Clin Exp Allergy 2002; 32:1713±1719

Speci®c sensitization to common allergens and pulmonary function in the

European Community Respiratory Health Survey

A. JaeÂn*, J. Sunyer*, X. BasaganÄa*, S. Chinn{, J. P. Zock, J. M. AntoÂ*{ and P. Burney{, on behalf of the European
Community Respiratory Health Survey (ECRHS)
*Respiratory and Environmental Health Research Unit, Institut Municipal d'Investigacio MeÁdica (IMIM), Barcelona, Spain, {Department of Public Health
Sciences, King's College, London, UK and {Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain

Summary
Background The role of atopy in the evolution to chronic obstructive disease remains controversial.
Aim We aimed to assess the association between individual sensitization to common allergens and
lung function.
Method We analysed data from 12 687 subjects aged 20 to 44 years, from 34 centres in 15 countries
participating in the European Community Respiratory Health Survey (ECRHS). Participants
performed a blood test, lung function test, methacholine challenge, and answered an administered
questionnaire. The relationships between specific IgE, FEV1 and FEV1/FVC ratio were assessed for
each study centre stratified by sex, followed by random effects meta-analysis.
Results Asthmatics sensitized to house dust mite had a lower FEV1 ( 119 mL in women and
112 mL in men) and FEV1/FVC ratio ( 1.95%, and 2.48%) than asthmatics without sensitiza-
tion. Asthmatics sensitized to cat had a lower FEV1 (statistically significant for women only) and a
lower FEV1/FVC ratio. Asthmatic women sensitized to grass had a lower FEV1 and a lower ratio,
and those sensitized to Cladosporium had a lower FEV1. A weak association was found with
sensitization to cat and to Cladosporium among non-asthmatic women, which disappeared after
adjusting for BHR.
Conclusion We conclude that atopy was related to a lower lung function, which was only apparent
among asthmatics. This relationship was explained by specific sensitization to cat and to house dust
mite, the latter being homogeneous across areas.
Keywords airflow obstruction, allergens, asthma, ECRHS, lung function, sensitization
Submitted 25 April 2002; revised 15 July 2002; accepted 12 August 2002

Introduction remains controversial. A longitudinal study in young asthmat-

The role of atopy in the evolution of chronic irreversible air¯ow
obstruction remains uncertain, both in the development of
COPD in subjects without asthma, and in the natural history
of asthma. Among middle-aged and older non-asthmatic males,
the US Normative Ageing Study [1] found an association of
speci®c skin reactivity to common aeroallergens with an ele-
vated annual decline of FEV1 and FEV1/FVC ratio, which was
not found in a population of male smokers [2], nor in a popula-
tion of grain elevator workers [3]. Two studies strati®ed by
smoking, one in elderly people [4], the other in middle-aged
and older men [5], found an inverse association between atopy
(skin test) and levels of total immunoglobulin E (IgE) with
decline of FEV1 in smokers, but a third study found this associ-
ation in adults who had never smoked [6]. In asthmatics the role
of atopy in the evolution of chronic obstructive disease also
Correspondence: Angeles JaeÂn, Institut Municipal d'Investigacio MeÁdica
(IMIM), C/Doctor Aiguader 80, E-08003 Barcelona, Spain. E-mail:
ajaen@imim.es
ics found a smaller decline of FEV1 in subjects with atopy than
without atopy [7], while a cross-sectional study in asthmatic
children found that sensitization to indoor allergens was asso-
ciated with a reduction in FEV1 [8]. Few studies have assessed
the speci®c role of individual allergens, which may vary at
different locations. Recently, Sunyer et al. [9], using Spanish
data from the European Community Respiratory Health
Survey (ECRHS), demonstrated an association of sensitization
to individual allergens with the level of FEV1, independently of
asthma, or smoking. However, these results refer to the Spanish
population, and there is geographical variation in the preva-
lence of asthma, and sensitization to individual allergens. The
ECRHS is a cross-sectional study that provides extensive data
from various centres in different countries collected with a
common methodology, and the heterogeneity can be assessed.
With the aim of elucidating the role of atopy in the degree of
air¯ow obstruction, we analysed data from the ECRHS to
assess relationships of sensitization to individual allergens
with lung function, and the role of asthma and smoking as effect
modi®ers.

ß 2002 Blackwell Science Ltd 1713

1714 A. JaeÂn et al.

Methods Statistical analysis

Sampling The relation of baseline FEV1 and FEV1/FVC ratio to each

The European study protocol has been described elsewhere [10].
At least 1500 males and 1500 females, aged 20 to 44 years, in
each centre were randomly selected from the general popula-
tion. During stage I, subjects answered a short questionnaire
enquiring about respiratory symptoms. During stage II, a 20%
random sample, along with a `symptomatic' sample that in-
cluded those who reported asthma-type respiratory symptoms
in the short questionnaire in stage I but who had not been
selected in the random sample, were re-contacted and answered
a more detailed administered questionnaire and underwent
blood tests, skin tests, lung function and airway challenge with
methacholine. Only those subjects from the random sample
were included in this study. Participation rates have been
reported previously [11±13]. The institutional committees on
ethical practice of the participating centres approved the study
protocol, and subjects gave written informed consent.
Asthma de®nition
Those subjects that answered `yes' to one of these questions
were considered to have current asthma: Have you been woken
by an attack of shortness of breath at any time in the last
12 months? Have you had an attack of asthma in the
last 12 months? Are you currently taking any medicines, includ-
ing inhalers, aerosols or tablets, for asthma?
Spirometric measurements
speci®c IgE and to total IgE was estimated using linear regres-
sion for each centre, adjusted for age and height. The coef®-
cients were then tested for heterogeneity and combined across
centres using random effects meta-analysis [15]. The analysis
was strati®ed by sex due to the important gender difference in
baseline lung function. To assess effect modi®cation by asthma
of the association between atopy and lung function, an inter-
action term between asthma and each speci®c IgE was included.
Smoking and season were adjusted for in the multivariable
models. BHR was also included in further analyses. Total IgE
titre was logarithmically transformed (a one unit increase in
log10 total IgE is equivalent to a 10-fold increase in kU/L).
Results
Study population
Subjects from the random sample of 34 centres in 15 countries
with complete information on lung function and serum testing
for IgE were included (n ˆ 12 687 out of 17 259). Descriptive
values for lung function by centre [14] and IgE by country [15]
have been reported elsewhere. The highest prevalences of sensi-
tization were found for house dust mite (HDM) (20.2%) and
grass (19.8%), followed by cat (9.5%) and Cladosporium (6.2%)
(Table 1). The means of baseline FEV1 and FEV1/FVC ratio
were 3.24 L and 83.7% in women, and 4.37 L and 81.5% in men,
respectively.
Table 1. Description of participants by sex

Spirometric methods have been described in detail elsewhere Women Men

[11, 14]. Brie¯y, baseline FVC (forced vital capacity) and FEV1 (n ˆ 6257) (n ˆ 6430)
(maximal one-second forced expiratory volume) were measured
Age (years)
in all subjects who agreed to these tests. Subjects were permitted
20±29 33.8% 35.1%
nine attempts to provide at least two technically acceptable
30±39 45.7% 44.2%
manoeuvres. Quality controls were performed at different
40±44 20.4% 20.7%
levels. All ®eld-workers involved in the study received identical
training, a quality control visit was made by investigators of the Height (metres)* 1.64 (0.07) 1.77 (0.07)
FEV1 in litres* 3.24 (0.51) 4.37 (0.71)
ECRHS, and there were also equipment quality controls.
FVC in litres* 3.88 (0.59) 5.38 (0.85)
FEV1/FVC in percentage* 83.7 (6.77) 81.5 (7.10)
Methacholine challenge Speci®c IgE (titre > 0.35 kUA/L)
Methacholine challenge methods have been reported elsewhere House dust mite 16.8% 23.5%
[12]. Methacholine was delivered via a Mefar dosimeter (Mefar, Cat 9.3% 9.5%
Bobezzo, Italy), using two methods of challenge, a long and Timothy grass 17.3% 22.4%
short schedule of doses, with a maximum cumulative dose of Cladosporium 5.1% 5.9%
1 mg. Bronchial responsiveness (BHR) was de®ned as any sub- Total IgE{ 27.8 (26.7±28.9) 38.1 (36.7±39.6)
ject with a $ 20% fall in FEV1 with respect to the highest Season{
post-diluent FEV1 during the methacholine challenge with a Summer 51.3% 48.1%
maximum cumulative dose of 5.117 mmol of methacholine. Winter 48.7% 51.9%
Current asthma§ 9.6% 8.1%
Bronchial responsiveness{ 17.2% 10.5%
Total and speci®c immunoglobulin E
Smoking status
Serum total IgE and speci®c IgE to cat, house dust mite (Der- Current smokers 33.6% 38.9%
matophagoides pteronyssinius), Cladosporium and timothy Ex-smokers 21.2% 21.5%
grass were measured using the Pharmacia CAP system (Phar- Never smokers 45.2% 39.6%
macia, Uppsala, Sweden). The measurement range for total
IgE was 2 to 2000 kU/L, and for speci®c IgE 0.35 to *Mean (SD). {Geometric mean (CI 95%). {Season: summer was defined
from May to October in northern hemisphere and November to April in
100 kUA/L. Speci®c IgE results were regarded as positive if the southern hemisphere. §Reporting a nocturnal attack of shortness of
> 0.35 kUA/L. The ®fth locally chosen speci®c IgE [13] is not breath, an attack of asthma during last year, or taking medication for
reported on here. asthma during last year. {PD20 < 1.0 mg in methacholine challenge.

ß 2002 Blackwell Science Ltd, Clinical and Experimental Allergy, 32:17131719

 Atopy and lung function 1715

Association of FEV1 and FEV1/FVC with sensitization
The associations between FEV1 and FEV1/FVC with sensitiza-
tion to allergens are shown in Table 2. After adjusting for age,
height, smoking and season we found signi®cant inverse associ-
ations between lung function parameters and sensitization to
HDM and cat in both sexes, and Cladosporium in women.
Modi®cation of the association between FEV1 and
FEV1/FVC with sensitization by asthma and BHR
On including asthma and interactions between asthma and
speci®c allergens there were signi®cant differences between
non-asthmatics and asthmatics for the associations with
HDM in both sexes and with cat and grass in women. Among
non-asthmatics (Table 3) we observed a weak association in
women with sensitization to cat and Cladosporium. Asthma-
tic women with sensitization to allergens had a lower FEV1 than
those not sensitized, but in men the difference was statistically
signi®cant only for HDM. Asthmatics with sensitization to
common allergen had also a lower FEV1/FVC ratio (Table 4).
On including BHR in the models these differences decreased
considerably (Tables 3 and 4) and remained only for FEV1
among asthmatic women sensitized to cat (P < 0.05) and grass
(P ˆ 0.057). Also the marginal associations in non-asthmatic
women were no longer signi®cant. The relation of FEV1 with
log serum total IgE, which was negative and signi®cant, became
non-signi®cant after adjusting for BHR. The analyses were also
carried out adjusting for BHR de®ned as dose/response slope
[12], and the results did not vary.
Heterogeneity between centres in the association of lung
function with sensitization to allergens
There was heterogeneity across the study centres for the associ-
ations between sensitization to cat (Fig. 1) and to grass (Fig. 2),
and both FEV1 and FEV1/FVC ratio (Tables 3 and 4). On the
other hand, there was no heterogeneity for sensitization to

Table 2. Random effects meta-analysis by centre for each sensitization. *Differences in FEV1 and FEV1/FVC and 95% con®dence intervals, sensitized
and non-sensitized subjects

FEV1 (ml) FEV1/FVC (%)

Sensitization{ Women Men Women Men

House dust mite 53 65 0.34{ 0.69

( 80, 27) ( 97, 33) ( 0.89, 0.20) ( 1.07, ± 0.32)
Cat 119{ 92{ 1.51{ 1.20{
( 166, 72) ( 152, 33) ( 2.31, ± 0.71) ( 1.93, ± 0.46)
Grass 28{ 30 0.10{ 0.43{
( 63, 7) ( 62, 3) ( 0.62, 0.49) ( 0.91, 0.05)
Cladosporium 80 10 0.75 0.50
( 127, 34) ( 70, 51) ( 1.56, ± 0.07) ( 1.20, 0.20)
Log10 total IgE 32 50 0.29{ 0.40{
( 47, 18) ( 72, 29) ( 0.55, ± 0.03) ( 0.67, ± 0.13)

*Results from different models for each sensitization adjusted by age, height, smoking and season of testing. {Specific IgE > 0.35 kUA/L. {P for
heterogeneity between centres < 0.1.

Table 3. Random effects meta-analysis by centre for each sensitization (speci®c IgE > 0.35 kUA/L). Differences in FEV1 in ml and 95% con®dence
intervals, sensitized and non-sensitized subjects, for non-asthmatics and asthmatics

Differences for each sensitization* Differences* including BHR

Women Men Women Men

Non-asthmatics
House dust mite 21 ( 50, 7) 17 ( 51, 17) 19 ( 10, 48) 20 ( 15, 55)
Cat 52 ( 100, 5){ 19 ( 70, 31) 14 ( 60, 32) 13 ( 38, 65)
Grass ±7( 26, 41){ 3( 32, 37) 35 ( 3, 72){ 23 ( 10, 57)
Cladosporium 53 ( 102, 4) 7( 57, 72) 35 ( 86, 16) 51 ( 12, 114)
Total log10 IgE 12 ( 27, 3) 26 ( 49, 2) 6( 10, 21) 1( 24, 26){
Asthmatics
House dust mite 119 ( 195, 43){ 112 ( 195, 30){ 21 ( 88, 45) 21 ( 121, 80)
Cat 202 ( 295, 110){{ 93 ( 218, 31){ 76 ( 144, 8) 32 ( 66, 130)
Grass 97 ( 188, 6){{ 41 ( 172, 90){ 83 ( 168, 2){{ 18 ( 83, 118)
Cladosporium 135 ( 248, 23){ 98 ( 14, 210) 47 ( 144, 50) 173 (60, 285)
Total log10 IgE 102 ( 161, 42){{ 104 ( 181, 28) 18 ( 70, 33) 6 ( 81, 92){

*Results from different models for each sensitization, model including interaction of asthma with sensitization, adjusted for age, height, smoking and
season of testing. BHR ˆ bronchial responsiveness. {P < 0.1 for heterogeneity between centres. {P < 0.05 for differences in values for non-asthmatics
and asthmatics.

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1716 A. JaeÂn et al.

Table 4. Random effects meta-analysis by centre for each sensitization (speci®c IgE > 0.35 kUA/L). Differences in FEV1/FVC ratio in percentage and 95%
con®dence intervals, sensitized and non-sensitized subjects, for non-asthmatics and asthmatics

Differences for each sensitization* Differences* including BHR

Women Men Women Men

Non-asthmatics
House dust mite 0.31 ( 0.23, 0.84){ 0.06 ( 0.49, 0.37) 0.90 (0.39, 1.40) 0.48 (0.07, 0.88)
Cat 0.21 ( 0.94, 0.53){ 0.00 ( 0.59, 0.59) 0.51 ( 0.21, 1.22){ 0.52 ( 0.05, 1.09)
Grass 0.63 (0.18, 1.08) 0.03 ( 0.42, 0.47) 0.89 (0.47, 1.32) 0.32 ( 0.08, 0.73)
Cladosporium 0.32 ( 1.06, 0.4) 0.06 ( 0.68, 0.81) 0.36 ( 0.38, 1.11) 0.58 ( 0.15, 1.30)
Total log10 IgE 0.17 ( 0.06, 0.40) 0.11 ( 0.35, 0.14) 0.41 (0.17, 0.64) 0.27 (0.04, 0.50)
Asthmatics
House dust mite 1.95 ( 3.32, ± 0.55){{ 2.48 ( 3.74, 1.22){ 0.32 ( 1.57, 0.93){ 35 ( 1.71, 1.01){
Cat 3.17 ( 4.57, 1.77){{ 3.45 ( 5.58, 1.32){{ 0.60 ( 1.65, 0.45) 0.80 ( 2.20, 0.60){
Grass 1.61 ( 3.31, ± 0.13){{ 1.53 ( 3.17, 0.11){ 0.41 ( 1.64, 0.83){{ 0.32 ( 1.58, 0.94)
Cladosporium 0.59 ( 2.40, 1.21){ 0.23 ( 1.97, 1.52){ 0.35 ( 1.14, 1.85) 0.36 ( 1.10, 1.81)
Total log10 IgE 2.13 ( 3.00, 1.25){{ 1.49 ( 2.70, ± 0.28){{ 0.38 ( 1.25, 0.48) 0.02 ( 1.00, 0.96)

*Results from different models for each sensitization, model including interaction of asthma with sensitization, adjusted for age, height, smoking and
season of testing. BHR ˆ bronchial responsiveness. {P < 0.1 for heterogeneity between centres. {P < 0.05 for differences in values for non-asthmatics
and asthmatics.

IgE Cat − asthmatic women

ALBACETE (1%)
OVIEDO (4%)
HUELVA (5%)
DUBLIN (5%)
GALDAKAO (5%)
GRENOBLE (6%)
BERGEN (6%)
VERONA (7%)
BERGEN_UP_ZOOM (7%)
PAVIA (7%)
WELLINTONG (7%)
HAWKES_BAY (7%)
IPSWICH (7%)
REYKJAVIK (8%)
ANTWERP_S (8%)
MONTPELLIER (8%)
PARIS (8%)
TURIN (8%)
GELEEN (8%)
ANTWERP_C (9%)
BORDEAUX (9%)
PORTLAND (9%)
GRONINGEN (10%)
MELBOURNE (11%)
ERFURT (11%)
NORWICH (11%)
HAMBURG (12%)
BASEL (12%)
GOTEBORG (13%)
CHRISTCHURCH (13%)
CAMBRIDGE (14%)
UPPSALA (15%)
UMEA (17%)
BARCELONA (20%)

Combined

−1.5 −1 −0.5 0 0.5 1

Differences in FEV1 (litres)
Fig. 1. Mean difference in FEV1 (litres), sensitized and non-sensitized asthmatic women with sensitization (speci®c IgE titre > 0.35 kUA/L) to cat by
centre (ranked from low to high prevalence of sensitization to cat). The area of each square is proportional to the reciprocal of the variance of the
estimate for the centre. - - - ˆ combined random effects estimate;  ˆ width of its 95% con®dence interval.

ß 2002 Blackwell Science Ltd, Clinical and Experimental Allergy, 32:17131719

 Atopy and lung function 1717

IgE Grass − asthmatic women

OVIEDO (9%)
ALBACETE (11%)
GALDAKAO (12%)
PARIS (12%)
REYKJAVIK (12%)
PAVIA (13%)
BARCELONA (14%)
ANTWERP_C (15%)
BERGEN (16%)
MONTPELLIER (16%)
DUBLIN (16%)
ANTWERP_S (17%)
GRENOBLE (17%)
GRONINGEN (18%)
GOTEBORG (18%)
VERONA (19%)
UPPSALA (19%)
BORDEAUX (20%)
UMEA (20%)
ERFURT (20%)
BERGEN_UP_ZOOM (20%)
HUELVA (20%)
TURIN (21%)
WELLINTONG (23%)
IPSWICH (23%)
GELEEN (24%)
HAWKES_BAY (25%)
NORWICH (25%)
HAMBURG (26%)
CAMBRIDGE (27%)
MELBOURNE )(29%)
CHRISTCHURCH (33%)
BASEL (33%)
PORTLAND (33%)

Combined

−1.5 −1 −0.5 0 0.5 1

Differences in FEV1 (litres)

Fig. 2. Mean difference in FEV1 (litres), sensitized and non-sensitized asthmatic women with sensitization (speci®c IgE titre > 0.35 kUA/L) to grass
(including BHR in the model) by centre (ranked from low to high prevalence of sensitization to grass). The area of each square is proportional to the
reciprocal of the variance of the estimate for the centre. - - - ˆ combined random effects estimate;  ˆ width of its 95% con®dence interval.

house dust mite, except in asthmatic women for the association
with the FEV1/FVC ratio. Heterogeneity between the centres
disappeared after controlling for BHR, except for grass in
women (Fig. 2).
Discussion
This is the ®rst multicentre study to evaluate the association
between sensitization to speci®c common allergens and lung
function, using the same methodology with standardized and
centralized measurement of IgE, and systematic measurement
of lung function. In general, a lower FEV1 and FEV1/FVC ratio
was found among asthmatics sensitized to house dust mite, cat
and grass in both sexes, although differences for cat and grass
were more pronounced among women. In addition, asthmatic
women with sensitization to Cladosporium had a lower FEV1.
These associations decreased after adjusting for BHR, and only
remained signi®cant for FEV1 among women with sensitization
to cat and grass. The associations varied between the centres,
with greater heterogeneity for cat and grass in both sexes, and
less heterogeneity for dust. However, on adjusting for BHR the
heterogeneity only persisted in women sensitized to grass.
Among non-asthmatic women there was a weaker association
between sensitization to allergens and FEV1 that disappeared
on adjusting for BHR. Overall, we found a consistent associ-
ation between sensitization to house dust mite (homogeneous
across centres) and sensitization to cat (heterogeneous), and
lung function among asthmatics. On the other hand, we only
found an effect of sensitization to grass and to Cladosporium
among asthmatic women.
Several studies have shown an association between exposure
and sensitization of allergens with prevalence and acute exacer-
bations of asthma [16, 17]. We found a lower level of FEV1 and
FEV1/FVC ratio in sensitized asthmatics, which could indicate
a role of allergens in the evolution of lung function impairment.
However, our study is cross-sectional. We do not know if there
is a temporary fall in the level of FEV1, or whether the lower
level of FEV1 is a chronic process. Age of asthma onset and age
of sensitization onset could in¯uence lung function impairment
and explain the different results between studies within different
age cohorts [7, 8]. Lange et al. [18] found a greater decline in
FEV1 in asthmatics, while Grif®th et al. [19] found a lower level
of FEV1 in older asthmatics but not a steeper decline. Despite
the cross-sectional limitation our results come from a general
population, while studies limited to asthmatics may be in¯u-
enced by several factors such as patient selection, treatment or
social class, although our results did not vary after accounting
for steroid treatment or educational level. The mechanisms by
which allergens affect lung function are not clear. The allergens
provoke acute episodes of asthma through in¯ammatory pro-
cesses and bronchial responsiveness that could develop into
chronic air¯ow obstruction independently of smoking or ster-
oid treatment [20]. We found that sensitized asthmatics had

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1718 A. JaeÂn et al.
signi®cantly more asthma attacks, longer duration of asthma
and a higher prevalence of steroid treatment and bronchial
responsiveness than non-sensitized asthmatics (data not
shown), and this could be the pathway from allergen sensitiza-
tion to pulmonary impairment.
Previous studies have associated allergen exposure [21] and
allergen sensitization [22, 23] with asthma severity. On the other
hand, it is dif®cult to interpret in asthmatics the reduction of
associations between allergen sensitization and lower FEV1 and
FEV1/FVC ratio after adjusting for BHR. The cross-sectional
design of this study made it dif®cult to study causal mechanisms
properly. BHR may therefore play an intermediate role or a
confounding role in the association between atopy and lung
function. If BHR is an intermediate step (atopy is associated
with impairment of lung function through bronchial respon-
siveness in the causal pathway), the regression models are over-
adjusted and the most valid results are those from the models
without including BHR. Also, it is possible that our estimates of
the effect of allergens after controlling for BHR were biased if
bronchial responsiveness was an effect rather than a cause of the
low FEV1 [24]. However, independently of BHR, sensitization
has a residual effect on lung function in asthmatic women.
Gottlieb et al. [1] suggested an hypothesis of sensitization to
allergens through in¯ammatory processes leading to air¯ow
obstruction, and this in¯ammatory process could be related to
mast cell degranulation and emphysema.
We have found that in asthmatics of age 20 to 44 years sensi-
tization to common allergens has a greater effect than smoking
in impairment of lung function, and no signi®cant interaction
with smoking was found (data not shown). Moreover, we found
more pronounced associations between speci®c sensitization to
allergens (except HDM) and FEV1 in women, but we did not
®nd these differences for the FEV1/FVC ratio. These results can
not be explained by differences in smoking between sexes. Other
studies have also found a stronger effect in females [8, 9]. Also,
we have observed an important role of cat allergy in obstructive
disease, apart from the effect on lung function of HDM previ-
ously reported [8, 25]. The lack of association between speci®c
sensitization and lung function for men could be due to insuf®-
cient statistical power, or perhaps due to a differential selection
bias in our men and women. However, sensitivity studies in
ECRHS have found minimal differences after adjustment for
non-participation, in the prevalence of bronchial responsive-
ness [12], sensitization to allergens and distribution of total IgE,
even when the participation rates were less than 25% [13]. In
addition, it is very unlikely that these differences of participa-
tion by sex or age can truly have an in¯uence on the association
between lung function and sensitization to allergens, as subjects
were selected from the population independently of their atopic
status, and both measurements, IgE and lung function, were
objective.
We observed different effects for different speci®c allergens
and for different study centres. This has also been observed
between BHR and allergy [15]. On the other hand, it is import-
ant to emphasize that the association between lung function and
sensitization to dust is homogeneous between centres. The pre-
sent study can not explain the heterogeneity for the observed
associations. Centres with a higher prevalence of speci®c sensi-
tization did not show a greater association with lung function.
The mechanism for this heterogeneity could be related to the
immunogenicity of the speci®c allergens, but also to differences
ß 2002 Blackwell Science Ltd, Clinical and Experimental Allergy, 32:17131719
in the environmental concentration and exposure characteris-
tics by allergen. The important heterogeneity between centres
that we found for sensitization to cat could be due to differences
in community prevalence of cat ownership or differences in cat
keeping. In ECRHS [26] there was an increased risk of cat
sensitization in cat owners who did not have symptoms when
exposed to pets and allowed cats to be indoors. The community
prevalence of cat ownership was also positively correlated with
the prevalence of respiratory symptoms in the presence of pets,
asthma and asthma medication.
In contrast to other studies [1, 9], we did not ®nd a signi®cant
association after adjusting for BHR among non-asthmatics,
perhaps due to the young age in our study and heterogeneity
between countries.
We conclude that sensitization to common allergens is related
to lung function impairment. This relationship was only appar-
ent among asthmatics, and was dependent on the speci®c aller-
gen. A consistent effect was found for sensitization to house
dust mite, being homogeneous across areas, and sensitization to
cat, being heterogeneous across areas. Sensitization to grass and
to Cladosporium was less consistently related to lung function.
Acknowledgements
Co-ordination of the ECRHS. Department of Public Health
Sciences, King's College, London, UK: P. Burney, S. Chinn,
C. Luczynska, D. Jarvis, J. Potts.
Participating centres providing information. Australia:
M. Abramson, J. Kutin (Melbourne). Belgium: P. Vermeire,
F. van Bastelaer (Antwerp South, Antwerp Central). Germany:
H. Magnussen, D. Nowak (Hamburg); H.E. Wichmann,
J. Heinrich (Erfurt). Iceland: T. Gislason D. Gislason (Reykja-
vik). Ireland: J. Prichard, S. Allwright, D. MacLeod (Dublin).
Italy: M. Bugiani, C. Bucca, C. Romano (Turin), R. de Marco
lo Cascio, C. Campello (Verona), A. Marinoni, I. Cerveri,
L. Casali, L. Perfetti (Pavia). the Netherlands: B. Rijcken, J.P.
Schouten, M. Kerkhof, H.M. Boezen (Groningen, Bergen op
Zoom, Geleen). New Zealand: J. Crane, S. Lewis, N. Pearce
(Wellington, Christchurch, Hawkes Bay). Norway: A. Gulsvik,
E. Omenaas (Bergen). Spain: J.M. AntoÂ, J. Sunyer, J. Soriano,
M. Kogevinas, A. TobõÂas, J. Roca (Barcelona),
N. Muniozguren, J. Ramos GonzaÂlez, A. Capelastegui (Galda-
kao), J. MartõÂnez-Moratalla, E. Almar (Albacete)
J. Maldonado PeÂrez, A. Pereira, J. SaÂnchez (Huelva),
J. QuiroÂs, I. Huerta (Oviedo). Sweden: G. Boman, C. Janson,
E. BjoÈrnsson (Uppsala), L. Rosenhall, E. Norrman
B. LundbaÈck (Umea), N. Lindholm, P. Plaschke, K. ToreÂn
(GoÈteborg). Switzerland: N. KuÈnzli (Basel). United Kingdom:
R. Hall (Ipswich), B. Harrison (Norwich), J. Stark (Cam-
bridge). USA: S. Buist, W. Vollmer, M. Osborne (Portland).
Grants. The European Commission supported the co-
ordination of this work. The following grants helped to fund
the local studies: Australia: Allen and Hanbury's. Belgium:
Belgian Science Policy Of®ce, National Fund for Scienti®c
Research. Germany: GSF, and the Bundesminister fuÈr For-
schung und Technologie, Bonn. Italy: Ministero dell'Universita
e della Ricerca Scienti®ca e Tecnologica, CNR, Regione Veneto
grant RSF n. 381/05.93. The Netherlands: Ministry of Welfare,
Public Health and Culture. New Zealand: Asthma Foundation
of New Zealand, Lotteries Grant Board, Health Research

Council of New Zealand. Norway: Norwegian Research Coun-
cil project no. 101422/310. Spain: Ministerio Sanidad y Con-
sumo FIS grants #91/0016060/00E-05E, #92/0319, #93/0393,
CIRIT 1999SGR00241, Hospital General de Albacete, Hos-
pital General Juan RamoÂn JimeÂnez, Consejeria de Sanidad
Principado de Asturias. Sweden: The Swedish Medical Re-
search Council, the Swedish Heart Lung Foundation, The
Swedish Association against Asthma and Allergy. Switzerland:
Swiss National Science Foundation grant 4026±28099. United
Kingdom: National Asthma Campaign, British Lung Founda-
tion, Department of Health, South Thames Regional Health
Authority. USA: United States Department of Health,
Education and Welfare Public Health Service Grant #2 S07
RR05521-28.
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