Seminar

Burden and clinical features of chronic obstructive

pulmonary disease (COPD) Lancet 2004; 364: 613–20
See Comment page 564
Romain A Pauwels, Klaus F Rabe Department of Respiratory
Diseases, Ghent University
Hospital, Ghent, Belgium
Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality and represents
(Prof R Pauwels MD); and
a substantial economic and social burden throughout the world. It is the fifth leading cause of death worldwide and Department of Pulmonology,
further increases in its prevalence and mortality are expected in the coming decades. The substantial morbidity Leiden University Medical
associated with COPD is often underestimated by health-care providers and patients; likewise, COPD is frequently Center, Leiden, Netherlands
(Prof K Rabe MD)
underdiagnosed and undertreated. COPD develops earlier in life than is usually believed. Tobacco smoking is by far
the major risk for COPD and the prevalence of the disease in different countries is related to rates of smoking and Correspondence to: Professor
Romain Pauwels, Department of
time of introduction of cigarette smoking. Contribution of occupational risk factors is quite small, but may vary Respiratory Diseases, Ghent
depending on a country’s level of economic development. Severe deficiency for alpha-1-antitrypsin is rare and the University Hospital, B9000
impact of other genetic factors on the prevalence of COPD has not been established. COPD should be considered in Ghent, Belgium
any patient presenting with cough, sputum production, or dyspnoea, especially if an exposure to risk factors for the [email protected]

disease has been present. Clinical diagnosis needs to be confirmed by standardised spirometric tests in the presence
of not-fully-reversible airflow limitation. COPD is generally a progressive disease. Continued exposure to noxious
agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations. Smoking
cessation is the only intervention shown to slow the decline. If exposure is stopped, the disease may still progress
due to the decline in lung function that normally occurs with aging, and some persistence of the inflammatory
response.

Chronic obstructive pulmonary disease (COPD) is a progressive and associated with an abnormal
major cause of chronic morbidity and mortality inflammatory response of the lungs to noxious particles
worldwide. The 2002 WHO World Health Report1 listed or gases.”3
COPD as the fifth leading cause of death in the world Chronic bronchitis and emphysema are related terms
(table 1), and further increases in its prevalence and but they describe different conditions. Chronic
mortality are expected in the coming decades.2 In 2001, bronchitis, or the presence of cough and sputum
the Global Initiative for Chronic Obstructive Lung production for at least 3 months in each of 2 consecutive
Disease (GOLD) issued and now updates yearly years, remains a clinical and epidemiologically useful
guidelines3 that aim to improve prevention and term. However, not all patients with chronic bronchitis
management of COPD through a concerted worldwide have or will develop chronic airflow limitation.4 The
effort and to encourage renewed research interest in this presence of chronic mucus hypersecretion in patients
highly prevalent disease. with COPD is, however, associated with an excess
decline in lung function and an increased rate of
Definition hospitalisation and death from COPD.5
For years, clinicians, physiologists, pathologists, and Emphysema—ie, destruction of the gas-exchanging
epidemiologists have struggled with the definitions of surfaces of the lung (alveoli)—is a common pathological
disorders associated with chronic airflow limitation. The term. Although radiological techniques such as CT
definition of COPD as given by GOLD is now rapidly scanning and measurements of lung density have
gaining general acceptance: “COPD is a disease state improved, they do not fully capture the structural
characterized by airflow limitation that is not fully abnormalities that underlie airflow limitation in
reversible. The airflow limitation is usually both COPD—ie, respiratory bronchiolitis and parenchymal
destruction.
Number of deaths

Ischaemic heart disease 7 181 000

Search strategy
Cerebrovascular disease 5 454 000
Lower respiratory tract infections 3 871 000 The material covered in this review is based on an extensive
HIV/AIDS 2 866 000
COPD 2 672 000
literature search and participation in expert meetings during
Perinatal conditions 2 504 000 the writing and updating of the GOLD guidelines, and on
Diarrhoeal disease 2 001 000 many years of research in the subject. We did a systematic
Tuberculosis 1 644 000 MEDLINE search for articles in English or with English
Trachea/bronchus/lung cancer 1 213 000
Road traffic accidents 1 194 000
abstracts with keywords COPD, prevalence, morbidity,
burden, cost, pollution, occupation, genetic, and severity, up
Total population 6 122 210 000.1
to June, 2004.
Table 1: Ten most frequent causes of death in the world in 2001

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 Seminar

Asthma is another major cause of chronic airflow

limitation, but its pathogenesis and pathology are clearly 450 Diagnosed with COPD
different from those of COPD.6 Airflow limitation in 400 Airflow limitation

asthma is usually reversible either spontaneously or 350

(per 1000 of population)

after treatment. Long-standing asthma can, however, 300
lead to airflow limitation that is not fully reversible.7 A 250
history of asthma and a higher reversibility of the airflow 200
limitation to an inhaled 2 agonist are helpful to 150
clinically differentiate the two diseases. A clinical overlap 100
between asthma and COPD will obviously occur in 50
asthmatic patients who smoke. Other pulmonary 0
25–44 45–54 55–64 65–74 75
diseases such as cystic fibrosis, sarcoidosis, and
Age (years)
interstitial lung diseases, can also cause chronic airflow
limitation, but COPD can usually be differentiated from
Figure 2: Prevalence of airflow limitation and diagnosis of COPD in the USA
these diseases on the basis of the clinical picture and
Data from reference 10.
radiological findings.

Prevalence administration of a bronchodilator (postbronchodilator

COPD prevalence and morbidity data probably greatly FEV1 is measured after the inhalation of a short-acting
underestimate the true burden of the disease, because it is bronchodilator).
not usually recognised until it is clinically apparent and An important issue in defining airflow limitation
moderately advanced. Studies of COPD prevalence have spirometrically is whether to use an age-dependent
used self-reported respiratory symptoms, physician FEV1/FVC ratio, since the limits of a normal FEV1/FVC
diagnosis of COPD, or the presence of airflow limitation ratio decrease with age. Some investigators use an age-
as criteria. Use of self-reported symptoms will include dependent definition whereas others use a cutoff value
people with chronic bronchitis but without airflow of 0·7 for all age groups. There are no data on whether
limitation. the decrease in FEV1/FVC ratio with age might be the
More recent epidemiological surveys have used result of subclinical airflow limitation caused by the
spirometric tests and the presence of airflow limitation lifetime exposure to air pollution.8
as an accurate estimate of the true burden of COPD. The A population survey9 of men and women in Spain aged
use of different cutpoints to define airflow limitation 40–69 years showed that, with an age-dependent and
makes comparison of results between studies rather postbronchodilator definition, spirometrically confirmed
difficult. Airflow limitation is usually defined as a COPD was present in 9·1 % of the population, 15% of
decreased ratio of forced expiratory volume in 1 s (FEV1) smokers, 12·8% of ex-smokers and 4·1% in non-
over forced vital capacity (FVC) (figure 1). Not-fully- smokers. Prevalence was 14·3% in men and 3·9% in
reversible airflow limitation is characterised by an FEV1 women. 78·2% of people identified with the disease had
and an FEV1/FVC ratio that is still decreased after not been previously diagnosed. Only 49·3% of patients
with severe COPD, 11·8 % of patients with moderate
6
COPD, and 10% of patients with mild COPD were
receiving treatment for the disease.
5 A large US survey on COPD10 reported that during
Normal
2000, an estimated 10 million adults in the USA
4 FEV1 reported physician-diagnosed COPD, but that about
COPD 24 million adults had evidence of airflow limitation,
FVC (L)

3
again indicating that COPD is largely underdiagnosed
(figure 2). The prevalence of moderate obstructive lung
FEV1 disease (FEV1/FVC <0·7 and FEV1< 80% predicted) was
2
FEV1 FVC
7·2 % in the 45–54 years age-group, 14% between age 55
FEV1/FVC
Normal 4·150 5·200
and 64 years, 20·7 % at age 65–74 years, and 22·9 % at
1 0·8
COPD 2·350 3·900 0·6
age 75 years and older. A study in the northern part of
Sweden11 also reported a prevalence of chronic airflow
0 limitation (FEV1/FVC <0·7 and FEV1 <80% predicted) of
0 1 2 3 4 5 6 7
14% above age 45 years and 50% in elderly smokers.
Time (s)
These three studies, which use an objective
Figure 1: Spirograms showing postbronchodilator FVC in a patient with
measurement of airflow limitation, show the high
COPD and a person without COPD prevalence of COPD and the frequent underdiagnosis
Reproduced with permission from WHO.1 and undertreatment.

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 Seminar

The European Community Respiratory Health with an early stage of COPD visit their doctor more
Survey12 of more than 18 000 young adults (age often, use more medications, attend the emergency
20–44 years) reported that, after exclusion of patients department more often, and are more frequently
with asthma, 11·8% had chronic respiratory symptoms admitted for respiratory difficulties.12
of cough, sputum, or dyspnoea, and 3·6% had airflow In the USA, the death rate from COPD was 67 per
limitation. These data suggest that COPD develops at an 100 000 in 2000, compared with 44 per 100 000 in the
earlier age than is usually believed. rest of the world. The annual COPD death rate has been
COPD has a substantial morbidity that is increasing in the USA in the past 20 years,10 in contrast
underestimated by health-care providers and by patients. with a decreasing mortality for other major chronic
In an international survey,13 patients with COPD diseases (figure 3).17
seriously underestimated their morbidity, as shown by
the high proportion of people whose basic daily life Economic burden
activities were limited by the disease, frequent absence Because of the high prevalence of the disease and the
from work (45% of COPD patients younger than potential for severe disability, COPD represents a
65 years reported absence from work in the past year), substantial economic and social burden. It is, therefore,
and frequent use of health care. surprising how little information is available on the
COPD also has a major effect on health status,14 with direct and indirect costs resulting from morbidity and
poor status being quite strongly associated with premature death from COPD.
impaired exercise performance and functional capacity. Some countries have attempted to assess the economic
The presence of daily symptoms and a high exacerbation burden of COPD, separating costs directly and indirectly
frequency are other important factors. Anxiety and attributable to the disease. Data from developing
depression are quite common in patients with COPD countries are not yet available, but data from the USA
and contribute to their poor health status. Elderly and some European countries show the enormous
patients with COPD show a substantial impairment in economic and social burden of COPD for these societies
health status depending on the severity of airway and their respective insurance payers.
obstruction; symptoms related to the disease may be For Sweden, the direct cost of COPD-related medical
exaggerated by mood deflection.15 care was estimated at about $US180 million in 1991.18
COPD accounts for many visits to health-care workers. The estimated indirect cost of COPD amounted to an
In the UK, general practice consultations for COPD in additional $281 million. The direct cost of COPD in the
1 year ranged from 4·17 per 1000 in people aged Netherlands was estimated to exceed $256 million—or
45–64 years, to 8·86 per 1000 in 65–74-year-olds and to $813 per patient per year. Although medications
10·32 per 1000 in 75–84-year-olds.16 These rates are two- contribute to 23% of these costs, admissions consume
to-four times those for chest pain caused by ischaemic more than 50% of the total budget. Mathematical
heart disease. In the USA, in 2000, COPD resulted in projections suggest that the direct costs of COPD in the
8 million visits to doctors and hospital outpatient Netherlands will rise to $410 million by 2010.
departments (45 per 1000 head of population), Similar data exist from NHS surveys in the UK where
1·5 million emergency department visits (8·7 per 1000), the direct cost of COPD was estimated to be about
and 726 000 admissions (4·1 per 1000).10 Young adults $1·4 billion or roughly $1900 per person per year.19 The
indirect cost of the disease including disability, work
3·0 absence, and reduced productivity amounted to more
than $3·0 billion,16 representing about 24 million days of
+163% COPD
2·5 work lost.
Data from the USA have estimated the total annual
economic burden of COPD at $23·9 billion in that
Proportion of 1965 rate

2·0
country.20 From these total costs, $14·7 billion were
attributable to direct expenditures for medical care
1·5
services, and the remaining $9·2 billion were related to
indirect morbidity and premature death. The total
1·0 –7% all other causes number of COPD cases in the USA is thought to be
–35% other
cardiovascular disease
around 15 million,21 so that the estimated direct cost of
0·5 –59% coronary heart disease COPD amounts to about $1500 per COPD patient per
–64% stroke year.
0 Data from a US national medical expenditure survey22
1965 1998 show that admission costs for COPD patients, based on
1987 estimates, are $5409 per admission—2·7 times the
Figure 3: Change in age-adjusted death rates for cardiovascular and
pulmonary diseases in the USA 1965–98 expenditures for patients without COPD. Data from
Adapted from reference 3. 1992, have shown that the annual health insurance costs

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 Seminar

Noxious agent WHO region 1990 prevalence (per 1000) (men/women)

(tobacco smoke, pollutant, occupational agent) Established market economies 7·0/3·8
Former socialist economies Europe 7·3/3·4
● Genetic factors
● Respiratory India 4·4/3·4
infection China 2·6/2·4
● Other*
Other Asia and islands 2·9/1·8
Sub-saharan Africa 4·4/2·5
COPD Latin America 3·4/2·7
Middle east crescent 2·7/2·8
Figure 4: Interaction between risk factors in the pathogenesis of COPD Data from reference 30.
*Includes airway hyperresponsiveness, lung growth, and socioeonomic status.
Adapted from reference 1. Table 2: Worldwide COPD prevalence

for patients older than 65 years with COPD were symptoms in adults.25 However, the effects of
$8482—2·5 times the amount for people without the environmental tobacco smoke on lung function are
disease.21 small and probably have limited clinical relevance for the
Estimates of the economic burden of COPD are likely development of COPD.
to be underestimations since society does not, for
example, acknowledge the economic value of the care Air pollution
provided by family members. Long-term home care An important risk factor for the development of COPD
provided by relatives for patients with severe COPD worldwide is exposure to indoor air pollution caused by
frequently has a detrimental effect on professional heating and cooking with biomass fuel in poorly
careers, not only for patients, but also for other family ventilated dwellings, leading to high levels of particulate
members. Taken together, COPD represents a major matter indoors.26–29 That women are usually more
global threat to economies and more studies into the exposed to this risk factor might explain why the
true effects of this disease are needed, in both developed prevalence of COPD in women is almost the same as
and less-developed countries. that for men in countries such as India, China, Latin
America, and the middle east, despite a clear difference
Risk factors between the sexes with respect to cigarette smoking
Most evidence about exogenous risk factors for COPD (table 2).30
comes from cross-sectional epidemiological studies that The role outdoor air pollution has in COPD is unclear,
identify associations rather than links between cause but it seems to be small when compared with that of
and effect3 (figure 4). cigarette smoking.

Tobacco smoke Occupational exposure

The most convincing evidence for a direct causal Sufficiently intense occupational exposure to dust,
relationship in COPD is for tobacco smoke. Many gases, or fumes is associated with an increased risk of
epidemiological studies have shown that cigarette developing COPD, independent of cigarette smoking,
smoking is by far the most important risk factor for but the effects of occupational exposure and cigarette
COPD. Cigarette smokers have more respiratory smoking are additive.31 Both inorganic and organic dust
symptoms and lung function abnormalities, a greater exposure can accelerate the decline in FEV1.32
annual rate of decline in FEV1, and a greater death rate
from COPD than do non-smokers. Age at smoking Genetic factors
commencement, total pack-years smoked, and current Although we know the risk of developing COPD is
smoking status are predictive of COPD mortality. Not all dependent on the amount and duration of cigarette
smokers develop clinically significant COPD, but the smoking, it is clear that there is a high variation in
most recent epidemiological studies show that most susceptibility to the disease between individuals. The
smokers, if they live long enough and smoke enough, effects of exposure to other risk factors are cumulative
will develop airflow limitation.9–11 Stopping smoking with those from tobacco smoke, but this still does not
slows the decline in FEV1.23 Further evidence for the role explain the differences between smokers in the rate of
of cigarette smoke in causing COPD comes from animal FEV1 decline. Proof that genetic factors are involved in
models where COPD-like pathology can be induced by the pathogenesis of COPD comes from the observation
exposing mice to cigarette smoke.24 Pipe and cigar that individuals with severe deficiency for alpha-1-
smokers have greater COPD morbidity rates and antitrypsin, a major inhibitor of serine proteases, have
mortality than do non-smokers, although their rates are an increased risk of developing COPD.33 Individuals
lower than those of cigarette smokers. with a severe deficiency for alpha-1-antitrypsin who
Passive exposure to cigarette smoke (ie, environmental smoke cigarettes tend to develop more severe COPD at
tobacco smoke) increases the frequency of respiratory an earlier age than do non-smokers with a comparable

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 Seminar

severe deficiency.34 Besides cigarette smoking, other by means of standard questionnaires.42 Wheezing and
environmental factors such as occupational exposure chest tightness are non-specific and variable symptoms,
interact with severe deficiency for alpha-1-antitrypsin in and their absence does not exclude the diagnosis of
the risk of developing COPD. COPD.
There are indications that genetic factors other than
alpha-1-antitrypsin might contribute to the risk of Severe disease
developing COPD.35 Current or ex-smoking first-degree With severe disease, weight loss and anorexia are
relatives of patients with severe early onset COPD common.43 During respiratory infections, haemoptysis
without alpha-1-antitrypsin deficiency have a higher can occur,44 and requires further investigation. The
prevalence of COPD than do controls with the same development of cor pulmonale caused by secondary
smoking habits.36 Segregation analysis and linkage pulmonary hypertension is often seen in advanced
studies have not been consistent in identifying major COPD45 and can present with typical signs and
genes for COPD other than alpha-1-antitrypsin. symptoms of depression, anxiety, or both.
Associations have been described between COPD and
different gene polymorphisms, including alpha-1- Physical examination
antichymotrypsin, microsomal epoxide hydrolase, In mild to moderate COPD, physical examination alone
glutathione S-transferase, haeme oxygenase-1, and is not helpful for diagnosis, since physical signs are not
TNF.35 However, results have been inconsistent in usually present until significant impairment of lung
different populations. function has occurred,46,47 and their detection has low
sensitivity and specificity. Likewise, palpation and
Clinical features percussion are not very helpful for diagnosis, but may
COPD should be considered in any patient presenting sometimes serve to indicate lung hyperinflation. The
with cough, sputum production, or dyspnoea, especially frequently observed reduction in breath sounds is a
if the patient has been exposed to risk factors for the clinical guide, but does not allow for diagnosis.48
disease. Clinical diagnosis is confirmed by standardised
spirometric tests that show the presence of airflow Measurement of airflow limitation
limitation (ie, postbronchodilator FEV1 <80% of the Lung function measurements should be undertaken for
predicted value in combination with an any patient who may have COPD, even in patients
FEV1/FVC <0·7). Clinical symptoms and signs, such as presenting primarily with chronic cough and sputum
abnormal shortness of breath and increased forced production in the absence of dyspnoea. Although
expiratory time, can be used to help with the diagnosis. spirometric tests only measure a small aspect of the
effect of COPD on a patient’s health, they remain the
Symptoms gold standard for diagnosis because of their high
Cough and sputum reproducibility and availability. The monitoring of
Cough may initially occur intermittently but it is usually disease progression, the effects of drug interventions,
the first symptom of COPD to develop.37 It may be and progress of rehabilitation might also be assessed by
unproductive38 and is frequently neglected as a clinical additional functional measurements known to be related
sign by patients. Regular production of sputum for to health status such as the measurement of
3 months or more in 2 consecutive years has been the hyperinflation, residual volume, and inspiratory
epidemiological definition of chronic bronchitis39 for capacity.49,50
many years but this pattern of sputum production is not Spirometric tests should measure FVC and FEV1, and
really the same as that seen in COPD patients, which is the ratio of these two measurements (FEV1/FVC) should
generally very variable and sometimes difficult to be calculated (figure 1). Spirometric measurements are
assess.4 assessed by comparison with reference values based on
age, height, sex, and race.51 Patients with COPD typically
Dyspnoea show a decrease in both FEV1 and FVC and a decreased
Breathlessness in COPD is usually the first symptom FEV1/FVC ratio. Specific spirometric cutpoints (eg, FEV1
that drives patients to seek a medical consultation. It is >80% of predicted) to define different stages of COPD
characteristically persistent and progressive. Patients are used for simplicity; these cutpoints have not been
may first notice impairments in daily activities39 before clinically validated and might underestimate the
their disease progresses to a more severe state and they prevalence of COPD in some groups, such as elderly
may become confined to their homes. people.
Patients frequently describe their dyspnoea as a The airflow limitation in COPD patients is not fully
sense of increased effort to breathe, heaviness, air reversible; but this does not mean that there is no
hunger, or gasping,40 although a large variety in reversibility. In fact, many patients with COPD will show
terminology exists.41 Dyspnoea in COPD needs to be some degree of reversibility after inhalation of a short
distinguished from other causes, and can be quantified acting bronchodilator (2 agonist or an anticholinergic

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Suggestive features
Measurement of packed-cell volume may be useful in
patients with severe COPD, since continued smoking
COPD Onset in midlife
Symptoms slowly progressive can explain the limited effects of long-term oxygen
Long smoking history therapy to correct increased red-cell mass.57
Dyspnoea during exercise A chest radiograph is seldom diagnostic in COPD, and
Largely irreversible airflow limitation
CT scans of the chest are not routinely recommended.
Asthma Onset early in life (often childhood)
Symptoms vary from day to day Both techniques, however, might help in the differential
Symptoms at night or early morning diagnosis.
Allergy, rhinitis, or eczema also present
Family history of asthma
Largely reversible airflow limitation
Differential diagnosis
In some patients with severe or chronic asthma, a clear
Table 3: COPD: differential diagnosis clinical distinction from COPD is not possible, despite
use of imaging and physiological testing techniques, and
agent). A high degree of reversibility (eg, 20% or more) it is assumed that asthma and COPD coexist in these
is usually evidence of the presence of asthma. patients. In these patients, COPD management is
Measurement of peak expiratory flow cannot routinely similar to that for asthma. Nevertheless, physicians
be recommended since in COPD the relation between should aim to differentiate asthma from COPD if
this variable and FEV1 is poor and furthermore, it may possible, which might include trying a course of oral
underestimate the degree of airways obstruction in steroids, since management strategies for mild to
patients with the disease.52 It should only be used if moderate disease differ (table 3).
spirometric tests are not available.53–55
Natural history
Other investigations Studies on the natural history of COPD show that it is
Arterial blood gases should be measured in all patients usually a progressive disease, although differences exist
who have FEV1 less than 40% of predicted, or clinical between individuals. Continued exposure to noxious
signs of respiratory failure or right heart failure. agents promotes a more rapid decline in lung function
Additional investigations may be useful in such patients. and increases the risk for repeated exacerbations
Arterial blood-gas measurements are best for obtaining (figure 5). If exposure to noxious agents is stopped, the
acid-base information, which will guide oxygen therapy disease may still progress because of the age-related
and help to decide whether patients with exacerbations decline in lung function, and the persistence of aspects
require ventilatory support. of the inflammatory response.58 Nevertheless, efforts
The measurement of diffusing capacity should not need to concentrate on stopping exposure to noxious
routinely be done, but may be helpful in the case of agents, since some improvements in lung function and
diagnostic uncertainty or for preoperative assessment of slowing—or even halting—the progression of the
patients with severe COPD who are undergoing lung
resections or lung volume reduction surgery.56
Panel: GOLD classification of COPD by severity
Stage 0: at risk
100 Normal spirometry
Never smoked Chronic symptoms (cough, sputum)
or not susceptible
to smoke Stage I: mild
FEV1 (% of value at age 25 years)

75 FEV1/FVC <0·7; FEV1 >80% predicted

With or without symptoms (cough, sputum)

Smoked regularly Stopped at Stage II: moderate

50 45 years FEV1/FVC <0·7; 50% <FEV1 < 80% predicted
and susceptible
to its effects of age
With or without chronic symptoms (cough, sputum,
Disability dyspnoea)
25 Stopped at
65 years Stage III: severe
Death of age FEV1/FVC <0·7; 30% <FEV1 <50% predicted
With or without chronic symptoms (cough, sputum,
0
45 50 55 70
dyspnoea)
25 30 35 40 60 65 75
Age (years) Stage IV: very severe
FEV1/FVC <0·7; FEV1 < 30% predicted or FEV1 <50%predicted
Figure 5: Fletcher-Peto diagram showing the natural history and the change over time of the FEV1 in
non-smokers and smokers
respiratory failure or clinical signs of right heart failure
Adapted from reference 61 with permission.

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disease may be expected in patients, even people with 8 Churg A, Brauer M, AvilaCasado MD, Fortoul TI, Wright JL.
substantial airflow limitation.23 Chronic exposure to high levels of particulate air pollution and
small airway remodeling. Environ Health Perspect 2003; 111:
The degree of airflow limitation in COPD is only 714–18
loosely related to symptom severity, which introduces 9 Pena VS, Miravitlles M, Gabriel R, et al. Geographic variations
difficulties in disease staging. The recommended in prevalence and underdiagnosis of COPD: results of the
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driven, requiring a pragmatic approach to the 10 Mannino DM, Homa DM, Akimbani LJ, Ford ES, Redd SC.
assessment of disease severity and the prescription of Chronic Obstructive Pulmonary Disease Surveillance - United
States, 1971–2000. MMWR 2002; 51: 1–16.
drug treatment. Furthermore, for educational purposes 11 Lundback B, Lindberg A, Lindstrom M, et al. Not 15 but 50%
COPD is defined on the basis of airflow limitation of smokers develop COPD? Report from the Obstructive
(panel), but in practice patients report symptoms that Lung Disease in Northern Sweden Studies. Resp Med 2003;
97: 115–22.
affect their lifestyle. Recent data also suggest that
12 de Marco R, Accordini S, Cerveri I, et al, for the European
differences in health status are not evident until GOLD Community Health Survey Study Group. An international
stages 3 and 4.59 In principle, COPD can be diagnosed at survey of chronic obstructive pulmonary disease in young
adults according to GOLD stages. Thorax 2004; 59: 120–25
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13 Rennard S, Decramer M, Calverley PM, et al. Impact of COPD
patient’s history, objective lung-function measurements, in North America and Europe in 2000: subjects’ perspective of
and the presence of characteristic symptoms such as Confronting COPD International Survey. Eur Respir J 2002; 20:
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14 Jones PW. Health status measurement in chronic obstructive
Recently, a multidimensional grading system using pulmonary disease. Thorax 2001; 56: 880–87.
body-mass index, airflow obstruction, dyspnoea, and 15 Peruzza S, Sergi G, Vianello A, et al. Chronic obstructive
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18 Jacobson L, Hertzman P, Lofdahl C-G, Skoogh B-E, Lindgren B.
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Conflict of interest statement 119: 344–52.
None declared.
23 Anthonisen NR, Connett JE, Murray RP. Smoking and lung
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