in this field is growing rapidly. The Department of Community Medicine is monitoring this through different databases and will aim to carry out the analysis using a state-of-the-art approach. This will enhance the utility of the outputs and ensure comparability as far as possible with studies in other countries (Katsouyanni, Schwartz, Spix et al 1996).10

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2.0 Scope and objectives

2.1 to examine the variation of daily air pollution data i.e. 24 hour average for sulphur dioxide, nitrogen dioxide and respirable suspended particulates and 8 hour average for ozone, among the various monitoring stations in Hong Kong for the years 1995-1996, as available;
   
2.2 to investigate the availability and the use of the various health outcome measures including data on hospital admissions and hospital deaths due to respiratory and circulatory problems collected routinely in the Hong Kong hospitals;
   
2.3 to investigate the short-term effects of the air pollutants considered in 2.1 (in the same day and one or more days lagged) individually and compositely on some of the health outcome measures considered in 2.2 above, with adjustment for seasonal variations, secular trends as well as meteorological conditions including temperature and humidity;
   
2.4 to validate and update models developed earlier and to develop a mechanism for the use and maintenance of the model for continuous study by the Environmental Protection Department.

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3.0 Materials and methods

3.1 Study design

It was an ecological study utilizing routinely collected hospital admission data, air pollutant concentration data and weather data by the Hospital Authority, Environmental Protection Department and the Observatory respectively. Variations in the daily number of hospital admissions due to circulatory and respiratory diseases were studied, and their relationships with each of the pollutants were modelled to assess the effects of air pollution on health after adjustment for time trends, seasonality, weather conditions and some other factors including days of week, holidays and days after holidays.

This study follows a previous one performed by the Chinese University of Hong Kong (CUHK)11 which followed the general approach of the protocol of the APHEA (a European approach using epidemiological time series data), developed within the frame of the EC Environment 1991-94 Programme. However data for some disease categories (ICD Rubrics) included in the APHEA protocol were not analysed in the CUHK study. The data sets and disease categories used for this new study are shown in Table 1 below. Those categories which were excluded or missing from the CUHK study are indicated in the table.
Table 1: Number of hospital admissions by disease groups
 
Disease groups 1995   1996 1997*
I. Diseases of the Circulatory System (ICD9 390-459)12:
  Acute rheumatic fever (390-392)** 32 - 12 11
  Chronic rheumatic heart disease (393-398)** 1,572 - 1,626 672
  Hypertensive disease (401-405)*** 4,396 (0) 4,319 2,000
  Ischaemic heart disease (410-414) 12,281 (11,884) 13,741 6,560
  Disease of pulmonary circulation (415-417) 291 (289) 274 144
  Other forms of heart disease (420-429) 15,494 (15,549) 17,567 8,932
  Cerebrovascular disease (430-438) 12,474 (10,224) 13,326 6,826
  Diseases of arteries, arterioles and capillaries (440-448)** 1,909 (1,300) 2,144 944
  Diseases of veins and lymphatics, and other diseases of circulatory system (451-459)** 5,591 - 6,448 3,240
  Sub-total: 54,040 (39,246) 59,457 29,329
II. Diseases of the Respiratory System (ICD9 460-519):
  Acute respiratory infections (460-466) 13,845 (13,871) 16,906 9,968
  Other diseases of upper respiratory tract (470-478)** 3,005 (2,228) 3,650 1,641
  Pneumonia and influenza (480-487) 12,567 (12,574) 14,944 7,648
  Chronic obstructive pulmonary disease and allied conditions (490-496) 25,330 (25,357) 28,344 13,567
  Pneumoconioses and other lung diseases due to external agents (500-508)*** 386 (0) 471 275
  Other diseases of respiratory system (510-519)** 11,358 - 13,478 7,733
  Sub-total: 66,491 (54,030) 77,793 40,832
I & II Total: 120,531 (93,276) 137,250 70,161
* first half year
** data for ICD9 390-392, 393-398, 446-448, 451-459, 470 and 510-519 were not included for analysis in the CUHK Final Report
*** data for ICD9 401-405 and 500-508 were missing in the CUHK data files and were not analysed in the CUHK Final Report
( ) CUHK data in brackets
- not included for analysis in the CUHK study

In order not to exclude categories which might show effects from air pollution (e.g. hospital admissions for cardiovascular diseases under ICD9 390 - 429 which were found to be related to respirable suspended particulates and carbon monoxide by Schwartz (1997)13 but not all included in the CUHK study) and to ensure comparability to the results of those studies which follow the APHEA protocol (Bacharova 1996; Schouten 1996),14,15 we decided to follow strictly the categories recommend by the APHEA protocol for this study.

Data for 1995-1996 (generated and cleaned by the Department of Community Medicine, the University of Hong Kong in this study) were used in establishing the statistical models and in estimating the effects; and data for first half year of 1997 were used for validation of the established models. It was also decided that data for the year 1994, which were used by the CUHK group, should not be used in this study because the data quality is not consistent with that of the 1995-96 data set to be used in this study. In 1994 only 3 of the 12 hospitals under study had already adopted the MRAS database; but the number increased to 7 in 1995. Besides, the percentages of valid daily data for air pollutant concentrations from the monitoring stations were lower in 1994 than those in the other years.
   
3.2 Databases

Hospital admission data: Hospitals included for generation of hospital admissions were the publicly funded hospitals (accounting for 90% of hospital beds in Hong Kong) which either had an accident and emergency department, or was a referral base from the accident and emergency department of another nearby hospital (9) or had a 24-hour outpatient department (2). 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. The hospitals included in the study, together with the type of information system they were using and an indication as to whether they had an A & E department, were listed in Table 2 below:
Table 2: List of HA hospitals included in the study
 
Hospital Information system* Whether having A&E
1. Kong Wah Hospital (KWH) MRAS Yes
2. Our Lady of Maryknoll Hospital (OLM) IPAS No
3. Princess Margaret Hospital (PMH) IPAS/MRAS Yes
4. Pok Oi Hospital (POH) IPAS Yes
5. Prince of Wales Hospital (PWH) MRAS Yes
6. Pamela Youde Nethersole Hospital (PYN) MRAS Yes
7. Queen Elizabeth Hospital (QEH) MRAS Yes
8. Queen Mary Hospital (QMH) IPAS/MRAS Yes
9. Ruttonjee Hospital (RH) MRAS No
10. Tuen Mun Hospital (TMH) MRAS Yes
11. United Christian Hospital (UCH) MRAS Yes
12. Yan Chai Hospital (YCH) IPAS/MRAS Yes
* IPAS - Integrated Patient Administrative System
MRAS - Medical Records Abstracting System

Patients admitted to hospitals between 1.1.1995 and 30.6.1997 with data on: dates of admission and discharge, socio-demographic information (age, gender, marital status, ethnic group, district of residence, pseudo identifier of patient), admission source, discharge diagnosis in ICD9 codes and discharge status were retrieved from the databases for each of the hospitals under study. In order to validate the completeness of the retrieved data, the total number of inpatients for the period 1.4.1995 to 31.3.1996, for each hospital, were compared with those reported in the Hospital Authority Statistical Report 1995/96. When there were big differences between the two, the Hospital Authority Information Technology Department was ask for an explanation and we then revised the databases if necessary until they were reasonably close to each other. This process took almost a half year to complete. The data are shown in Table 3 below:
Table 3: Comparison of total hospital discharges between HKU data obtained from the HA IPAS/MRAS and those from HA Statistical Report 95/96
 
  1.4.1995 - 31.3.1996#
  HKU < HA
Kong Wah Hospital (KWH) 63,583 63,583
Our Lady of Maryknoll Hospital (OLM) 8,564 8,564
Princess Margaret Hospital (PMH) 104,149 104,149
Pok Oi Hospital (POH) 11,432 11,432
Prince of Wales Hospital (PWH) 104,679 104,679
Pamela Youde Nethersole Hospital (PYN) 66,672@ 61,263
Queen Elizabeth Hospital (QEH) 112,557 112,559
Queen Mary Hospital (QMH) 87,308 87,313
Ruttonjee Hospital (RH) 16,727 16,727
Tuen Mun Hospital (TMH) 83,117 83,118
United Christian Hospital (UCH) 51,266 51,293
Yan Chai Hospital (YCH) 39,508 39,508
Total: 749,562 744,188
# total hospital patient discharges
@ The excess 5409 cases in the HKU data set were day cases which could not be excluded when the Information Technology Department generated the data set due to missing of the identifier.

The total data sets were then extracted for circulatory (ICD9 390-459) and respiratory (ICD9 460-519) diseases. The numbers of hospital admissions by disease groups in the three years were as shown in the previous Table 1 and subset of specific disease categories are shown in Table 4 below:
Table 4: Number of hospital admissions by specific diseases
 
Disease 1995 1996 1997*
Asthma (ICD-9 493) 8,682 9,672 3,803
Chronic obstructive pulmonary disease (ICD-9 490-496) 25,330 28,344 13,567
Ischaemic heart disease (ICD-9 410-414) 12,281 13,741 6,560
* first half year

Acute myocardial infarction was not analysed, as had been done by the CUHK, because diagnosis for the disease has been changing and subject to misclassification over the past years.

Pollutant concentration data: Pollutant concentration data in CD-ROM were made available by the Air Services Group of the Environmental Protection Department with hourly data from all monitoring stations in Hong Kong. The following stations in various urban, suburban and industrial areas were included in the study:
Table 5: 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 (SSPO) 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, 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, were excluded from the study. The pollutants included in this study are in Table 6 below:
Table 6: List of pollutants used in the study
 
Pollutant Unit
1. Nitrogen Dioxide {24-hr} (NO2)  
2. Sulphur Dioxide {24-hr} (SO2) All in micrograms/
3. Respirable Suspended Particulates {24-hr} (TEOM)* cubic metre
4. Ozone {9.00 am - 5.00 pm} (O3)  
* TEOM - Tapered Element Oscillating Microbalance, an instrument for the continuous measurement of particulates matter in air

In order to maintain consistency and similar quality standards in the data, missing data were defined and replaced in accordance with the APHEA recommendations. The guidelines were slightly modified to suit local situations and these are described in Table 7 below:
Table 7: Definitions of and methods for and replacement of missing daily data
 
Procedure Computation
(a) Define non-missing daily data on a particular day (i) For SO2, NO2 and RSP, if number of non-missing hourly data in that day 318, it will be defined as non-missing.
(ii) For O3 (9 am - 5 pm), if number of non-missing hourly data in that day (during the 8 hour interval) 36, it will be defined as non-missing
(b) Exclude pollutant from a station for further analysis (i) For each of SO2, NO2 and O3, if the proportion of non-missing daily data in a station over the study period <75%, it will be excluded from the analysis.
(ii) For RSP, if the proportion of non-missing daily data in a station over the study period <67%, it will be excluded from the analysis.#
(c) Compute non-missing daily data   Mean of non-missing hourly data in that day
(d) Define seasonal i

(i = 1, 2, 3, 4) in a particular year (December include in the next coming year)
  w(i)=Mean for non-missing daily data in the station in season i / Mean for non-missing daily data in all the other stations in season i

1 = December - February

2 = March - May

3 = June - August

4 = September - November
(e) Define a weight w(i) for a station in a particular season i of the year   i = 1, 2, 3, 4

w(i) will be missing if the proportion of non-missing daily data in either the above numerator or denominator are less than 75% for SO2, NO2 and O3 and less than 67% for RSP.#
(f) Define missing daily data in a particular day   Data in the day not regarded as non-missing according to (a) were missing data
(g) Replace missing daily data in a particular day during a particular season i for a particular station   Mean of all non-missing daily data over all the other stations multiply by a seasonal weight w(i) defined in (e)
Note: RSP measured by TEOM.

# A minimum of 67% non-missing daily data was used as criteria for inclusion of a pollutant in the analysis instead of 75%. This was set in the computer programme at the beginning of the study when the HKU was trying to adopt a similar procedure as that used by the CUHK. However this might not be necessary for data after 1994 as the data were more complete.

The data in monthly averages were comparable to those in the EPD 1995 and 1996 statistical reports. The percentage of data valid after replacement are shown in the following Table 8:
Table 8: Percentage of valid daily measures of air pollutants by stations in the study (1995-96 and first half of 1997)
 
  Station#
Pollutant C/W KC KT SSPO ST TP TW
NO2 (24-hr average)
1995 92.60 92.33 95.89 89.04 97.26 96.71 95.34
1996 93.44 95.90 94.81 90.16 95.63 94.54 93.17
1997* 94.48 93.37 87.85 97.24 96.69 95.03 86.74
SO2 (24-hr average)
1995 98.08 96.71 97.26 93.42 99.45 - 95.07
1996 97.54 95.08 98.36 89.07 98.91 - 97.54
1997* 96.69 98.90 98.34 98.90 98.90 - 85.08
TEOM (24-hr average)
1995 85.21 94.79 79.18 - 87.40 - 94.25
1996 98.63 97.81 91.80 - 87.43 - 86.07
1997* 93.92 99.45 92.82 - 96.13 - 86.19
O3 (8-hr average)
1995 94.25 93.15 - - - - -
1996 92.35 94.54 - - - - -
1997* 91.16 96.69 - - - - -
* the data are available only for first half year of 1997
- not available
# Abbreviations referred to Table 5. A daily mean concentration representing the pollution level in all Hong Kong areas were obtained from valid data of all the stations for each of the pollutants under study.

Meteorological data: Daily means for temperature and relative humidity were obtained from the Environmental Protection Department which derived the data from the Observatory. The monthly means for the years 1995 and 1996 were comparable with those reported in the Hong Kong Annual Reports.
   
3.3

Statistical modelling

The statistical modelling methods followed the guidelines recommended by the APHEA protocol and are outlined as follows:
(a) Poisson regression with adjustment for overdispersion using quasi-likelihood method was used to model the health count outcome and pollutant after adjusting for covariates.
   
(b) The following covariates, which are considered to be potential confounders, were fitted to each model so as to obtain the core model before adding in the pollutant concentration variable:
Variable Explanation
t (day) Daily trend
t2 Daily curvature
year Year (1995, 1996)
cos (2 p /365) Seasonality: cosine curve - 1 cycle
cos (4 p /365) 2 cycles
cos (6 p /365) 3 cycles
cos (8 p /365) 4 cycles
sin (2 p /365) sine curve - 1 cycle
sin (4 p /365) 2 cycles
sin (6 p /365) 3 cycles
sin (8 p /365)  4 cycles
Monday Sunday (reference) vs Monday
Tuesday Sunday vs Tuesday
Wednesday Sunday vs Wednesday
Thursday Sunday vs Thursday
Friday Sunday vs Friday
Saturday Sunday vs Saturday
Holiday1 Holiday effect
Holiday2 After holiday effect
Temperature Linear effect of temperature
Humidity Linear effect of humidity
   
(c) Each pollutant concentration was included into the model both without lag effect and with cumulative lag effect for up to three previous days (mean of cumulative concentration as an independent variable) for SO2, NO2 and RSP; and with cumulative lag effect for up to the previous five days for O3 .
   
(d) Akaiki Information Criteria (AIC) was used to select the best model in c) above (Appendix C).
   
(e) The final model for each of the age groups 0-14, 15-64 and 65 years or above was obtained using the best model from d) above.
   
(f) In order to obtain an indicator of the amount (proportion) of variation in the health outcome explained, the number of admissions was transformed by taking the logarithm and multiple regression was then applied. The value R2 was used to quantify the variation explained by the core module without pollutant.
   
(g) Interaction effect between each pollutant (in its original scale) and 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 fitted model.
   
(h) When there were interaction effects, the effect was estimated for high and low levels of the other pollutant (using results from the model).
   
(i) Interactions between pollutants and seasons were checked by defining the four seasons as follows: spring, March-May; summer, June-August; autumn, September-November; winter, December-February, multiplying each pollutant concentration by each season dummy variable to obtain the interaction terms and fitting each interaction term in the model.
   
(j) To account for the correlations among the pollutants, a composite score is generated from the concentration levels of the four pollutants by principal component analysis using the 1995-1996 data. The composite score is a weighted average of the original concentration levels using the loadings from principal component analysis as weights but scaled so the total weight is equal to one.
Validation of the model for 1995-96 was achieved internally by comparing the predicted with the observed number of health outcomes in the data set as well as by comparing the observed on the first half year of 1997 with the predicted from the model developed using 1995-96 data. Externally the effects per 50 ug/m3 concentration estimated by other studies following the APHEA protocol and those obtained from the CUHK study were compared with those in this study.

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4.0 Findings

4.1 Descriptive statistics

Summary statistics of daily hospital admissions for circulatory and respiratory diseases, both combined and separately by 3 month periods are shown in Basic Table A5.1 to A5.3 (in Appendix). Summary statistics of all the health outcomes used in this study are shown in Tables 9-12 below:
Table 9: Summary statistics of daily hospital admissions by disease groups (1995-96)
 
Disease No.
(days)
Mean SD Min P25 Median P75 Max
Combined* 731 352.6 61.38 209 311 349 388 556
Circulatory 731 155.3 34.73 68 126 160 180 260
Respiratory 731 197.4 37.25 116 170 190 219.5 320
Asthma 731 25.1 8.42 9 19 24 30 63
COPD 731 73.4 15.85 40 62 72 84.5 128
IHD 731 35.6 10.61 8 28 35 44 76
* Combined circulatory and respiratory diseases
COPD - Chronic obstructive pulmonary disease
IHD - Ischaemic heart disease  
Table 10: Summary statistics of daily hospital admissions by disease groups (1997#)
 
Disease No. (days) Mean SD Min P25 Median P75 Max
Combined* 181 387.6 54.32 220 352 391 420 524
Circulatory 181 162.0 32.64 85 135 170 187 234
Respiratory 181 225.6 36.11 132 200 223 251 332
Asthma 181 21.0 5.60 7 17 21 24 41
COPD 181 75.0 11.84 47 67 74 82 112
IHD 181 36.2 9.16 16 29 37 43 61
* Combined circulatory and respiratory diseases
# first half year
COPD - Chronic obstructive pulmonary disease
IHD - Ischaemic heart disease  
Table 11: Summary statistics of daily hospital deaths by disease groups (1995-96)
 
Disease No. (days) Mean SD Min P25 Median P75 Max
Combined* 731 21.1 6.43 6 16 21 25 46
Circulatory 731 10.5 3.90 1 8 10 13 24
Respiratory 731 10.6 4.19 1 8 10 13 27
* Combined circulatory and respiratory diseases  
Table 12: Summary statistics of daily hospital deaths by disease groups (1997#)
 
Disease No. (days) Mean SD Min P25 Median P75 Max
Combined* 181 22.2 5.33 9 18 22 26 39
Circulatory 181 10.3 3.49 4 8 10 12 19
Respiratory 181 11.9 3.72 5 9 12 14 24
* Combined circulatory and respiratory diseases
# first half year

Summary statistics of daily mean temperature, relative humidity, and mean concentration of each of the pollutants are shown in the Basic Tables B1-2 and C4-7.

The correlations among the four pollutants, and between each pollutant and the health outcomes are shown in Table 13.  
Table 13: Spearman's rank correlation coefficient (r) between daily concentrations of pollutant, meteorological measures and hospital admissions (1995-1996)
 
  Circulatory Respiratory Circulatory + Respiratory
  r (p-value) r (p-value) r (p-value)
SO2 (24-hr) 0.16 (0) 0.14 (0) 0.18 (0)
NO2 (24-hr) 0.28 (0) 0.14 (0) 0.22 (0)
RSP (24-hr) 0.19 (0) 0.02 (0.55) 0.11 (0)
O3 (8-hr) 0.02 (0.53) -0.06 (0.1) -0.03 (0.42)
Temperature -0.13 (0) -0.06 (0.13) -0.09 (0.01)
Humidity -0.09 (0.01) 0.07 (0.06) -0.01 (0.84)
SO2 and NO2 were correlated with both circulatory and respiratory admissions, combined and separately. For RSP it correlated with circulatory admissions and circulatory and respiratory admissions combined. In studying whether these pollutants have an effect on early health outcome, it is important to adjust for confoundings which might explain the correlation.

The correlations among the pollutant concentrations, temperature and humidity are shown in the following Table 14.
Table 14: Matrix of Spearman's rank correlation coefficient (r) between daily concentrations of pollutant and meteorological measures (1995-1996)
 
  NO2 RSP O3 (8-hr) Temperature Humidity
  r (p-value) r (p-value) r (p-value) r (p-value) r (p-value)
SO2 0.38 (0) 0.31 (0) -0.17 (0) 0.12 (0) -0.05 (0.17)
NO2     0.84 (0) 0.45 (0) -0.47 (0) -0.38 (0)
RSP         0.55 (0) -0.39 (()) -0.54 (0)
O3 (8-hr)             -0.08 (0.03) -0.54 (0)
Temperature                 0.29 (0)

 

   
4.2 Statistical modelling

Core models for hospital admissions: The following Tables 15-17 show the results of core models which explain the hospital admissions due to circulatory and respiratory disease categories in terms of daily linear and quadratic time trends, year effect, seasonality (using sine and cosine functions), day of week (compared with Sunday), holidays and days after the holidays, temperature and relative humidity. (Air pollutant concentrations are not included at this stage.)

For the two disease groups, both combined and separately, there were positive daily linear and quadratic trends over the two year period; and weekdays (Monday to Friday relative to Sunday), day after holidays, higher temperature and lower humidity were positively associated with hospital admissions (p<0.012, except for Friday effects in respiratory admission where p=0.708). Each model explained 64-79% of the variation in the health outcomes.

Similar effects were also found in individual age groups (younger than 15 years, 15-64 and 65 years and older age groups), for both disease categories separately, except in those younger than 15 years for respiratory diseases, (most p<0.10) (Basic Tables E 7-12). The above models explained 39-77% of the variations in the health outcomes.

For admissions due to asthma, chronic obstructive pulmonary and ischaemic heart diseases the effects due to the whole set of meteorological, seasonality and trend were similar except that numbers of hospital admissions were associated with lower temperature (p<0.044) (Basic Tables E 4-6). The models explained 31% to 49% of the variations in the health outcome.
 
Table 15: Core model of Poisson regression for hospital admissions due to circulatory and respiratory diseases in 1995-96 (N = 731)
Multiple R-Square = 0.7518 (from multiple regression on logarithmic transformed counts of health outcomes)
Independent variable* Coefficient Standard error t-value p-value 
Intercept 7.6180 2.9925 2.5457 0.0109
t 0.0006 0.0001 5.9284 0.0000
t2 0.0000 0.0000 -3.9367 0.0001
year -0.0229 0.0317 -0.7214 0.4706
cos (2¹ t/365)# 0.0503 0.0107 4.7210 0.0000
cos (4¹ t/365)# -0.0165 0.0048 -3.4561 0.0005
cos (6¹ t/365)# -0.0215 0.0046 -4.7016 0.0000
cos (8¹ t/365)# 0.0131 0.0046 2.8230 0.0048
sin (2¹ t/365)# 0.1673 0.0124 13.4915 0.0000
sin (4¹ t/365)# 0.0332 0.0071 4.6997 0.0000
sin (6¹ t/365)# -0.0468 0.0056 -8.2948 0.0000
sin (8¹ t/365)# -0.0103 0.0052 -1.9989 0.0456
Monday 0.2737 0.0122 22.4151 0.0000
Tuesday 0.1811 0.0126 14.3995 0.0000
Wednesday 0.2324 0.0123 18.8229 0.0000
Thursday 0.1841 0.0125 14.7472 0.0000
Friday 0.1363 0.0126 10.8002 0.0000
Saturday 0.0043 0.0130 0.3337 0.7386
holiday1 -0.1800 0.0148 -12.1695 0.0000
holiday2 0.0778 0.0197 3.9517 0.0001
temperature 0.0093 0.0016 5.7843 0.0000
humidity -0.0013 0.0004 -3.4697 0.0005
*Notes:
 
  1. t denotes daily linear trend (values: 1,2,3,... ,731)
  2. t2 denotes daily quadratic trend (1,4,9,... ,534361)
  3. year denotes year effect (95,96)
  4. #cos {2k¹ t/365} and sin {2¹ kt/365}; where k = 1,2,3,4 are used to model one year, six months, four months and three months cycle respectively. But for the leap year 1996, 366 are used instead of 365 for number of days in a year.
  5. Monday, Tuesday,... , Saturday effects relative to Sunday
  6. holiday1 denotes holiday effect for all public holidays (includes the Sunday before and after the holiday); and holiday2 denotes day after each of the holidays.
  7. temperature denotes daily mean temperature
  8. humidity denotes daily mean relative humidity
Table 16: Core model of Poisson regression for hospital admissions due to circulatory diseases in 1995-96 (N = 731)
Multiple R-Square = 0.7869 (from multiple regression on logarithmic transformed counts of health outcomes)
Independent variable* Coefficient Standard error t-value p-value
Intercept 3.8665 3.5342 1.0940 0.2740
t 0.0005 0.0001 3.8582 0.0001
t2 0.0000 0.0000 -3.7549 0.0002
year 0.0070 0.0374 0.1871 0.8516
cos (2p t/365)# 0.1013 0.0129 7.8713 0.0000
cos (4p t/365)# -0.0110 0.0057 -1.9286 0.0538
cos (6p t/365)# -0.0104 0.0055 -1.8901 0.0587
cos (8p t/365)# -0.0016 0.0056 -0.2907 0.7713
sin (2p t/365)# 0.1043 0.0148 7.0651 0.0000
sin (4p t/365)# 0.0324 0.0084 3.8688 0.0001
sin (6p t/365)# -0.0218 0.0067 -3.2381 0.0012
sin (8p t/365)# -0.0183 0.0062 -2.9603 0.0031
Monday 0.4666 0.0151 30.8715 0.0000
Tuesday 0.3324 0.0156 21.2877 0.0000
Wednesday 0.4209 0.0153 27.5933 0.0000
Thursday 0.3429 0.0155 22.1293 0.0000
Friday 0.3152 0.0156 20.2303 0.0000
Saturday 0.0123 0.0167 0.7381 0.4604
holiday1 -0.3527 0.0193 -18.2530 0.0000
holiday2 0.0799 0.0231 3.4506 0.0006
temperature 0.0093 0.0020 4.7657 0.0000
humidity -0.0011 0.0005 -2.5104 0.0121
* For explanation of variables, refer to Table 15.
Table 17: Core model of Poisson regression for hospital admissions due to respiratory diseases in 1995-96 (N = 731)
Multiple R-Square = 0.6406 (from multiple regression on logarithmic transformed counts of health outcomes)
Independent variable* Coefficient Standard error t-value p-value
Intercept 9.9914 3.8859 2.5712 0.0101
t 0.0008 0.0001 5.4589 0.0000
t2 0.0000 0.0000 -2.5986 0.0094
year -0.0533 0.0412 -1.2946 0.1955
cos (2p t/365)# 0.0085 0.0136 0.6253 0.5318
cos (4p t/365)# -0.0201 0.0061 -3.2875 0.0010
cos (6p t/365)# -0.0306 0.0059 -5.2079 0.0000
cos (8p t/365)# 0.0232 0.0059 3.9030 0.0001
sin (2p t/365)# 0.2181 0.0160 13.6331 0.0000
sin (4p t/365)# 0.0348 0.0091 3.8242 0.0001
sin (6p t/365)# -0.0654 0.0073 -9.0004 0.0000
sin (8p t/365)# -0.0042 0.0066 -0.6353 0.5252
Monday 0.1326 0.0154 8.6384 0.0000
Tuesday 0.0744 0.0158 4.7227 0.0000
Wednesday 0.0944 0.0156 6.0727 0.0000
Thursday 0.0710 0.0156 4.5354 0.0000
Friday 0.0060 0.0159 0.3751 0.7076
Saturday -0.0004 0.0159 -0.0241 0.9808
holiday1 -0.0653 0.0179 -3.6487 0.0003
holiday2 0.0747 0.0256 2.9193 0.0035
temperature 0.0090 0.0020 4.4334 0.0000
humidity -0.0015 0.0005 -3.0204 0.0025
* For explanation of variables, refer to Table 15. The daily number of hospital admissions in all ages due to circulatory and respiratory diseases combined and separate, due to asthma, chronic obstructive pulmonary and ischaemic heart diseases, as observed and predicted by the core models are depicted in Figures 5 (a1 - f1). The numbers of hospital admissions predicted by the models with pollutants for each of the corresponding health outcomes are depicted in Figures 5 (a2 - f2). For specific age groups and for circulatory and respiratory diseases combined and separately, the numbers of admissions are depicted in Figures 7 (a1 - b3). From the graphs there were strong seasonal variations which are predicted closely by the core models. However the observed numbers were varying to a greater extent than that of the predicted. After adding in the pollutant concentration to the core model, some of the excess variations were explained. In general both the observed and predicted numbers were more crowded in the upper bound than in the lower bound. Core models for hospital deaths: For hospital deaths in all ages due to circulatory and respiratory diseases combined together and separately, the models explained 24% to 39% of the variations (Basic Tables E 13-15). The daily number of observed deaths and those predicted by the core models in 1995-96 are depicted in Figures 6 (a1 - c1). The numbers predicted by models with pollutants for each of the health outcomes are depicted in Figures 6 (a2 - c2). Because of the small observed numbers, the observed varied from the expected to a much greater extent for hospital deaths than for hospital admissions.

Models with pollutants for hospital admissions: The relative risks (RR) with 95% confidence intervals (95% CI) for hospital admissions in all ages due to each of the disease categories are shown in Table 18 below, with comparison to similar estimates from the CUHK reports. As the CUHK study used data of 1994-95 (instead of 1995-96) and included different ICD9 codes for circulatory and respiratory diseases, the results will not be directly comparable to those from the HKU study. All relative risks in the tests and in Tables 18-21 below were referred to 50 ug/m3 changes in concentration of the pollutants. However relative risks for 100 ug/m3 changes were also presented in Tables 18a-21a (Appendix B) for the pollutants correspondingly.
 
Table 18: Relative risks (RR) and 95% confidence interval (95% CI) for 50 micrograms per cubic metre increase in the concentration of air pollutants for hospital admissions of (i) combined circulatory and respiratory, (ii) circulatory, (iii) respiratory, (iv) asthma, (v) chronic obstructive pulmonary diseases and (vi) ischaemic heart diseases (1995-96)
 
(i) Circulatory + Respiratory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0 :1.07 (1.04,1.09)*** 0-1 :1.11 (1.09,1.14)***
SO2 (24-hr) 0 :1.04 (1.01,1.07)* 0 :1.07 (1.03,1.10)***
RSP (24-hr) 0-1 :1.04 (1.02,1.06)*** 0-3 :1.10 (1.07,1.23)***
O3 (8-hr) 0-2 :1.07 (1.05,1.10)*** 0-5 :1.14 (1.10,1.17)***

 

(i) Circulatory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0-2 :1.08 (1.04,1.11)*** 0-1 :1.06 (1.03,1.10)***
SO2 (24-hr) 0-1 :1.05 (1.01,1.10)* 0-1 :1.09 (1.03,1.14)***
RSP (24-hr) 0-3 :1.03 (1.00,1.06)* 0-2 :1.03 (1.00,1.06)*
O3 (8-hr) 0-5 :1.07 (1.03,1.10)*** 0-5 :1.06 (1.02,1.11)**

 

(iii) Respiratory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0 :1.08 (1.05,1.11)*** 0-3 :1.18 (1.14, 1.23)***
SO2 (24-hr) 0 :1.03 (1.00,1.08) 0 :1.06 (1.02, 1.11)**
RSP (24-hr) 0-1 :1.05 (1.02,1.07)*** 0-3 :1.15 (1.12, 1.19)***
O3 (8-hr) 0-2 :1.10 (1.07,1.13)*** 0-3 :1.18 (1.14, 1.22)***

 

(iv) Asthma
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag RR (95% CI)
NO2 (24-hr) 0-3 :1.12 (1.02,1.22)* 0-3 :1.27 (1.17, 1.37)***
SO2 (24-hr) 0-3 :0.91 (0.78,1.06) 0 :1.12 (1.01, 1.23)*
RSP (24-hr) 0-3 :1.10 (1.03,1.18)** 0-3 :1.16 (1.08, 1.24)***
O3 (8-hr) 0-2 :1.16 (1.08,1.24)*** 0-2 :1.23 (1.14, 1.33)***

 

(v) Chronic obstructive pulmonary diseases
  HKU (Lag 0-n)#
Pollutant Lag :RR (95% CI)
NO2 (24-hr) 0 :1.13 (1.09,1.17)***
SO2 (24-hr) 0 :1.12 (1.06,1.18)***
RSP (24-hr) 0-3 :1.08 (1.04,1.13)***
O3 (8-hr 0-2 :1.14 (1.09,1.18)***

 

(vi) Ischaemic heart diseases
  HKU (Lag 0-n)#
Pollutant Lag :RR (95% CI)
NO2 (24-hr) 0-2 :1.09 (1.03,1.16)**
SO2 (24-hr) 0-1 :1.03 (0.95,1.12)
RSP (24-hr) 0-1 :1.04 (1.00,1.09)
O3 (8-hr) 0-2 :1.04 (0.99,1.10)
* p < 0.05;
** p < 0.01;
*** p < 0.001

# Notes: Lag0-n denotes the mean of cumulative effects of lag from day 0 (same day) up to previous n days using up to 5 days (Lag0-5) for ozone and up to 3 days (Lag0-3) for other pollutants

The results will be discussed in 5.2-5.4.

Models of pollutants and hospital deaths: The relative risks (RR) with 95% confidence intervals (95% CI) for hospital deaths due to each disease category are shown in Table 19 below, with comparison to similar estimates from the CUHK reports:
 
Table 19: Relative risks (RR) and 95% confidence interval (95% CI) for 50 micrograms per cubic metre increase in the concentration of air pollutants for hospital deaths of (i) combined circulatory and respiratory, (ii) circulatory and (iii) respiratory diseases (1995-96)
 
(i) Circulatory + Respiratory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0-1 :1.12 (1.05,1.20)*** 0-3 :1.14 (1.05,1.24)**
SO2 (24-hr) 0-3 :0.93 (0.81,1.06) 0-1 :1.11 (0.99,1.24)
RSP (24-hr) 0-1 :1.04 (0.99,1.09) 0-3 :1.06 (0.99,1.14)
O3 (8-hr) 0-2 :1.07 (1.05,1.10)*** 0-5 :1.20 (1.10,1.32)***

 

(ii) Circulatory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0-1 :1.10 (1.01,1.21)* 0-3 :1.10 (0.98,1.24)
SO2 (24-hr) 0-3 :0.89 (0.74,1.07) 0-2 :1.10 (0.72,1.31)
RSP (24-hr) 0-3 :1.05 (0.96,1.14) 0-3 :1.03 (0.96,1.10)
O3 (8-hr) 0-5 :1.15 (1.03,1.28)** 0-5 :1.13 (1.04,1.22)**

 

(iii) Respiratory
  HKU (Lag 0-n)# CUHK (Lag 0-n)#
Pollutant Lag :RR (95% CI) Lag :RR (95% CI)
NO2 (24-hr) 0-1 :1.14 (1.04,1.25)** 0-3 :1.14 (1.04,1.26)**
SO2 (24-hr) 0 :1.08 (0.96,1.22) 0-1 :1.16 (0.98,1.37)
RSP (24-hr) 0-1 :1.05 (0.97,1.13) 0-3 :1.10 (0.99,1.22)
O3 (8-hr) 0-5 :1.22 (1.09,1.35)*** 0-5 :1.27 (1.11,1.46)***
* p < 0.05;
** p < 0.01;
*** p < 0.001
# Note: 1) Lag0-n denotes the mean of cumulative lag from day 0 (same day) up to previous n days

2) the cumulative lag days were up to 5 days for ozone and up to 3 days for other pollutants
The results will be discussed in 5.2-5.4.

Models with interactions between pollutants: The relative risks of hospital admissions for circulatory and/or respiratory disease in models with interaction terms between pollutants are as shown in Table 20 below:
Table 20: Effect in relative risk (95% confidence interval) per 50 ug/m3 of each pollutant at high and low level of each other co-pollutant (using median concentration as cut-off) of hospital admissions due to circulatory/respiratory diseases
(a) Effect of NO2 on circulatory and respiratory diseases
SO2 Relative risk (95% CI)
High 1.061 (1.035, 1.088)***
Low 1.122 (1.079, 1.166)***
(b) Effect of RSP on circulatory and respiratory diseases
O3 Relative risk (95% CI)
High 1.013 (0.992, 1.034)
Low 1.041 (1.016, 1.066)***
(c) Effect of NO2 on respiratory disease
SO2 Relative risk (95% CI)
High 1.068 (1.034, 1.103)***
Low 1.133 (1.077, 1.192)***
(d) Effect of NO2 on circulatory disease
SO2 Relative risk (95% CI)
High 1.054 (1.023, 1.087)***
Low 1.111 (1.059, 1.164)***
*** p < 0.001

 

NO2 interacted with SO2 for circulatory and/or respiratory diseases, with the estimated RR ranging from 1.11 to 1.13 at lower levels of SO2; and ranged from 1.05 to 1.07 at higher levels of SO2. RSP has an effect on circulatory and respiratory diseases combined at lower levels of O3 with RR 1.04 (95% CI: 1.02, 1.07) but no significant effect was seen at higher level of O3 . The effects for a pollutant were stronger at a lower level of the other pollutant interacting with it. The other pollutants for circulatory and respiratory diseases combined and separately were not significant.

Models with interaction between pollutant and seasons: In studying whether the pollutant effects on hospital admissions for circulatory and respiratory diseases combined and separately, varied between seasons (i.e. spring: March - May; summer: June - August; autumn: September - November; winter: December - February), only the relative risk associated with O3 were found to differ in the spring, being higher than in the other seasons.

The relative risk per 50 ug/m3 increase was 1.05 (95% CI 1.02, 1.08) in spring and 1.01 (0.99, 1.04) in other seasons for circulatory and respiratory diseases combined; and was 1.06 (1.03, 1.10) and 1.02 (0.99, 1.05) for respiratory disease alone.

Effect of composite score of pollutants: A composite score of the concentrations of the four pollutants was derived (for method, see footnote for Table 21), which extracts the maximum correlation among the pollutants and explains 68% of the variations among them. Using this composite score as the independent variable instead of each of the pollutants, the results with all those significant health outcomes are shown in Table 21 below.
 
Table 21: Relative risk (RR) with 95% confidence interval (95% CI) for composite score of air pollutant concentrations for 50 micrograms per cubic metre increase on (1) hospital admissions (2) hospital deaths Ð lag effects not analysed
 
(1) Hospital admissions due to:   RR (95% CI)
Circulatory and respiratory diseases (a) 1.06 (1.04, 1.08)***
Circulatory diseases (a) 1.04 (1.01, 1.07)**
  (b) 0.92 (0.78, 1.09)
  (c) 1.02 (0.98, 1.06)
  (d) 1.06 (1.03, 1.10)***
Respiratory diseases (a) 1.08 (1.04, 1.11)***
  (b) 1.06 (1.02, 1.11)**
  (c) 1.04 (1.00, 1.09)
  (d) 1.10 (1.06, 1.15)***
Asthma (a) 1.06 (0.99, 1.14)
Chronic obstructive pulmonary diseases (a) 1.11 (1.07, 1.16)***
Ischaemic heart diseases (a) 1.05 (0.99, 1.10)
(2) Hospital deaths due to:    
Circulatory and respiratory diseases (a) 1.07 (1.00, 1.14)*
Circulatory diseases (a) 1.05 (0.96, 1.15)
Respiratory diseases (a) 1.09 (0.99, 1.19)
* p < 0.05;
** p < 0.01;
*** p < 0.001

# Composite score was generated from four pollutants (NO2, SO2, TEOM and O3) by principal components analysis and the first principal component was used which explained 68% of the variance with loadings of 0.491, 0.105, 0.726 and 0.469 respectively.

(a) All ages
(b) 0-14 years old
(c) 15-64 years old
(d) 65 years or older

The results will be discussed in 5.2-5.4.

Adequacy of 1995-96 models (hospital admissions): The residues for hospital admissions due to circulatory and respiratory diseases combined and separately, after fitting the model for each of the pollutants are shown in Figures 9(a) - 9(c). Patterns indicating unexplained variations in the models are observed. There were no discernible patterns in the residuals for circulatory admissions. There were some unexplained patterns in the residual plots for respiratory and respiratory and circulatory admissions combined.

There may also be autocorrelations (i.e. correlation between consecutive observations) in the data. This was examined by the autocorrelation function plots in Figures 10(a) - 10(c). There was no evidence of autocorrelation in the circulatory admission residuals. However slight autocorrelation of less than 0.5 was present in the respiratory and respiratory and circulatory combined admission residuals.

Predictive validity of 1995-96 models (hospital admissions): After obtaining the models from the 1995-96 data, the predicted number of hospital admissions due to circulatory and respiratory diseases combined and separately in the first half year of 1997 were obtained. The observed numbers in the first half year of 1997 and the predicted numbers with model using each of the pollutants are depicted in Figure 8 (a-c). Overall the models for prediction of circulatory and for prediction of circulatory and respiratory admissions were better (i.e. closer to the observed) than those for the prediction of respiratory admissions. In all the three health outcomes observed there were rising trends in the later part of the first half of 1997. These phenomena were particularly prominent in respiratory admissions indicating that the long term effects of other determinants of the disease might have changed. The models developed according to two yearsÕ data were not able to pick up the changes. But it would not invalidate the models to be used for estimation of air pollution effect on health.

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5.0 Discussion

5.1 Validity and reliability of the models

The validity and reliability of the models were ensured and assessed in the following ways:
(a) checking of accuracy of the data

The validity of the models is very much dependent on the accuracy of the data from which the models are derived. As far as possible, all hospital admissions, pollutants and meteorological data were checked for consistency by comparisons with data from similar sources and with published reports on the same data. In this way several errors during the process of generating the data sets were detected and corrected.
   
(b) following the APHEA guidelines

Results from statistical models are subject to the choice of variables for inclusion in the models, the assumptions made about the distribution of the data and the methods of modelling. This is especially the case in statistical modelling for time series data in that the variables chosen in the model should be adequate to account for serial correlation, seasonality and trends which might be due to confounding but should not be over fitted to eliminate real effects of air pollutant which are also serially correlated, varying seasonality and with some time trends.

The APHEA guidelines are set to compromise the above two aspects of modelling and are recommended for all participating centres so that comparison can be made and effect estimates can be pooled up. We chose to follow the APHEA guidelines as strictly as possible in the disease categories, in the choice of independent variables, in the method to define and replace missing data, in the way to assess interaction among pollutants and stratification of the data by similar age groups. The results can therefore be compared with those from other APHEA studies.
   
5.2 Summary of findings

All relative risks referred to an increase of 50 ug/m3 in the concentration of the pollutant.

Hospital admissions: Time trends, seasonality and weather conditions explained 31% to 79% of the variations in all the health outcomes under study. (In the CUHK report only those for admissions and hospital deaths due to circulatory and respiratory diseases combined were reported, which were 66% and 31% respectively.)

Irrespective of the amount of variations unexplained after fitting the core model, all the pollutants under study showed significant effect on daily hospital admissions for circulatory and respiratory diseases combined and separately with relative risk (RR) estimates ranged from 1.03 to 1.10 in all ages overall. (The CUHK results were 1.03-1.18 in the RR estimates.)

In analysis by age groups, apparently the effects of pollutants on circulatory diseases were stronger for the older age groups with significant RR of 1.05 to 1.10 found in 65 or older age group; and for respiratory diseases the effects by age groups were apparently j-shaped with RR 0.93-1.08 in the 0-14 years age group, 0.90-1.06 in the 15-64 age group, and 1.06-1.19 for the 65 or older age group. (In the CUHK report there were no comparable results.)

For specific disease categories, NO2 , RSP and O3 were positively associated with admissions for asthma, RR 1.10-1.16; all pollutants were positively associated with chronic obstructive pulmonary diseases, RR 1.08-1.14; NO2 and RSP were significantly associated with ischaemic heart disease, RR 1.04-1.09. (In the CUHK results, only for asthma were available with RR (1.12-1.27.)

For all ages and the 65 and older age group, NO2 and RSP exhibited the most consistent effects with estimates for RR 1.07-1.14 for NO2 and 1.03-1.10 for RSP, significant for all health outcomes; O3 exhibited the strongest effects with RR 1.04-1.19 all were significant except for ischaemic heart disease; SO2 exhibited the least effects with RR 0.91-1.12, all were significant except for asthma and ischaemic heart diseases. However as the pollutants are highly correlated, a composite score which summarises the four pollutants, was constructed and was found to provide the most consistent (i.e. closely estimated) for all the health outcomes under study with RR 1.06-1.11, all statistically significant except for asthma and ischaemic heart disease. (No corresponding results were from the CUHK study.)

Hospital deaths: NO2 was positively associated with hospital deaths due to circulatory and respiratory diseases combined and separately with RR 1.10-1.14 (same RR 1.10-1.14 for CUHK results); and O3 was similarly associated with these health outcomes with RR 1.07-1.22 (CUHK 1.13-1.27). Similar to that for hospital admissions, the composite score for pollutant concentrations was also found to provide consistent estimates for effects of air pollution on hospital deaths with RR 1.05-1.09 (no corresponding results for CUHK).
   
5.3 Comparison with APHEA studies

The estimates of relative risks in the validation study showed stronger and significant effects when compared with pooled results of Western European cities on hospital admissions due to respiratory diseases, asthma and chronic obstructive pulmonary diseases with our significant RR of 1.02-1.06 versus theirs of 1.01-1.03 for the 15-64 age group and 1.06-1.19 versus 1.02-1.04 for the 65 and older age group.

Effects on hospital deaths were also more significant and higher in the HKU study than those in the pooled up estimates for total mortality from Western European studies with significant RR 1.10-1.15 versus 1.01-1.04 for circulatory diseases and RR 1.14-1.22 versus 1.04-1.05 for respiratory diseases.
   
5.4 Comparison with CUHK study

However the estimates from the validation study, when compared with those from the CUHK study, were smaller with RR 1.04-1.07 versus 1.07-1.14 for hospital admissions due to circulatory and respiratory diseases combined for all ages; about the same for admissions due to circulatory diseases (RR 1.05-1.10 versus 1.04-1.12 for 65 or older); and smaller for respiratory disease (RR 1.06-1.19 versus 1.13-1.22 for the 65 or older age group).

In the analysis for interaction effects between pollutants, the validation study followed the APHEA protocol in principle (i.e. defining the interaction term by multiplying a continuous pollutant concentration variable with the other pollutant dichotomized into high and low level in order to avoid multicollinearity10) and this is a more conservative approach. The CUHK study took a more aggressive approach (in that several co-pollutants with interaction terms were put in the same model and subject to model selection by means of a stepwise procedure). Relatively smaller numbers of interactions were found in the HKU study compared to the findings reported in the CUHK report.
   
5.5 Limitations of the Hong Kong study

 

Only two years of data: Unlike most studies in other places, the Hong Kong study only had two yearsÕ data for the analysis. It would not be realistic to confidently predict the health outcome in the third year of the study according to models developed in the previous two years, with reasonable accuracy. However the main objectives of this kind of studies were to assess the health effects of air pollution, but not to obtain prediction for health outcomes.

Non-linearity of the effects: Although a moving average method was used to take account of the lag effect of air pollution, all the other covariates were modelled for their linear effects. Some other smoothing functions would be useful and have to be used such as the generalised additive modelling, for modelling the non-linear relationship between the health outcome and covariates.

Refinement of models: There are discernible patterns in the residuals of some models. We have used different cycles (obtained from spectral analysis) in fitting the models and found that there were no changes in the fitness and estimates of the models. However plots of the residuals against pollution levels suggested that the unexplained variations are not related to air pollution. For the sake of uniformity we keep the same covariates of the original models for our results.

Discrepancies between hospital deaths and total deaths: The hospital deaths included in this study represented only about half of all deaths occurred in the period. Also, they were analysed with the air pollutant concentration on the date of admission to hospital rather than on the actual date of death. These will produce discrepancies in the estimates compared to those when all deaths are included and analyses were based on date of death.

New direction: There are new issues raised in the newly developed APHEA II16 protocol, such as in harvesting effects of air pollution on pre-mature deaths, and regional differences in the effect estimates. These issues were pointed out in a separate operation manual but were not addressed in this study. They should be taken into account in any future study.

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6.0 Conclusions

In this study we have examined the variations and covariations in daily concentrations of the four pollutants under study (objective 2.1). A composite score was derived from the four pollutants.

We have obtained, examined, cleaned and validated a series of hospital admission data (mostly from the Department? own resources) with health outcomes defined in accordance with the guideline of the APHEA project (objective 2.2).

We found and quantified the health effects of air pollution, representing by the daily concentrations of the four pollutants individually and compositely (objective 2.3). The estimates are consistent to but slightly greater than those from the APHEA studies.

We validated with the models developed in the earlier CUHK study by comparison with models independently developed and using different data which are comparable to those of the APHEA protocol. We have also obtained and provided in an operation manual the major source programmes, for the use and maintenance of the models for the continuous study by the Environmental Protection Department (objective 2.4). The critique of the CUHK study was in the following section and the operation manual in a separate documents.

6.1 Critique of CUHK study
(a) In the data

Admission data

Some diseases selected for study were not found in the CUHK data sets (i.e. ICD9 401-405 hypertension disease and ICD9 500-508 pneumoconioses and other lung disease due to external causes).

Some disease categories recommended by the APHEA protocol and used by some APHEA studies were not included in the CUHK (i.e. ICD9 390-392 acute rheumatic fever, ICD9 393-398 chronic rheumatic heart disease, ICD9 446-448 in diseases of arteries, arterioles and capillaries, ICD9 451-459 diseases of veins and lymphatics, and other diseases of circulatory system, ICD9 470 in other diseases of upper respiratory tract, and ICD9 510-519 other diseases of respiratory system).

Overall the CUHK used about 23% less than the total data available in 1995; all of the available data were used in the validation study. For the 1994 data, we were not able to validate as we did not and were not required to collect data for the year; but the data have the same problems in missing and excluding some disease categories from the analysis.

The HKU were only contracted to collect the hospital admission data for the period 1.7.1996-30.6.1997. However we had collected the data for period starting from 1.1.1995 involved in another study. We therefore have the completed data for 1995, 1996 and half year of 1997 independently collected from the HA but not for 1994. Due to incompleteness of the CUHK data and the EPD was not able to produce complete data for the 1994, the EPD agreed that we should base the study on data collected by us for period 1.1.1995-30.6.1997.

Air pollutant data

There were zero values for daily means in RSP and SO2 in the CUHK data in Figures 2 and 4. Zero values should not appear as the minimum daily values did not have zero (Tables 8 and 6). The zero values probably reflect missing values, indicating that there may be problems with the way in which missing data were handled in the CUHK study.

Meteorological data

There were discrepancies between data obtained from the EPD in diskette given to HKU for analysis, and those from the CUHK data sets (obtained directly from the Observatory and computed by the CUHK for the averages). The discrepancies were reflected in plotting the CUHK data against the EPD data. These might arise from using different precision or method in taking the average for daily data.

 

   
(b) In the methods

The CUHK report states that Poisson regression was mainly used in the data analysis. But in fact other approximate logistic regression methods were used and odds ratios were presented instead of relative risks (Table 14, pp 44). For a fuller assessment of the CUHK report it would be necessary to confirm for why Poisson regression was not used; and in using the approximate logistic regression methods, what denominator had been used.

Only results for one core model were presented in Tables 13 and 14, although there should be several core models, one for each health outcome under study. There was no mention of core model for other health outcomes.

In the CUHK study age groups 0-4, 5-64 and 65 or older were used. This classification of age groups is not comparable to that reported in APHEA studies which usually used 0-14, 15-64 and 65 or above age groups.

Interactions

In the CUHK study in obtaining interaction effects between pollutants, concentrations between pollutants were multiplied to obtain the interaction terms. All concentrations and their interaction terms were put in model and stepwise regression (pp60 of CUHK report) was used to select significant interaction variables. This process would have problem of multicollinearity (as the three pollutants put in the model, NO2, O3 and RSP, are correlated with coefficient 0.44-0.79) and is at risk of letting the noices in the data to choose the pollutants in a model.23
   
(c) In the results

In Table 15 of the CUHK report for admissions due to respiratory and circulatory combined and separately, asthma and AMI, the relative risks were sometimes too low (from 0.87 to 0.92 per 50 ug/m3 change in pollutant concentrations for AMI) or too high (from 1.12 to 1.27 for asthma admissions).

In Table 15a of CUHK report, relative risks for 0-4 age group in total respiratory and circulatory admissions were not presented. There are no reasons given (probably due to small numbers) for their absence while results for respiratory admissions were given for this age group.

In Table 16 of CUHK report, most of the relative risks tended to be high (from 1.03 to 1.27 per 50 ug/m3 change in pollutant concentrations).

In Table 17 to 25 of CUHK report, relative risks for the health effects of a pollutant at three specific concentrations of other pollutant were presented. These are different from relative risks in different range of the other interacting pollutants, which should be used to express synergistic effects.
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