Air Pollution and Child Respiratory Health

A Case-Crossover Study in Australia and New Zealand

Adrian G. Barnett, Gail M. Williams, Joel Schwartz, Anne H. Neller, Trudi L. Best, Anna L. Petroeschevsky,
and Rod W. Simpson
School of Population Health, University of Queensland, Herston; Faculty of Science, Health and Education, University of the Sunshine Coast,
Maroochydore DC, Queensland, Australia; and Exposure, Epidemiology, and Risk Program, Harvard School of Public Health, Harvard
University, Boston, Massachusetts

Rationale: The strength of the association between outdoor air pollution and hospital admissions in children has not yet been well
defined. Objectives: To estimate the impact of outdoor air pollution
on respiratory morbidity in children after controlling for the confounding effects of weather, season, and other pollutants. Methods:
The study used data on respiratory hospital admissions in children
(three age groups: 1, 14, and 514 years) for five cities in Australia
and two in New Zealand. Time series of daily numbers of hospital
admissions were analyzed using the case-crossover method; the
results from cities were combined using a random-effects metaanalysis. Measurements and Main Results: Significant increases across
the cities were observed for hospital admissions in children for
pneumonia and acute bronchitis (0, 14 years), respiratory disease
(0, 14, 514 years), and asthma (514 years). These increases were
found for particulate matter with a diameter less than 2.5 m (PM2.5)
and less than 10 m (PM10), nephelometry, NO2, and SO2. The
largest association found was a 6.0% increase in asthma admissions
(514 years) in relation to a 5.1-ppb increase in 24-hour NO2. Conclusions: This study found strong and consistent associations between
outdoor air pollution and short-term increases in childhood hospital
admissions. A number of different pollutants showed significant
associations, and these were distinct from any temperature (warm
or cool) effects.
Keywords: air pollutants; Australasia; meta-analysis; respiration disorders

Many studies have found associations between selected air pollutants and adverse health effects in children (1). These adverse
health effects include the following: childhood hospital admissions (26), school absences (7), physician visits for upper and
lower respiratory illness (8), deficits in lung function growth
rates (9), bronchitis and chronic cough (10, 11), and increased
infant mortality (1214). A recent review in Europe strongly
recommended a reduction in childrens exposure to air pollution
(15). However, the strength of the association is still not well
defined because of the small number of studies of hospital admissions (which represent a common and serious outcome in children), and the complexity of the time-series modeling. In addition, there are few studies that have been able to examine a range
of pollutants. When multiple pollutants have been examined,

(Received in original form November 25, 2004; accepted in final form March 9, 2005)
Supported by the Environment Protection and Heritage Council, and partly supported by the National Health and Medical Research Council of Australia (grant
252834).
Correspondence and requests for reprints should be addressed to Rod W. Simpson,
Ph.D., Dean and Chair in Environmental Science, Faculty of Science, Health and
Education, University of the Sunshine Coast, Maroochydore DC, QLD 4558, Australia. E-mail: rsimpson@usc.edu.au
This article has an online supplement, which is accessible from this issues table
of contents at www.atsjournals.org
Am J Respir Crit Care Med Vol 171. pp 12721278, 2005
Originally Published in Press as DOI: 10.1164/rccm.200411-1586OC on March 11, 2005
Internet address: www.atsjournals.org

the independent effect of each pollutant is usually addressed in

multipollutant models, but these are sensitive to the assumptions
inherent in the time-series models. If the association with one
pollutant is nonlinear, or varies by season, then a two-pollutant
model assuming a linear relationship with each pollutant might
not give the independent effect of the second pollutant. This
suggests that an approach less sensitive to model assumptions
is desirable.
This study used the case-crossover method to examine the
effects of air pollution exposure on daily counts of hospital
admissions for children. The case-crossover design (16) is a
method for investigating the effects of acute exposures that can
also examine multiple exposures and interactions between exposures. This approach has been applied to the analysis of the
acute effects of environmental exposures, especially air pollution
(1719), and additional detail on this method is provided in the
online data supplement.
Many of the previous studies investigating the health effects
of air pollution in children used an age group of 0 to 14 years.
However, this combines infants and teenage children, two groups
that have a very different lung function and immune system,
and that are also in very different environments (prior to school
and school). This study examined three age bands: 0, 1 to 4, and
5 to 14 years.
The emphasis here is on identifying which air pollutants have
significant impacts on the respiratory health of children using
hospital admissions data, and on assessing the consistency of
such associations across cities in Australia and New Zealand.
Some of the results of this study have been previously reported
in the form of an abstract (20).

METHODS
Respiratory Health Data and Air Pollutant Data
Daily hospital and pollution data were collected for the period 1998
2001 in five of the largest cities in Australia (Brisbane, Canberra,
Melbourne, Perth, and Sydney) and the two largest cities in New
Zealand (Auckland, Christchurch). In 2001, these cities comprised 53%
of the Australian population and 44% of the New Zealand population.
Health data for all respiratory admissions of children aged 14 years
or younger were collected from state government health departments
in Australia and the New Zealand Health Information Service (Ministry
of Health), and details, including International Classification of Disease
codes, are provided in the online supplement.
The air pollutants considered were particulate matter less than 2.5 m
in diameter (PM2.5; g m3) and less than 10 m in diameter (PM10;
g m3), coefficient of light-scattering by nephelometry (an indicator
of fine particles 0.12 m in diameter [bsp]; in 104 m1), nitrogen
dioxide (NO2; in ppb), carbon monoxide (CO; in ppm), sulfur dioxide
(SO2; in ppb), and ozone (O3; in ppb). Additional information on how
these pollutants were measured is provided in the online supplement.

Statistical Methods
The case-crossover method controlled for long-term trend, seasonal
changes, and respiratory epidemics by design. Matched case-crossover

Barnett, Williams, Schwartz, et al.: Air Pollution and Child Health

1273

analyses were also used to investigate whether some pollutant effects

were related to those of other pollutants (21). The fixed 28-day-window
case-crossover approach was used, with a 1-day exclusion period around
the case day (22). Using covariates, there were additional controls for
the following: temperature, current minus previous days temperature,
relative humidity, pressure, extremes of hot and cold (coldest and warmest 1% of days), day of the week, public holiday (yes/no), and day after
a public holiday (yes/no).
To estimate the average effect for all cities, the estimates were
combined across cities using a random effects meta-analysis (23), and
the differences (heterogeneity) between cities were quantified using
the I-squared statistic (24). Analyses were conducted using the SAS
package (SAS System for Windows, version 8; SAS Institute, Inc.,
Cary, NC).
In the absence of an a priori opinion of which pollutants were
important to child health in Australia, we used a statistical significance
level of 5% with no correction for multiple comparisons. Although this
increased the chances of finding spurious associations, it reduced the
chances of missing any important associations during this early stage
of investigation of the effects of air pollution in Australia and New
Zealand.
To test whether one city had an undue influence on the metaanalysis, the meta-analyses were repeated with each city left out in turn
(a leave-one-city-out sensitivity analysis) (23).

RESULTS
Summary statistics of hospital admissions and demographic data
for each city are given in Table 1. Summary statistics of the air
pollutant and meteorology data in each city are given in Table 2.
Pollutant exposures used were the average of the current and
previous day. Estimates of the percentage increase in morbidity
are shown for an interquartile range increase (using the mean
interquartile range across cities). This made the increases from
different pollutants more comparable because the results showed
the changes to be expected for the cities under study, and allowed
the largest impacts to be identified.
The statistically significant increases in hospital admissions
for all cities are shown in Table 3, together with the estimated
differences (heterogeneity) between cities and the leave-onecity-out sensitivity analyses (see online Tables E1E3 for a com-

plete set of results). Statistically significant increases were found

for PM2.5, PM10, bsp, NO2, and SO2, but not for CO or O3. Results
are shown for an interquartile increase to facilitate comparisons
across pollutants. These interquartile ranges were as follows:
3.8 g m3 for 24-hour PM2.5, 7.5 g m3 for 24-hour PM10, 0.18
104 m1 for 24-hour bsp, 9.0 ppb for 1-hour NO2, 5.1 ppb for
24-hour NO2, 5.4 ppb for 1-hour SO2, and 9.8 ppb for 1-hour O3.
As with most cities around the world, there were strong correlations between some pollutants (see Table E4), because they
often arise from the same emission source (e.g., motor vehicles).
Given these correlations, matched pollutant models were run
where significant increases were found with more than one pollutant (Table 4) to identify whether the pollutant impacts are different or are related to each other (or some other pollutant arising
from the same emission sources). Matched control days were defined as follows: 24-hour PM2.5 within 2 g m3, 24-hour PM10
within 3 g m3, 24-hour NO2 within 1 ppb, 1-hour SO2 within
1 ppb, and temperature within 1C.
Differences between the Cities and Countries

The I-squared statistic represents the proportion of total variation in the estimated increase that is caused by heterogeneity
between cities and was used to identify any differences between
cities. This measure allowed the estimation of the average effect
of an air pollutant on hospital admissions using all the data, and
to identify if this effect is the same across all cities (positive or
negative) or whether the results for some cities are different
from others. In this way, we can conclude whether any identified
impact is the same for all cities or whether there are different
results arising from factors not identified in the analyses. The
I-squared statistic was generally very low, except for NO2 (Table
3), where all seven cities were available for analysis. The contrasting increases between cities are apparent in Figure 1, which
shows three of the significant meta-analysis increases for respiratory admissions (age groups: 0, 14, and 514 years).
To look for differences between countries, separate metaanalyses were run for the Australian and New Zealand cities.
The differences in the associations with NO2 between the five

TABLE 1. SUMMARY STATISTICS FOR DEMOGRAPHIC DATA AND HOSPITAL ADMISSION RATES
PER MILLION POPULATION (19982001)
Auckland
Demographic data
Total population
Median weekly individual income, $*
Population 15 yr, %
Population 65 yr, %
Daily hospital admissions, mean (range)
Respiratory
0 yr
14 yr
514 yr
Asthma
14 yr
514 yr
Pneumonia acute bronchitis
0 yr
14 yr

* Australian dollars.

Brisbane

Canberra Christchurch Melbourne

1,158,891 1,627,535 311,518

400499 300399 500599
22.9
21.0
21.2
10.0
11.0
8.3

316,224
300399
19.3
13.7

Perth

Sydney

3,366,542 1,339,993 3,997,321

400499 300399 400499
19.8
20.7
20.2
12.1
11.3
11.9

4.6
(029)
4.7
(019)
2.1
(011)

2.1
(09)
4.2
(012)
2.1
(09)

1.9
(023)
4.8
(023)
3.9
(032)

4.7
(029)
7.9
(035)
3.2
(022)

1.4
(06)
3.1
(09)
1.6
(07)

2.4
(016)
4.7
(013)
2.2
(010)

2.2
(010)
4.5
(113)
2.1
(09)

1.6
(08)
1.0
(07)

1.7
(07)
1.3
(07)

1.3
(013)
1.0
(016)

2.2
(019)
1.3
(013)

1.3
(06)
0.9
(07)

1.9
(08)
1.3
(07)

1.9
(010)
1.2
(08)

3.6
(025)
1.9
(013)

1.4
(07)
1.0
(05)

1.3
(019)
1.3
(016)

2.8
(029)
1.6
(016)

0.9
(06)
0.6
(03)

1.3
(014)
0.9
(07)

1.2
(08)
1.0
(05)

1274

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 171 2005
TABLE 2. SUMMARY STATISTICS FOR DAILY AIR POLLUTANT AND WEATHER DATA (19982001)
Auckland
Daily pollutant levels, mean (range)
24-h PM2.5, g m3
No. monitors
24-h PM10, g m3
No. monitors
24-h bsp, 104 m1
No. monitors
1-h NO2, ppb
24-h NO2, ppb
No. monitors
8-h CO, ppb
No. monitors
1-h SO2, ppb
24-h SO2, ppb
No. monitors
1-h O3, ppb
4-h O3, ppb
8-h O3, ppb
No. monitors
Weather, mean (range)
Temperature, C
Relative humidity, %

Brisbane

11.0*
9.7
(2.137.6) (3.2122.8)
1
1
18.8*
16.5
(3.2101.4) (3.850.2)
6
4

0.2
(01.7)
0
4
19.1
17.3
(4.286.3)
(444.1)
10.2
7.6
(1.728.9) (1.419.1)
2
7
2.1
1.7
(0.27.9)
(07)
3
1

7.6
(046.5)
4.3
1.8
(024.3)
(08.2)
1
2
23.9
31.5
(8.844.2)
(792.3)
22.9
28.9
(8.242.7) (5.475.2)
21.6
25.5
(7.440.1) (3.758.4)
2
7

Canberra Christchurch Melbourne

0
20.6
(1.3156.3)
2

0
0.3
(02.1)
1
17.9
(053.7)
7.0
(022.5)
1
0.9
(05.8)
1

0
23.7
(075.3)
22.1
(062.8)
19.5
(057.7)
1

15.7
20.0
13.7
(6.324.1) (9.530.4)
(128)
79.1
72.4
69.9
(52.1100) (29.396.3) (24.197)

Perth

Sydney

8.1
9.4
(1.729.3) (2.482.1)
2
3
16.5
16.6
(4.468.9) (3.7104.7)
1
11
0.2
0.3
(0.11.6)
(03.4)
5
9
21.3
22.6
(4.448)
(5.251.4)
9.0
11.5
(223.3)
(2.524.5)
5
13
1.0
0.8
(0.14)
(04.5)
3
4

3.7
(0.120.2)

0.9
(03.9)
0
0
6
23.8
33.6
31.7
(1.785.4)
(1385)
(3.2126.7)
21.8
31.3
28.9
(1.373.1) (10.672.8) (2.2105.1)
19.0
28.5
24.9
(0.863)
(864)
(1.486.8)
8
3
12

11.6
(027.2)
75.9
(3199)

15.3
18.2
17.8
(5.931.8) (8.232.3) (8.530.1)
68.7
67.8
70.6
(25.195.5) (2898.5) (26.397.1)

0
15.7
(1.254.6)
7.1
(0.224.5)
1
0.5
(05.4)
2
10.1
(0.142.1)
2.8
(011.9)
2

8.9
(2.843.3)
2
16.6
(3.171.1)
4
0.3
(03.6)
7
23.2
(4.462.5)
11.7
(229.5)
8
1.0
(0.18)
3

Definition of abbreviation: bsp an indicator of fine particles 0.12 m in diameter; PM2.5 particle matter less than 2.5 m
in diameter; PM10 particle matter less than 10 m in diameter.
* Tapered Element Oscillating Microbalance (TEOM) data were not available for Auckland in the study period. PM data in
Auckland were recorded once every 6 days (Hi-Vol); this was not suitable for the case-crossover analysis.

Australian cities and the two New Zealand cities are shown in
Table 5. The increases are quite different, but clearly not all of
the heterogeneity between the increases for all the cities is caused
by the difference in countries.
Multiple pollutant models showed that the results for NO2
were often independent of the effects of other pollutants, although some impacts caused by particles and SO2 could not be
separated from those found for NO2.
Differences by Season

To test whether any pollutant effects were dependent on season,

case-crossover analyses were separated into a (southern hemisphere) cool season of May to October, and a warm season of
November to April. The significant effects of pollutants were
analyzed separately for cool and warm seasons (Table 6), because some pollutants (e.g., O3) peak significantly in the warm
periods (because of the formation of photochemical smog) and
these smog impacts may affect the results. The increase in
respiratory admissions in the younger-than-1-year age group
associated with bsp (Australian cities only) was a cool-season
effect, indicating these results are not caused by summer smog
episodes. However, the increases in respiratory admissions in
the 1- to 4-year age group that were associated with PM2.5 and
PM10 were warm-season effects, and the increases in respiratory
admissions in the 5- to 14-year age group associated with NO2
were larger in the warm season.

Effect Modification

Where differences in impacts were found for different cities,

possible reasons for this were explored by examining whether
the effect estimates for each city were related to different city
characteristics. These reasons may include some cities having
more pollution than others, having a larger proportion of children younger than 15 years, or being hotter (or colder) than
others. A hierarchic model in which the increases in admissions
in each city were regressed against potential city-level effect
modifiers was used to incorporate variables that may differ between cities and therefore modify the results (effect modifiers).
The effect modifiers examined included the following: average
pollutant level, number of monitors, temperature, and percentage of the population younger than 15 years. Statistical significance was assessed using the estimate of the regression slope.
The only differences between the cities that could be related to
the different effect estimates were related to climate. The only
significant effect modification found was that cities with higher
average temperatures had greater increases in hospital respiratory admissions in the 1- to 4-year age group for increases in
1-hour NO2.

DISCUSSION
This study has shown statistically significant relationships between outdoor air pollution and child health in Australia and

Barnett, Williams, Schwartz, et al.: Air Pollution and Child Health

1275

TABLE 3. STATISTICALLY SIGNIFICANT INCREASES IN HOSPITAL ADMISSIONS IN CHILDREN

USING A META-ANALYSIS OF CASE-CROSSOVER ESTIMATES (URBAN AUSTRALIA
AND NEW ZEALAND, 19982001)
Children
Age Group (yr)

Cities

Pneumonia acute bronchitis

0
B, M, P, S
B, Ca, M, P, S
14
B, M, P, S
B, Ch, S
Respiratory admissions
0
B, M, P, S
B, Ca, M, P, S
B, Ch, S
14
B, M, P, S
B, Ch, M, P, S
B, Ca, M, P, S
A, B, Ca, Ch, M,
B, Ch, S
514
B, Ch, M, P, S
A, B, Ca, Ch, M,
A, B, Ca, Ch, M,
Asthma admissions
514
A, B, Ca, Ch, M,

Pollutant (units)

Increase %*
(95% CI)

I-squared
(% )

Range in
Increases (% )

24-h PM2.5 (g m3)

24-h bsp (104 m1)
24-h PM2.5 (g m3)
1-h SO2 (ppb)

1.7
2.1
2.4
6.9

(0.0,
(0.3,
(0.1,
(2.3,

3.4)
3.9)
4.7)
11.7)

0
0
16.3
0

1.1
1.8
0.9
5.6

(M), 2.3 (B)

(M), 2.2 (P, S)
(S), 3.3 (B)
(B), 8.5 (Ch)

P, S
P, S

24-h PM2.5 (g m3)

24-h bsp (104 m1)
1-h SO2 (ppb)
24-h PM2.5 (g m3)
24-h PM10 (g m3)
24-h bsp (104 m1)
1-h NO2 (ppb)
1-h SO2 (ppb)
24-h PM10 (g m3)
1-h NO2 (ppb)
24-h NO2 (ppb)

2.4
2.5
3.2
1.7
1.7
2.2
2.8
2.7
1.9
4.7
5.8

(1.0,
(1.1,
(0.3,
(0.7,
(0.5,
(1.2,
(0.7,
(0.6,
(0.1,
(1.6,
(1.7,

3.8)
4.0)
6.3)
2.7)
2.9)
3.2)
4.9)
4.8)
3.8)
7.9)
10.1)

0
0
0
0
0
0
46.9
0
0
52.0
54.0

2.0
2.2
3.0
1.3
1.4
1.9
2.1
1.9
1.4
3.8
4.5

(S), 2.8 (B)

(B, S), 3.2 (M)
(Ch), 3.6 (B)
(S), 2.1 (B)
(S), 2.3 (Ch)
(S), 2.4 (Ca)
(S), 3.5 (A)
(Ch), 3.2 (S)
(S), 2.5 (M)
(A), 5.5 (P)
(A), 6.9 (P)

P, S

24-h NO2 (ppb)

6.0 (0.2, 12.1)

61.9

4.3 (A), 7.7 (B)

P, S

Definition of abbreviations: A Auckland; B Brisbane; bsp an indicator of fine particles 0.12 m in diameter; Ca
Canberra; Ch Christchurch; CI confidence interval; M Melbourne; P Perth; PM2.5 particle matter less than 2.5 m
in diameter; PM10 particle matter less than 10 m in diameter; S Sydney.
* Percentage increase in admissions for an interquartile range increase in pollutant using the average over the current and
previous day.

I-squared is the percentage of total variation in the estimated increase that is due to heterogeneity between cities.

Minimum and maximum increases using a leave-one-city-out sensitivity analysis; the city in parentheses was the city left out.

New Zealand. Levels of air pollution in these two countries

are generally low compared with countries in Europe or North
America where similar associations have been found (1).
When studying the health effects of a hazardous exposure,
children are often considered as if they were small adults; however, children represent the largest subpopulation susceptible to
the adverse health effects of air pollution (25). Infants and children inhale and retain larger amounts of air pollution per unit
of body weight than adults; the air intake of a resting infant is
twice that of an adult. As children grow, their organ systems are
still developing, and their normal growth may be affected when
exposed to pollutants at critical periods (25). Children also spend
more time outdoors than adults, and concentrations of pollutants
of an ambient origin are higher outdoors than indoors. Children
playing outdoors also engage in exercise that increases ventilation. This is particularly true in afternoons, when photochemical
pollutant concentrations (O3 and particulate sulfate) are highest.
This study found an association with respiratory admissions in
the 1- to 4-year age group and 1-hour ozone exposure during
warm months.
We can only identify associations here, not causes, but other
studies have reviewed the air pollution effects on human respiratory diseases (2628). It has been suggested that NO2 effects
arise from the NO2 exposure, making people more susceptible
to respiratory viral infections that exacerbate asthma (27), and
that the direct effects of NO2 on health are less important than
its role as a precursor to the onset of photochemical smog leading
to the formation of ozone and secondary particles. SO2 effects
have been related to decreases in pulmonary function in controlled human exposure studies (28) but may also contribute to
acid sulfate aerosol formation (26, 28). Diesel exhaust particles
have been found to increase airway inflammation and exacerbate
asthma (28), and there have been a number of studies on the

inflammatory impacts of O3 on respiratory disease (28). The

emissions from motor vehicles increase the concentrations of
all the pollutants under study, making it difficult to separate the
differing impacts.
Pollutants Confounding Each Other

If a health outcome was significantly associated with more than

one pollutant, there was always the question as to whether one
pollutant effect is actually showing the impact of another with
which it is correlated. To examine whether some of the impacts
were interrelated, multipollutant models were run using a
matched case-crossover method, a traditional approach to control for potential confounding in epidemiology. By choosing
control days for each subject that are both nearby in time and
also matched on the level of another pollutant, the effect estimate
cannot be confounded by the other pollutant (21).
For respiratory admissions in the 5- to 14-year age group,
the significant association with PM10 disappeared after matching
on NO2, indicating that this result could not be separated from
that for NO2. However, the association with NO2 remained after
matching on PM10. Similar results were found in a southern
California study, which concluded that NO2 deserved greater
attention as a potential cause of the chronic symptoms of bronchitis in children with asthma (29). For respiratory admissions
in the 1- to 4-year age group, the effects of both PM10 and
PM2.5 (only four Australian cities involved) became larger when
matched with each other, indicating separate effects. Also, the
PM2.5 and SO2 impacts could not be separated and may indicate
pollution from the same emission source. None of the significant
associations found were confounded by temperature, because
associations matched to within 1C of temperature changed very
little when compared with the unmatched result. Hence, the
pollutant impacts are not related to temperature effects but are

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AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 171 2005
TABLE 4. MULTIPOLLUTANT MODELS: STATISTICALLY SIGNIFICANT INCREASES IN HOSPITAL
ADMISSIONS IN CHILDREN AND INCREASES AFTER MATCHING FOR OTHER EXPOSURES
(INCREASE IN EVENTS AND 95% CONFIDENCE INTERVALS)
Outcome
Pneumonia and bronchitis, 14 yr

Respiratory
0 yr

14 yr

514 yr

Single
Pollutant

Increase %*
(95% CI)

Matched
Exposure

24-h PM2.5

2.4 (0.1, 4.7)

1-h SO2

6.9 (2.3, 11.7)

1-h SO2
Temperature
24-h PM2.5
Temperature

24-h PM2.5

2.4 (1.0, 3.8)

1-h SO2

3.2 (0.3, 6.3)

24-h PM2.5

1.7 (0.7, 2.7)

24-h PM10

1.7 (0.5, 2.9)

1-h SO2

2.7 (0.6, 4.8)

1-h NO2

2.8 (0.7, 4.9)

24-h PM10

1.9 (0.1, 3.8)

24-h NO2

5.8 (1.7, 10.1)

1-h SO2
Temperature
24-h PM2.5
Temperature
24-h PM10
1-h SO2
1-h NO2
Temperature
24-h PM2.5
1-h SO2
1-h NO2
Temperature
24-h PM2.5
24-h PM10
1-h NO2
Temperature
24-h PM2.5
24-h PM10
1-h SO2
Temperature
24-h NO2
Temperature
24-h PM10
Temperature

Increase %*
(95% CI)
1.9
2.3
4.7
7.1

(1.7, 5.6)
(0.4, 5.1)
(1.4, 11.1)
(2.1, 12.5)

3.1 (0.5, 5.7)

1.8 (0.2, 3.4)
0.6 (3.4, 4.9)
3.2 (0.1, 6.5)
2.9 (0.2, 5.6)
1.3 (1.8, 4.4)
1.5 (3.2, 0.2)
1.5 (0.2, 3.1)
5.5 (0.2, 11.5)
3.2 (0.3, 6.1)
0.0 (2.1, 2.1)
2.3 (0.6, 3.9)
0.4 (3.2, 2.4)
3.8 (3.3, 11.5)
0.9 (8.4, 11.0))
2.8 (1.1, 6.9)
8.5 (0.7, 16.9)
0.7 (10.1, 12.7)
5.3 (2.6, 8.1)
2.3 (0.7, 5.4)
1.2 (1.8, 4.4)
3.6 (1.4, 5.8)
6.4 (3.0, 9.8)
6.5 (3.6, 9.5)

Cities Included in
Match
B,
B,
B,
B,

S
M, P, S
S
Ch, S

B, S
B, M, P, S
B, S
B, Ch, S
B, M, P, S
B, S
B, M, P, S
B, M, P, S
B, M, P, S
B, Ch, S
B, Ch, M, P,
B, Ch, M, P,
B, S
B, Ch, S
B, Ch, S
B, Ch, S
B, M, P, S
B, Ch, M, P,
B, Ch, S
All
B, Ch, M, P,
B, Ch, M, P,
B, Ch, M, P,
B, Ch, M, P,

S
S

S
S
S
S

Definition of abbreviations: B Brisbane; Ch Christchurch; CI confidence interval; M Melbourne; P Perth; PM2.5

particle matter less than 2.5 m in diameter; PM10 particle matter less than 10 m in diameter; S Sydney.
* Percentage increase in admissions for an interquartile range increase in pollutant using the average over the current and
previous day.

separate and different impacts. However, both of the associations

with PM10 increased by approximately 50% when matched on
temperature.
Heterogeneity and Comparison between Australian
and New Zealand Cities

The differences (heterogeneity) between cities for the significant

associations were low except for associations with NO2 (although

the number of cities involved for this pollutant was always larger
than the others). Figure 1 shows that the four largest Australian
cities (Brisbane, Melbourne, Perth, and Sydney) usually showed
different results to the New Zealand cities and Canberra (the
coldest Australian city). The only significant effect modification
found was that cities with higher average temperatures had
greater increases in hospital respiratory admissions in the 1- to
4-year age group for increases in 1-hour NO2. The average tem-

Figure 1. Selected statistically significant increases and 95% confidence intervals for hospital respiratory admissions in children, with city-specific
and meta-analysis estimates by age group. (A ) Age group 12 months: 24-hour average PM2.5 (average lag, 01); (B ) age group 14 years:
1-hour maximum NO2 (average lag, 01); and (C ) age group 514 years: 1-hour maximum NO2 (average lag, 01).

Barnett, Williams, Schwartz, et al.: Air Pollution and Child Health

1277

TABLE 5. INCREASES IN HOSPITAL ADMISSIONS IN CHILDREN: DIFFERENCES BETWEEN

META-ANALYSIS RESULTS IN AUSTRALIAN AND NEW ZEALAND CITIES

Age Group (yr)

Respiratory admissions
14
514
Asthma admissions
514

Pollutant

All Cities
Increase %*
(95% CI)

1-h NO2
1-h NO2
24-h NO2

2.8 (0.7, 4.9)

4.7 (1.6, 7.9)
5.8 (1.7, 10.1)

24-h NO2

6.0 (0.2, 12.1)

Australian Cities
Increase %*
(95% CI)

New Zealand Cities

I-squared
(% )

Increase %*
(95% CI)

I-squared
(% )

3.6 (1.5, 5.7)

4.0 (1.1, 7.1)
4.4 (1.4, 7.5)

42.2
46.2
32.6

0.7 (4.7, 3.4)

6.7 (5.3, 20.3)
12.7 (1.4, 25.3)

0.0
68.3
46.1

3.8 (1.3, 9.3)

62.9

18.4 (6.7, 31.4)

0.0

Definition of abbreviation: CI confidence interval.

* Percentage increase in admissions for an interquartile range increase in pollutant using the average over the current and
previous day.

I-squared is the percentage of total variation in the estimated increase that is due to heterogeneity between cities.

peratures of Christchurch and Canberra are lower than the other

cities (Table 2). Aucklands average temperature is slightly
higher than Melbournes, but its maximum is much lower. There
is evidence of seasonal impacts on asthma and respiratory admissions (5- to 14-year age group) for NO2; on respiratory admissions
(1- to 4-year age group) for PM2.5, PM10, and O3; and for pneumonia and acute bronchitis admissions (1- to 4-year age group) for
PM2.5 and SO2.
In examining the effects of pollution, it is important to be
able to identify the sources of pollutants. Most of the nitrogen
oxide pollution in Australian and New Zealand cities comes
from motor vehicle exhausts in summer and a combination of
motor vehicle exhausts and home heating in winter. Diurnal pat-

terns for NO2 show the morning peak-hour traffic times to be

particularly notable, especially on weekdays. Also, the NO2 levels
are generally much higher in winter, especially at night, and the
differences between summer and winter are much more marked
in the New Zealand cities than in most of the Australian cities.
A recent meta-analysis of three European studies of respiratory admissions in children aged 0 to 14 years reported a 1.0%
increase in admissions for a 10 g m3 increase in PM10 (95%
confidence interval, 0.2, 2.1%) (30). In this study, we found a
relationship between PM10 and respiratory admissions in the
5- to 14-year age group of 1.9% (95% confidence interval, 0.1,
3.8) for a 7.5 g m3 increase in PM10.
Unfortunately, not all pollutants were available in all cities.

TABLE 6. INCREASES IN HOSPITAL ADMISSIONS IN CHILDREN SPLIT BY COOL AND WARM

SEASONS USING A META-ANALYSIS OF CASE-CROSSOVER ESTIMATES (URBAN AUSTRALIA
AND NEW ZEALAND, 19982001)
Cool
Age Group (yr)
Pneumonia acute bronchitis
0
14
Respiratory admissions
0

14

514

Asthma admissions
514

Pollutant (units)
24-h PM2.5 (g m3)
24-h bsp (104 m1)
24-h PM2.5 (g m3)
1-h SO2 (ppb)
24-h PM2.5 (g m3)
24-h bsp (104 m1)
1-h SO2 (ppb)
24-h PM2.5 (g m3)
24-h PM10 (g m3)
24-h bsp (104 m1)
1-h NO2 (ppb)
1-h SO2 (ppb)
1-h O3 (ppb)*
24-h PM10 (g m3)
1-h NO2 (ppb)
24-h NO2 (ppb)
24-h NO2 (ppb)

Increase % (95% CI)

1.1
1.8
2.0
4.9

(0.7,
(0.1,
(0.4,
(0.6,

Warm
I-squared

3.0)
3.7)
4.5)
10.8)

0
0
7.1
0

1.8 (0.2, 3.4)

2.3 (0.5, 4.2)
3.3 (0.3, 7.0)
1.1 (0.1, 2.3)
0.6 (0.8, 2.1)
2.2 (0.9, 3.5)
2.7 (0.7, 4.8)
3.1 (0.3, 5.9)
3.4 (7.4, 0.8)
2.1 (0.2, 4.6)
5.7 (1.9, 14.0)
6.0 (0.7, 13.0)

0
14.0
0
0
0
0
0
0
55.2
0
73.7
66.0

7.0 (2.4, 17.3)

66.8

Increase % (95% CI)

2.2 (3.1, 7.8)
2.2 (7.7, 3.7)
3.3 (6.1, 13.6)
10.4 (2.1, 19.4)
2.8
0.7
2.6
3.0
3.1
1.6
3.4
2.8
3.5
1.9
8.6
9.6

(0.9, 6.7)
(3.0, 4.5)
(2.8, 8.2)
(0.8, 5.2)
(0.2, 6.0)
(0.5, 3.7)
(1.6, 8.6)
(4.4, 10.6)
(1.8, 5.2)
(2.4, 6.4)
(4.0, 13.3)
(3.3, 16.3)

10.2 (2.6, 18.4)

I-squared
0
0
58.4
0
0
0
0
0
27.5
0
68.3
72.4
9.7
51.1
39.8
37.6
49.2

Definition of abbreviations: bsp an indicator of fine particles 0.12 m in diameter; CI confidence interval; PM2.5 particle
matter less than 2.5 m in diameter; PM10 particle matter less than 10 m in diameter.
* Result not significant for overall (whole season) effect.

Cool May to October; Warm November to April.

Percentage increase in admissions for an interquartile range increase in pollutant using the average over the current and
previous day.

I-squared is the percentage of total variation in the estimated increase that is due to heterogeneity between cities.

1278

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 171 2005

This reduced the power for some comparisons, and means that
comparisons across pollutants are also (to a varying degree)
comparisons across cities.
Conclusions

This study has shown strong and consistent associations between

childrens hospital admissions and outdoor air pollutants in the
urban centers of Australia and New Zealand for NO2, particles,
and SO2. The largest association found in this study for all cities
was a 6.0% increase in asthma admissions in the 5- to 14-year
age group related to a 5.1-ppb increase in 24-hour NO2. These
impacts also appeared to be distinct from any temperature (warm
or cold) effects. NO2 effects were often the strongest and appeared to be generally independent of the impact of other pollutants. However, there were differences in the impacts between
cities with different climates (impacts were higher in the warmer
cities). There were also differing impacts in summer and winter
because of summer smog events.
Conflict of Interest Statement: A.G.B. does not have a financial relationship with
a commercial entity that has an interest in the subject of this manuscript; G.M.W.
does not have a financial relationship with a commercial entity that has an interest
in the subject of this manuscript; J.S. does not have a financial relationship with
a commercial entity that has an interest in the subject of this manuscript; A.H.N.
does not have a financial relationship with a commercial entity that has an interest
in the subject of this manuscript; T.L.B. does not have a financial relationship with
a commercial entity that has an interest in the subject of this manuscript; A.L.P.
does not have a financial relationship with a commercial entity that has an interest
in the subject of this manuscript; R.W.S. does not have a financial relationship
with a commercial entity that has an interest in the subject of this manuscript.
Acknowledgment : The authors acknowledge the contributions made to this project by Queensland Health, NSW Health, EPA Victoria, Western Australian Department of Environmental Protection, Environment ACT, New Zealand Ministry for
the Environment, Auckland Regional Council, Environment Canterbury, and the
project steering committee. Daily weather data were provided by the Australian
Bureau of Meteorology and the New Zealand National Climate Database. This
study used monitoring data provided by the relevant monitoring agency in each
city. The datasets have been used without extensive analysis or corrections beyond
the basic quality control needed to ensure data validity for the case-crossover
analysis. Some datasets have not been fully used (e.g., the PM10 data from Auckland), as they did not fully meet the strict requirements of the study, but they
are still regarded as valid datasets for the purposes for which they were gathered.

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