Vous êtes sur la page 1sur 23

INT J TUBERC LUNG DIS 8(1):214 2004 IUATLD

The burden and impact of COPD in Asia and Africa


M. Chan-Yeung,* N. At-Khaled, N. White, M. S. Ip,* W. C. Tan
* Department of Medicine, Division of Respiratory and Critical Care Medicine, the University of Hong Kong, Hong Kong; Respiratory Division, University of British Columbia, Vancouver, Canada; International Union Against Tuberculosis and Lung Disease, Paris, France; Department of Medicine, UCT Lung Institute, University of Cape Town and Groote Schuur S U M M A RY Hospital, Cape Town, South Africa; Department of Medicine, National University of Singapore, Singapore

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. The World Health Organization (WHO) estimated that COPD is currently the seventh leading cause of death and disability worldwide, but will rise to the fifth position by 2020. The estimated prevalence of COPD worldwide in 2001 was 1013/100 000 population; it was highest in the Western Pacific Region and lowest in Africa. The mortality from COPD followed the same pattern. The prevalence of smoking is slowly decreasing in the industrialised world and rising in developing countries, especially in Asia and Africa. Cigarette consumption per adult has also decreased in the Americas, remained the same in Europe but increased in all other regions, especially the Western Pacific. Indoor air pollution from combustion of biomass/traditional fuels and coal, previous tuberculous infection, outdoor air pollution and childhood respiratory infections are other important risk factors for COPD in developing countries. The rise in morbidity and mortality from COPD will be most dramatic in Asian and African countries over the next two decades, mostly due to progressive increase in the prevalence of smoking. As developing countries can ill afford the added economic burden of COPD and other smoking-related diseases, there is an urgent need for multi-dimensional actions in reducing the main risk factor of cigarette smoking. KEY WORDS: COPD; epidemiology; risk factors

CHRONIC obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. The World Health Organization (WHO) estimated that COPD is currently the seventh leading cause of death and disability worldwide, and that it will rise to the fifth position by 2020.1,2 The increase is largely driven by two factors: the rise in tobacco-related mortality and morbidity, and the ageing population. As these factors are rapidly increasing in the developing world, COPD will become one of the toughest public health challenges, exerting huge demands on the economic and health care resources of these countries. The purpose of this review is to update readers on the epidemiology and risk factors of COPD in Asia and in Africa as examples of the problems and challenges the developing world is and will be facing in the next two decades.

DEFINITION The overall burden of COPD is not adequately appreciated worldwide.3 This is due to a number of factors. First, COPD is often not recognised, as symptoms of cough are frequently attributed to the acceptable irritant effects of smoking itself, to other respiratory diseases or even to ageing. These beliefs, which appear to be widely prevalent in Asia, hinder early diagnosis of the disease.4,5 Second, the term COPD has been used in two ways: as a functional disorder and as a disease entity. The term COPD had commonly been used for describing a functional disorder which is the consequence of several diseases, such as bronchiectasis, chronic asthma, panbronchiolitis, bronchiolitis obliterans, chronic post-tuberculosis lung disease and smoking-related airway disease, all of which are characterised by chronic airflow limitation. The introduction of the term COPD to describe the disease entity of chronic bronchitis and emphysema due largely to smoking dates back to 1969 in the United Kingdom6 and 1972 in the United States,7 while COPD as a smoking-related entity was officially introduced in Japan as recently as 1995.5 Thirdly, the term COPD is unfamiliar to the public and even physicians in many parts of the world. In many countries in Asia, for example, asthma is used generically to describe all types of chronic airway diseases.4 The consensus worldwide is to regard COPD as a distinct clinical entity, as shown in many guidelines

Correspondence to: Moira Chan-Yeung, Department of Medicine, Division of Respiratory and Critical Care Medicine, University of Hong Kong, Hong Kong. Tel: (_852) 2855 4385. Fax: (_852) 2855 1143. e-mail: mmwchan@hkucc.hku.hk

STATE OF THE ART

3 for management of this disease.812 Definitions of COPD have been prepared by expert panels of the European Respiratory Society (ERS) in 1995,9 the American Thoracic Society (ATS) in 1995,10 the British Thoracic Society (BTS) in 1997,11 and the Global Initiative for Chronic Obstructive Disease (GOLD) in 2001.12 All four expert panels made essentially the same key points in the definition for COPD: irreversible airflow obstruction; limited reversibility of airflow obstruction in response to bronchodilator drugs; chronic airflow obstruction due to other diagnosable conditions, such as asthma that is fully reversible, tuberculosis, cystic fibrosis, obliterative bronchiolitis or panbronchiolitis, is not included in COPD; tobacco smoking is the major, but not the only, risk factor for COPD; the cause of irreversible airflow obstruction in COPD is the presence in the lungs of bronchiolitis or small airway disease and emphysema, which are present in a variable mix among patients. The GOLD definition further states that airflow limitation is usually
The burden and impact of COPD in Asia and Africa

both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases.12 The case definition for COPD is problematic for developing countries, where the prevalence of lung infections, including tuberculosis, is still high and a proportion of patients develop chronic irreversible airflow obstruction as a result of these conditions or from both smoking and sequelae of lung infections. The appropriateness of using inhaled steroids on a long-term basis for COPD patients with Stage IIb COPD and the frequent use of short courses of oral steroids has not been adequately evaluated for patients with functional impairment associated with sequelae of lung infections and tuberculosis. Any change in the definition of COPD from a purely functional one to one including aetiological factors requires further discussion. Many international and national societies have recommended spirometric criteria for COPD. The criteria for cut-off values for forced expiratory volume (FEV)/forced vital capacity (FVC) differ in the various recommendations. The BTS,11 the South African Thoracic Society (SATS)13 and GOLD12 have recommended a cut-off point of FEV/FVC _70%, while in 1995 the ERS recommended that the ratio be _88% and _89% of predicted in men and women, respectively.9

EPIDEMIOLOGY OF COPD Most of the available information on the disease burden of chronic lung diseases comes from industrialised countries.12 However, comparison of published epidemiological data on prevalence, morbidity and mortality from the industrialised world is difficult, as they vary appreciably due to the different methodologies and definitions for COPD. This is because estimates of morbidity and mortality are usually based on in-formation recorded on medical records and death certificates. The imprecise and variable definitions of COPD have made it hard to quantify the morbidity and mortality of this disease in industrialised and developing countries. Available prevalence and morbidity data on COPD are likely to underestimate the total burden, as COPD is usually not recognised and is not diagnosed until it is moderately advanced. Global Burden of Disease study The Global Burden of Disease study was initiated by the WHO and the World Bank. Estimates were made by invited experts on the basis of published and unpublished studies, and when no data were available informed estimates were made.1,2 Worldwide mortality, prevalence and incidence of various diseases have been estimated, including those of COPD. Table 1 shows the global estimates of mortality, incidence and prevalence per 100 000 population and disabilityadjusted life years (DALYs) for COPD in 2001 in various regions.14 DALYs, the sum of years lost due to

premature mortality and years lived with disability, adjusted for the severity of the disability, has been proposed by the World Bank and the WHO as a measure of the global burden of disease. There is considerable variation across different regions in mortality, incidence, prevalence and DALYs. The high incidence and DALYs in the Western Pacific Region is due to the very high incidence and mortality of the disease in China.14
Region Population million Mortality /100 000 Incidence /100 000 Prevalence /100 000 DALYs million Africa 639.63 18.1 29.8 179 1.11 Americas 827.37 26.8 95.5 1390 2.99 Eastern Mediterranean 481.65 18.3 28.6 301 3.71 Europe 873.57 32.6 91.7 1329 1.00 South East Asia 1535.63 40.0 43.5 474 7.38 Western Pacific 1687.30 79.8 176.6 1675 13.7 World 6045.17 44.2 92.1 1013 29.9

Table 1 Global estimates of mortality, incidence and prevalence of COPD and DALYs of COPD in the world and six regions in 2001*

* Derived from reference 14. The rates were obtained by dividing the number of deaths, or of new cases, or cases at that point in time estimated by the WHO in each region by the population of that region divided by 100 000. COPD _ chronic obstructive pulmonary disease; DALYs _ disability-adjusted life years.

4 The International Journal of Tuberculosis and Lung Disease Prevalence There have been very few studies on the prevalence of COPD worldwide, especially in developing countries. The estimated prevalence of COPD worldwide in 2001 was 1013/100 0001206/100 000 in men and 810/100 000 in women (approximately 30% higher in men than in women).14 It was highest in the Western Pacific Region (1675/100 000) and lowest in Africa (179/100 000).14 As the estimates include all ages, the study grossly underestimates the disease in adults and the elderly, as COPD occurs mainly in these age groups. Precise estimates of the incidence of physiciandiagnosed COPD or spirometric airflow limitation in the community are not available. In the US, the prevalence of airflow obstruction (FEV/FVC _70%) in the white population was 14.2% among current smokers, 6.9% in ex-smokers and 3.3% in never smokers.15 The prevalence of self-reported lifetime emphysema or chronic bronchitis in the US in 2000 was 4.6% in men and 7.3% in women. The prevalence has shown a progressive decline in men but a progressive increase in women during the past decade.16 In Canada, the prevalence of chronic bronchitis or emphysema diagnosed by a health professional in 1998/99 was 2.8% and 3.6% in men and women, respectively, over the age of 35 years.17 The prevalence of chronic airflow obstruction has been estimated to be 46% of the adult population in Nordic countries, increasing with

age, with little difference between the sexes.1820 When airflow obstruction was defined as FEV/FVC _70%, the prevalence of airflow obstruction was 6% in the general population aged 1873 years in Norway. 20 In Northern Italy, the prevalence of airflow obstruction, defined in the same manner, was the same; about 1% of the population was found to have severe COPD with FEV at one second (FEV1) _50% predicted.21 In the developing world, which comprises a large part of the Asia and Africa, epidemiological data are either lacking, patchy or localised, or published in the native language. Community-based prevalence surveys are rare due to the high cost and complexity of organising them. Illiteracy requiring administration of questionnaires, sometimes in several languages in the same country, and unavailability of lung function equipment except in a few specialised services, are other barriers. The Asia Pacific Round Table Group/Asia Pacific Task Force used a statistical model to project the prevalence of COPD in 2000 in individual countries of the Asia Pacific region for comparison.22,23 The results of the study suggest that the prevalence of COPD in the region may be significantly greater than previously anticipated (Table 2). The combined prevalence of 6.3% for these countries is considerably higher than the overall rate of 3.9% extrapolated from WHO data.1,2 The estimated rate for China was 6.5%, 2.5 times greater than that estimated in the WHO study. The COPD prevalence rates projected by the model reflect the high prevalence of risk factors for the disease in Asia (cigarette smoking, exposure to high risk occupations, biomass fuels indoors and air pollution outdoors). The low prevalence of COPD in Africa is thought to be a reflection of Africas young population, with 44% under 15 years and only 3.2% over 65 years, and because of the low prevalence of smoking. Three reviews on chronic bronchitis and asthma in Africa have been published.2426 In Africa, the majority of the prevalence surveys on chronic bronchitis have been conducted in limited and specific population groups: miners, agricultural or industrial workers, civil servants and hospital patients. These studies used the British Medical Research Council questionnaire, de-fining chronic bronchitis as the presence of chronic productive cough sputum for at least 3 months in 2 successive years.27 The results only give a reflection of the prevalence of COPD, as airway obstruction occurs in only a proportion of chronic bronchitis cases.28 Many studies were conducted in occupational settings (Table 3).2942 The prevalence of chronic bronchitis in non-exposed workers varied between 3.5% and 17%,29,35 and was always higher

in exposed workers (4.1 to 38.5%).2941 The South African Demographic and Health Survey (SADHS) was a 1998 national, stratified household sample of over 14 000 South African adults aged _15 years.42 Chronic bronchitis occurred in 2.3% of males and 2.8% of females. These symptoms were most common in the age group 5564 years in men (9.3%) and _65 years in women (7.8%). Educational status had a strong protective effect, whereas nonurban residence appeared to be a risk factor for men (2.6%) and particularly for women (3.75%). An
Table 2 Prevalence of moderate/severe COPD in 2000 for 12 countries in the Asia-Pacific region (projected by model)*
Country/region Moderate/severe COPD cases Prevalence % Australia 558 000 4.7 China 38 169 000 6.5 Hong Kong, SAR, China 139 000 3.5 Indonesia 4 806 000 5.6 Japan 5 014 000 6.1 South Korea 1 467 000 5.9 Malaysia 338 000 4.7 Philippines 1 691 000 6.3 Singapore 64 000 3.5 Taiwan 636 000 5.4 Thailand 1 502 000 5.0 Vietnam 2 068 000 6.7 Total 56 553 000 6.3

* From reference 22. The COPD prevalence estimation model is an algorithm embedded in a software programme. It estimates the current COPD population for a specific region or country based on the local prevalence of four risk factors for COPD (cigarette smoking, biomass fuel use, moderate/severe air pollution, occupational exposure) and the population exposed to these risk factors. COPD _ chronic obstructive pulmonary disease.

5 abnormal peak expiratory flow rate (PEFR), defined as _2 standard deviation from predicted, based on the predicted from the same sample, was 4.0% in men and 4.1% in women. Hospital utilisation Hospital utilisation is usually studied by analysing health care use such as hospitalisation and clinic visits. Data on health service utilisation are not helpful for assessing burden of disease in an area where utilisation is strongly influenced by the supply of medical services. Data that are routinely available, even though not validated, may provide useful information. In the US, the rate of hospitalisation was 424/ 100 000 in men and 402/100 000 in women in 2000.16 During the past decade, the rate of hospitalisation has shown a progressive decrease in men but a progressive increase in women.17 In Canada, the differences between the sexes are similar; the projected increase in hospitalisations for women is higher than for men (Figure 1) due to the increasing proportion of women in the older age groups.17 The trends in Asian countries are similar. Hospitalisation
The burden and impact of COPD in Asia and Africa

records from Hong Kong and other regions in Asia have shown a steady increase over the years, with higher demands on the use of intensive care services, thus increasing the health care burden.4,5,4345 Among patients hospitalised in specialised chest services in Africa, the proportion of chronic bronchitis varies among countries, from 2.7% in a Conakry chest clinic to 14% in a specialised hospital in Morocco (Table 4).4651 The proportion of COPD among patients hospitalised for chronic bronchitis is more than 50%55% in national surveys in Algeria46 and Morocco,48 and 65% in Tunisia.51 This proportion differs from one clinic to another in the same country. By contrast, in Botswana, airways diseases are relatively uncommon. In returns on all causes for admissions by all hospitals to the Ministry of Health in 1997, asthma/COPD accounted for only 1.9% of discharge diagnoses and 0.7% of in-patient mortality _15 years of age in Botswana, but pulmonary tuberculosis, AIDS and pneumonia accounted for respectively 15.7%, 15.5% and 8.3% of in-patient mortality in the same year.52

Figure 1 Number of individuals hospitalized with chronic obstructive pulmonary disease actual and projected, Canada excluding territories, 19852016.17 Table 3 Prevalence of chronic bronchitis in various occupational settings in some African countries
Number of subjects Chronic bronchitis (%) Population Nonexposed Exposed Nonexposed Exposed Reference Algeria, Annaba Steel/fertiliser industries 200 400 3.5 10.3 Messadi29 Morocco Marrakech cement workers 230 38.3 El Bouanani30 Industrial workers El Meziane et al.31 Men 1829 10.7 Women 48 0 Male cement workers 403 23.5 Male cement workers 167 4.1 Chelil 32 Cement workers 120 120 6.7 11.7 Laraqui et al.33 Flour mill workers 373 120 4.3 13.1 Laraqui et al.34 South Africa, Cape Town Grain mill workers 153 582 17 35 Yach et al.35 Foundry workers 107 15.9 Myers et al.36 Sudan Chromite ore miners 27 177 7 26 Ballal37 Tanzania Sisal brushers 88 12 Mustapha et al.38 Tunisia Various sectors 4331 10.0 Maalej et al.39,40 Men 3646 10.4 Women 665 8.5

6 The International Journal of Tuberculosis and Lung Disease It is anticipated that more reliable information concerning health service utilisation will become available within the context of the WHO-sponsored programme Practical Approach to Lung Health (PAL),

which is currently being launched in a number of lowand middle-income countries. Mortality In 2001, the WHO estimated that global mortality from COPD was 44.2/100000.14 Mortality was highest in the Western Pacific region (79.8/100 000) and lowest in Africa (18.1/100 000). Throughout all regions, the mortality rate in men was higher than in women, except in the Western Pacific region, where mortality in women was higher than in men (90 vs. 70/100 000). There were 2.67 million deaths from COPD worldwide in 2001, and the trend is increasing. Despite the difficulties of case definition, the possible misclassification of COPD and the changes in the International Classification of Diseases (ICD), mortality rates from national statistics are the only epidemiological data that are readily available for comparison. In the US, COPD is the only common disease (including stroke and coronary heart disease) in which the death rate is increasing instead of falling; the increase in mortality is mostly in women.15 In 2000, the mortality from COPD was 82.6/100 000 in men and 56.7/100 000 in women in the US.16 In Canada, the mortality rate from COPD has increased progressively in both men and women during the past decade; the projected rise in COPD mortality rate in women is higher than in men (Figure 2).17 Mortality rates from COPD in Asian countries are similar to or even higher than in those in the West. In Japan, mortality from COPD in 1999 was 10.4/ 100 000, making it the seventh leading cause of death.5 In China, deaths from chronic respiratory disease rank first as the cause of all deaths. In 1994, the mortality
Figure 2 Number of chronic obstructive pulmonary disease deaths, actual and projected, Canada excluding territories, 19872016.17 Table 4 Prevalence of chronic bronchitis in health services in some African countries
Population n Age group Chronic bronchitis % COPD in chronic bronchitis % Reference Algeria In-patientsspecialised departments, 1982 5596 Adults 5.5 55 Oussedik and At-Khaled46 Out-patientschest department Stif, 19831984 1533 Adults 3.1 93 Rouiba, 19831984 968 Adults 3.3 66 Patientslung function laboratory 2160 Adults 13 54 At-Khaled et al.47 Casablanca, Morocco In-patientsgeneral hospital 368 3060 14 60 Bartal et al.48 Men 198 20.2 Women 170 6.5 Casablanca, Morocco In-patientsspecialised service Bouhayad (personal communication) 1988 234 Adults 4.3 1997 1131 Adults 10.8

Lome, Togo Out-patientschest department 5 years (19801984) 4640 Adults 8.2 Tidjani et al.49 2 years (19841985) 1400 Adults 7.7 Tidjani et al.50 Tertouba, Kairouan, Tunisia Women attending MCH centres 674 2050 14.9 65 Benmiled et al.51 Conakry, Guinea Chest service Sow (personal communication) In-patients 405 Adults 2.7 Out-patients 1667 Adults 10 Guinea Out-patients in primary health care 2564 Adults 3.3 Ottmani (personal communication) Ivory Coast Out-patients in primary health care 247 Adults 13.8 Ottmani (personal communication)
MCH _ Maternal and Child Health.

7 rate for the whole population was 161.57/100000 in the rural areas and 94.4/100 000 in cities, with a rising trend.53 In Hong Kong, COPD ranked as the fifth most common cause of death, accounting for 31.1/ 100 000 of the whole population in 1997.43 In Singapore, between 19911998, COPD deaths occurred in 163/100 000 population aged over 55 years, with four times higher rates in men (282/100 000) than in women (69/100 000), and more deaths in the minority ethnic groups (Table 5).44 In Thailand, mortality is reported to be 5004400/100 000 for men aged _51, and 6003400/100 000 in women.45 In Korea, according to national statistics, the overall death rates for COPD have risen from 0.4/100 000 in 1983 to 6.7/100 000 in 2000 (Figure 3).4 However, misclassification into asthma is likely to have accounted for this apparently low rate, as traditional doctors, who make up 20% of the medical profession, often classify COPD as asthma.4
The burden and impact of COPD in Asia and Africa

ECONOMIC AND SOCIAL BURDEN OF COPD Data on the direct (cost of health care resources) and indirect (cost of the consequences of the disability) cost of COPD are only available from industrialised countries. They showed that total cost for COPD is greater than for other common respiratory diseases such as asthma, influenza, pneumonia and tuberculosis. 54 In the US, the annual economic burden of COPD was estimated to be $23.9 billion in 1998 (direct and indirect cost). The cost per capita was $87 per year and about $1522 per patient per year. In the UK, the medical cost of COPD in 1996 was about $1900 per person per year, and the per capita cost of COPD was $65. Similar data are not available for developing countries.54 DALYs have been used by the WHO and the World Bank to estimate the economic and social burden of a particular disease for both low- and highincome countries. By this measure it is estimated that respiratory diseases account for 20% of the global burden for all diseases today. ETIOLOGY/RISK FACTORS Risk factors for COPD include both host predisposition and environmental exposures. The best-documented

host susceptibility factor is alpha-1-antitrypsin (_-1AT) deficiency.55 It is likely that other genetic factors play a role, but they have not yet been identified. The key environmental factors include tobacco smoke, occupational exposure to irritants, dusts and fumes and indoor air pollution caused by combustion of biomass/traditional fuels and coal. Other potential contributory risk factors include outdoor air pollution, allergy and bronchial hyperresponsiveness, prematurity, low birth weight and certain childhood respiratory infections. There is some evidence to suggest that these risk factors could be additive for development of COPD. Host factors

_-1-AT deficiency _-1-AT deficiency is the only known genetic factor that is definitely linked to the development of emphysema and COPD, even in non-smokers.55 _-1-AT is a major circulating inhibitor of serine proteases. People who carry the _-1-AT deficiency gene have a 40-fold increased risk of developing COPD compared with individuals without the deficiency gene. This genetic defect most often occurs in the people of Northern European origin, but is rare in Asians. In Japan, _-1-AT deficiency is rare and is due to the variant Siiyama.56 In China, studies reported no definite relationship between _-1-AT deficiency and COPD in Chinese patients as defined by serum _-1-AT level.57 Furthermore, studies involving genotyping of _-1-AT allelic gene and electrophoretic phenotyping found no cases of PiZ or PiS in Chinese. Small numbers of variants, such as MEtokyo and Mpirare, have been reported, but their pathogenetic relevance is unclear.58,59 The assessment of _-1-AT deficiency has been carried out in very few settings in Africa, and the prevalence of _-1-AT deficiency among African nations is unknown.
Table 5 COPD hospitalisation and mortality in population aged _5 years, by sex and ethnicity, Singapore 19911998*
Hospitalisation Mortality Characteristics Rate /10 000 Rate ratio (95% CI) Rate /10 000 Rate ratio (95%CI) Overall 52.4 16.3 Sex Females 18.2 1.00 6.9 1.00 Males 94.1 5.15 (1.071.68) 28.2 4.05 (3.404.84) Ethnicity Chinese 53.9 1.25 (1.041.50) 16.4 1.48 (1.032.14) Malay 45.1 1.07 (0.861.34) 19.3 1.76 (1.152.68) Indian 43.9 1.00 10.7 1.00

* From reference 44. COPD _ chronic obstructive pulmonary disease; CI _ confidence interval.

Figure 3 Age standardised mortality rates (per 100 000) for

chronic obstructive pulmonary disease versus asthma, 1983 2000 in Korea.4

The International Journal of Tuberculosis and Lung Disease

Airway hyperresponsiveness Airway hyperresponsiveness has also been linked to increased risk of development of COPD, a concept termed the Dutch hypothesis,60 which is popular among clinicians in several Asian countries. Smokers with airway hyperresponsiveness show greater decline of lung function than normal smokers.61 The exact relation is unknown, and is confounded by the fact that airway hyperresponsiveness could also result from exposure to tobacco smoke and environmental insults. There is no information on the role of airway hyperresponsiveness and atopy on the development of COPD in Africa and Asia. Environmental exposures Smoking Cigarette smoking is the main factor responsible for the development of COPD. The decline in lung function of susceptible smokers is twice that of nonsmokers. This causal relationship has been well established over 40 years in both cross-sectional62 and longitudinal studies.63,64 The cumulative amount of tobacco smoked, expressed as pack years, correlates with decline in lung function. The WHO estimated that there are about 1100 million smokers in the world, of which about 800 million are in developing countries (Table 6).65 Fortyseven per cent of men and 12% of women in the world are smokers. Smoking prevalence varies substantially among regions; it is lowest in Africa and highest in the Western Pacific, including China. The pattern of cigarette smoking changed globally between 19701972 and 19901992. It is slowly decreasing in the industrialised world, at a rate of 1% annually, and is rising in developing countries at a rate of 2%. Over the 20-year period, cigarette consumption per adult remained about the same in Europe, decreased in the Americas, and increased in all other regions, especially in the Western Pacific. In China, the estimated consumption of cigarettes per adults increased by 260% between 19701972 and 1990 1992; the rates of smoking are extremely high in both urban and rural areas, the respective rates being 60% and 64% in men and 15% and 9% in women.66 Table 7 shows the prevalence of smoking in adults and young adults by sex in selected Asian countries, the US and UK in the 1990s. In both adults and young adults, the prevalence of smoking in men in many Asian countries now exceeds those in the US and the UK.65 Compared to the US and the UK, the prevalence of smoking in adult women is lower in Asian countries; however, the prevalence in young women in some Asian countries is higher. There is a wide discrepancy

in the prevalence of smoking between men and women. The rates for women range from 2% to 4% for most South-East Asian countries to 14% in
Table 6 Estimated smoking prevalence for men and women, _15 years by WHO region, early 1990s*
WHO region Men % Women % Africa 29 4 The Americas 35 22 Eastern Mediterranean 35 4 Europe 46 26 South-East Asia 44 4 Western Pacific (includes China) 60 8 More developed countries 42 24 Less developed countries 48 7 World 47 12
* Derived from reference 65.

Table 7 Prevalence of smoking in adults and young adults in selected Asian countries by sex, and cigarette consumption per capita compared with two industrialised countries
Prevalence in adults (%) Prevalence in young adults (%) Cigarette consumption Country/region, year (Unit) Age (years) Male Female Age (years) Male Female Cambodia, 1994 1545 64.7* 86.3 NA _21 18.0* 58.0 NA NA China, 1996 1569 63.0 3.8 NA 23.0 5.0 1798 (1998) Hong Kong, 1998 15_ 27.1 2.9 1415 16.0 18.0 926 India, 19851986 2564 45.0 7.0 NA 12.8* 1.1* 129 Japan, 1998 15_ 52.8 13.4 1219 8.0 1.5 2403 Korea, 1997 NA NA NA 1315 35.3 8.1 2841 Malaysia, 1996 18_ 49.2 3.5 16 25.1 0.6 910 Philippines, 1999 20_ 75.0 18.0 NA NA NA 1688 Singapore, 1998 1864 26.9 3.1 920 3.0 0.2 1230 Taiwan, 1996 18_ 55.1 3.3 NA 23.8 8.2 NA Thailand, 1999 11_ 38.9 2.4 1114 0.4 0 1162 Vietnam, 1995 1892 72.8 4.3 15 20.0 NA 844 United States, 1997 18_ 27.6 22.1 1115 7.0 6.0 2255 United Kingdom, 19961997 16_ 29.0 28.0 1115 8.0 11.0 1748

Source (reference 67): National Tobacco Information Online System (NATIONS) from http://apps.nccd.cdc.gov/nations/nations/country-specific_indicators.asp * Urban. Rural. NA _ not available.

9 Japan. In men, the lowest rate was 27% in Singapore and Hong Kong, the highest is 73% in Vietnam, with intermediate high rates of 63% in China and South Korea, and 52% in Indonesia. Among Asian countries, Japan has the highest rate of smoking for women. Although smoking is still mainly a male habit, details from these national statistics indicate that there is an in-crease in the trend of smoking in women, especially those in their early twenties. In Africa, the overall consumption of tobacco is estimated to be 600 cigarettes per adult per year in 1990
The burden and impact of COPD in Asia and Africa

1992, about one third of the consumption of countries in the Organization for Economic Co-operation and Development (OECD) in the same period.65 However, tobacco consumption is growing at a faster rate in Africa than in any other part of the world: between 1985 and 1990, tobacco consumption rose by 2.4%. This rate is expected to rise to 3.2% between 1995 and 2000, compared to other developing countries, where the rise was expected to be 2.7% in the same period. The World Bank has estimated that a 10% increase in revenue in middle-income countries brings about a 7% increase in tobacco consumption, whereas the same increase in the poorest countries leads to an increase of 13%.65 Very little survey information on the prevalence of smoking is available for the African region. As of 1995, national survey data existed in only seven of the 46 countries, representing 33% of the regions total population aged _15 years. Population-weighted average prevalence estimates of smoking for these seven countries were 36% for men and 10% for women. The results of local surveys indicated that smoking prevalence in the other 46 countries was around 25% for men and 1% for women. The approximate population-weighted prevalence estimate for the WHO Africa Region is 29% for men and 4% for women. Currently, Mauritius and Botswana have consumption rates similar to those in industrialised countries. The consumption in middle-income countries such as Cameroon and Senegal is around 800/adult/year.65 In the SADHS it was established that in 1998, 42.3% of South African men and 10.7% of women were current daily or occasional smokers, with respectively 52.6% and 24.4% ever having smoked.42 Manufactured cigarettes were consumed by 80% of men and 84% of women. The mean age at starting smoking showed a trend towards a younger age, with men aged 3544 years having started at 20.8 years, compared to a mean of 16.3 years in the age group 1524 years. Ninety per cent of men and 94% of women were aware that tobacco was harmful to their health, and 66% of men and 83% of women current smokers had tried to quit. Nine per cent of pregnant women reported that they had smoked during pregnancy. Education had the strongest protective effect, with 50.5% of men with no formal education being current smokers, compared to 25.4% among those who had completed secondary education (Grade 10).42 With the declining sales in the industrialised countries, international tobacco companies are directing aggressive marketing campaigns in the developing countries, Asia and Africa alike, targeting not only men but also women and young boys.68 The Food and Agriculture Organisation (FAO) in Africa estimated

that if nothing were done to stop the rate of growth in cigarette sales, the level of consumption in Africa would soon be one of the highest in the world.65 This augurs badly for the future, as many countries in Asia and Africa can ill afford the health, social and economic burden of smoking-related diseases in general and the rising number of COPD patients in particular. Occupational exposure to dust and fumes Many studies documenting the relationship between occupational exposure to silica and chronic airflow obstruction even in non-smokers came from African gold miners.69 In addition, the association between occupational exposures to other dusts and chemicals (vapours, irritants and fumes) and COPD has been demonstrated in other studies of workers employed in other industries in Africa3138 and other countries.20,70,71 This association is not often fully appreciated, however, as diseases caused by these risk factors are often considered separately under the category of occupational lung diseases or pneumoconioses. The multiplicative effect of a combination of exposure to dust, gas and fumes has also been shown.71 Indoor air pollution In many countries in Asia and Africa, coal, wood and other biomass such as animal dung are used as cooking and heating fuels. Respirable particulate levels measured in these settings are typically 10002000 _g/m3, depending upon the specific fuel, ventilation, cooking duration and measurement interval.72 These levels are 1050 times higher than those observed for example in heavy urban traffic. The association of indoor air pollution from domestic fuel combustion in poorly ventilated houses and the development of COPD in non-smoking women has been widely reported in India, Nepal, Mexico and China,7378 and is considered an important non-smoking risk factor, especially in the developing countries, for nonsmoking women. In Africa, where biomass fuels are used extensively in rural areas, there are few data about any relationship with COPD. In one study conducted among women attending maternal child health centres in the rural mountainous areas of Tunisia,40 a very high prevalence of chronic bronchitis (14.9%) and COPD (9.2%) has been found. Another study of women from rural areas of South Africa that have very cold winters has documented COPD in association with mixed dust fibrosis, thought to be primarily related to 10 The International Journal of Tuberculosis and Lung Disease biomass fuels, particularly cow dung used in poorly ventilated houses.79 Outdoor air pollution The harmful effects of high levels of outdoor air pollution in patients with chronic cardiopulmonary diseases have been well documented, leading to increases

in morbidity, as reflected by increases in hospitalisations and mortality.8082 The role of the cumulative effects of outdoor air pollution in the development of COPD is unclear.82 This question is especially pertinent in many Asian countries that experience consistently high levels of urban air pollution and recurrent high peak levels of pollution, or haze due to forest fires.83 With progressive industrialisation, African countries may face the same problem as the Asian countries in the years to come. Infection

Childhood infection A review published by Samet et al. and a populationbased study in Brazil suggest a relationship between lower respiratory tract infections in childhood and the subsequent development of chronic bronchitis and COPD.84,85 However, this hypothesis remains unconfirmed. The prevalence of acute respiratory infections in sub-Saharan Africa is one of the highest in the world. Indoor air pollution has also been shown to be a risk factor for acute respiratory tract infection in children. In a South African study of acute respiratory infection in children, odds ratios (ORs) as a measure of risk for lower respiratory tract infection were estimated in a variety of domestic fuel scenarios based on care givers questionnaire responses:86 electrified vs. non-electrified (OR 2.9, 95%CI 1.46.2); electrified vs. partial electrification (OR 2.3, 95%CI 1.04.9); non-electrified urban exposed to wood and/or coal vs. non-exposed (OR 2.4, 95%CI 1.44.0); non-electrified rural exposed to wood and/or coal vs. non-exposed (OR 5.2, 95%CI 2.99.3). Pulmonary tuberculosis In many Asian and African countries, the occurrence of concomitant post-tuberculous lung disease and COPD is a significant problem, as risk factors for both conditions are prevalent. In patients with both risk factors, the lung function abnormality and the disability due to either disease interact and can be difficult to differentiate. In the SADHS a previous diagnosis of tuberculosis was an important risk factor for symptoms of chronic bronchitis and of airflow limitation.42 Other recent information on the clinical and functional abnormalities from this combined pathophysiology from South Africa indicates that among gold miners, 18.4% will have an FEV1 _80% predicted following one treatment episode for pulmonary tuberculosis, 27.1% in those with two and 35.2% in those with three treatment episodes.87 Other studies indicate that the degree of airflow obstruction in treated patients with pulmonary tuberculosis increased with age, the amount of cigarettes smoked, and the extent of the initial tuberculous disease.8890 Studies from hospital records in Indonesia suggest that some patients with mild tuberculosis may develop significant airway

obstruction.91 In addition to the role of tuberculosis itself in producing chronic airflow limitation, the association of tobacco smoking as a risk factor for both tuberculosis and COPD complicates the evaluation of the relationship of the individual risk factors with COPD, possibly acting as a confounder.

HIV HIV infection has been shown to accelerate the onset of smoking-related emphysema,92 and may add to the burden of smoking-related COPD. Population attributable fractions (PAF) There is no published literature on PAF of various risk factors for COPD, except for occupational exposure. Hnizdo et al. studied work exposure and COPD in the US population as part of the National Health and Nutrition Examination Survey (19881994), and estimated the fraction of COPD attributable to work to be 19.2% for the overall population and 31.1% for non-smokers.93 Data from the same survey showed that 45.4% of all subjects with low lung function (FEV1/FVC _70%) were smokers, 34.1% were exsmokers and 20.4% were non-smokers,94 suggesting that about 80% of obstructive lung diseases were due to smoking. Other risk factors were not studied. In Africa, 6085% of COPD patients were smokers in all studies except the Tunisa study, which was conducted in women.51 In the emphysema study of 102 patients in Algiers, 44.2% were smokers, 42.2% exsmokers and 14.7% non-smokers.31 Multivariate analysis of the SADHS has shown that in South Africa significant predictors for chronic bronchitis include a past history of tuberculosis in both men and women (OR 4.7, 95%CI 2.58.8 in men and OR 6.2, 95%CI 3.511.0 in women), smoking up to 15 cigarettes/day in women (OR 2.4, 95%CI 1.44.3) and occupational exposure in men (OR 1.6, 95%CI 1.02.5), while having _12 years education was protective in men (OR 0.2, 95%CI 0.10.9).42 In men, the estimated PAF for chronic bronchitis were 11% for a past history of tuberculosis, 20% for occupational exposure, 11% for smoking up to 15 cigarettes/ day and for 11% for more than 15 cigarettes/day. In women, the estimated PAF for chronic bronchitis was 11% for a past history of tuberculosis, 4.2% for occupational exposure and 1% for smoking fewer than 15 cigarettes/day. This South African study suggests that the epidemiology of COPD differs in high TB incidence countries, where previous tuberculosis is an important risk factor for COPD, and that The burden and impact of COPD in Asia and Africa 11 smoking contributes less to the development of COPD than in industrialised countries, while occupational exposure appears equally important in both contexts. For women in developing countries, indoor air pollution is probably an important contributory

factor. The lack of data makes it difficult for any firm conclusion to be drawn. The Burden of Obstructive Lung Disease (BOLD) initiative, which has been developed as a spin-off from the GOLD initiative to measure the prevalence, risk factors and burden of COPD in all countries using a standardised methodology, is a major step forward allowing inter-country and inter-region comparisons.

CONCLUSION Despite incomplete epidemiological data, there is persuasive evidence to support the fact that the burden of COPD is considerable worldwide, being apparently highest in the Western Pacific Region (especially in China) and lowest in parts of Africa. The morbidity and mortality of COPD is rising worldwide, and the rise is likely to be most dramatic in Asian and African countries over the next two decades, due to the projected increase in the prevalence of smoking. As developing countries can ill afford the added economic burden of COPD, there is an urgent need for multidimensional actions to reduce the main risk factor of cigarette smoking and to define the role of sequelae of lung infections in the development of COPD in these countries. Asian and African governments have a central role to play through the proven measures of enforced tobacco control legislation that, among other measures, increases the price of tobacco products through taxation, limits tobacco companies ability to advertise their products and controls the sale of tobacco products, particularly to children. Risk factors other than tobacco smoking, most notably the sequelae of lung infections (including tuberculosis), as well as occupational, environmental and domestic air pollution, are important in many parts of Asia and Africa, and must be evaluated more thoroughly to enable effective action. References
1 Murray C J L, Lopez A D. Evidence-based health policy lessons from the Global Burden of Disease Study. Science 1996; 274: 740743. 2 Murray C J L, Lopez A D. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injury and risk factors in 1990 and projected to 2020. Cambridge, MA: Harvard University Press, 1996. 3 Vermeire P. The burden of chronic obstructive pulmonary disease. Respir Med 2002; 96 (Suppl C): S3S10. 4 Shim Y S. Epidemiological survey of chronic obstructive pulmonary disease and alpha-1 antitrypsin deficiency in Korea. Respirology 2001; 6 (Suppl): S9S11. 5 Izumi T. Chronic obstructive pulmonary disease in Japan. Curr Opin Pulm Med 2002; 8: 102105. 6 Crofton J, Douglas A. Chronic bronchitis and emphysema. Respiratory diseases. Oxford and Edinburgh, UK: Blackwell, 1969: pp 330336. 7 United States Public Health Services. The health consequences of smoking. A report of the Surgeon General. DHES HSM, 727516. Washington, DC: US Government Printing Office, 1972. 8 Guidelines for the management of chronic obstructive pulmonary disease. The Thoracic Society of Australia and New

Zealand. Modern Med Australia 1995; 38: 132146. 9 Siafakas N M, Vermeire P, Pride N B, et al. ERS Consensus Statement. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). Eur Respir J 1995; 8: 13981420. 10 American Thoracic Society Statement. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 152 (Suppl): S77 S120. 11 The COPD guidelines Group of the Standards of Care Committee of the BTS. BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax 1997; 52: S1S28. 12 Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NIH, NHLBI 2701. Bethesda, MD: NHLBI/WHO report, April 2001. 13 Working Group for the South African Pulmonary Society. Guidelines for the management of chronic obstructive pulmonary disease. SAMJ 1998; 88: 9991010. 14 World Health Organization. World Health Report 2002. Geneva, Switzerland: WHO, 2002. www.who.int/whr/2002. 15 US Centers for Disease Control and Prevention. Vital and Health Statistics. Current Estimates from the National Health Interview Survey, 1995. DHHS, (PHS) 96-1527. Atlanta, GA: CDC, 1998. 16 Mannino D M, Homa D M, Akinbami L J, Ford E S, Redd S C. Chronic obstructive pulmonary disease surveillanceUnited States, 19712000. MMWR Surveillance Summaries 2002; 51: 116. 17 Health Canada. Chronic Obstructive Pulmonary Disease. In: Respiratory Disease in Canada. Tunneys Pasture, Ottawa, Canada: Health Canada, Sept 2001. www.hc-sc.gc.ca/pphb-dgspsp/ publicat/rdc-mrcol/index.html 18 Lange P, Groth S, Nyboe J, et al. Chronic obstructive lung disease in Copenhagen. Cross-sectional epidemiological aspects. J Int Med 1989; 226: 2532. 19 Gulsvik A. Prevalence and manifestations of obstructive lung disease in the city of Oslo. Scand J Respir Dis 1979; 60: 286296. 20 Bakke P, Baste V, Hanoa R, Gulsvik A. Prevalence of obstructive lung disease in a general population: relation to occupational title and exposure to some airborne agents. Thorax 1991; 46: 863870. 21 Viegi G, Carrozzi L, Di Pede F, et al Risk factors for chronic obstructive pulmonary disease in a North Italian rural area. Eur J Epidemiol 1994; 10: 17. 22 Tan W C, Seale P, Charoenrantakul S, et al. Chronic obstructive pulmonary disease (COPD) prevalence in 7 Asian countries. Projections based on the COPD prevalence model. Am J Respir Crit Care Med 2001; 163: A81. 23 Schau B S, Lopez-Vidriero M, Peabody J, et al. Chronic obstructive pulmonary disease: a prevalence estimation model. Am J Respir Crit Care Med 2000; 163: A799. 24 Chaulet P. Asthma and chronic bronchitis in Africa: evidence from epidemiologic studies. Chest 1996; 3 (Suppl): S334S339. 25 Becklake M R. International Union Against Tuberculosis and Lung Disease (IUATLD): initiatives in non-tuberculous lung disease. Tubercle Lung Dis 1995; 76: 493504. 26 Ait-Khaled N, Chaulet P, Enarson D A, Slama K. Epidemiology and management of stable obstructive pulmonary disease in Africa. In: Derenne P, ed. Clinical management of chronic obstructive pulmonary disease. New York, NY: Marcel Dekker, 2002; 165: 10071030.

12

The International Journal of Tuberculosis and Lung Disease

27 Medical Research Council Committee on the Aetiology of Chronic Bronchitis. Standardized questionnaires on respiratory symptoms. Br Med J 1960; 2: 1665. 28 Burrows B. Airway obstructive diseases: pathogenetic mechanisms and natural histories of disorders. Med Clin North Am 1990; 74: 547560. 29 Messadi M S. Prvalence de la bronchite chronique chez les

travailleurs de la zone industrielle de Annaba. Casablanca, Maroc: 5e Congrs de la fdration Maghrbine des Maladies Respiratoires, 1997. 30 El Bouanani M D. La prvalence de la bronchite chronique en milieu empoussir (Cimenterie Asmar Marrackech). Thse numro 512 soutenue la Facult de Mdecine et de Pharmacie de Casablanca, Maroc, 1984. 31 El Meziane A, Chellil C, El Bouanani M D, et al. Prvalence de la bronchite chronique en milieu industriel au Maroc. Alger, Algrie: Rapport Marocain au 13e Congrs mdical Magrhbin, 1984. 32 Chelil C. La prvalence de la bronchite chronique en milieu empoussir (Cimenterie de Casablanca). Thse numro 76 soutenue la Facult de Mdecine et de Pharmacie de Casablanca, Maroc, 1985. 33 Laraqui C H, Laraqui O, Rahhali A, et al. Prevalence of respiratory problems in workers of two manufacturing centers of ready-made concrete in Morocco. Int J Tuberc Lung Dis 2001; 5: 10511058. 34 Laraqui C H, Yazidi A A, Rahhali A, et al. The prevalence of respiratory symptoms and immediate hypersensitivity reactions in a population exposed to flour and cereal dust in five flour mills in Morocco [in French]. Int J Tuberc Lung Dis 2003; 7: 382389. 35 Yach D, Myers J, Bradshaw D, Benatar S R. A respiratory epidemiological survey of grain mill workers in Cape Town, South Africa. Am Rev Respir Dis 1985; 131: 505510. 36 Myers J E, Garisch D, Myers H S, Cornell J I. A respiratory epidemiological survey of workers in a small South African foundry. Am J Int Med 1987; 12: 19. 37 Ballal S G. Respiratory symptoms and occupational bronchitis in chromite ore minersSudan. J Trop Med Hyg 1986; 89: 223228. 38 Mustapha K Y, Lakha A S, Milla M H, Dahoma U. Byssinosis, respiratory symptoms and spirometric lung function tests in Tanzania sisal workers. Br J Ind Med 1978; 35: 123128. 39 Maalej M, Bouacha H, Benmiled T, Benkhedder A, Nacef T, El Gharbi B. Aspects pidemiologiques de la bronchite chronique en Tunisie. Enqute dans diffrents milieux professionnels in la bronchite chronique en Tunisie. Alger, Algrie: Rapport Tunisien au 13e Congrs Mdical Maghrbin, 1984. 40 Maalej M, Bouacha H, Bemiled T, Benkhedder A, El Gharbi T, El Gharbi B. La bronchite chronique en Tunisie. Aspect pidmiologique. Tunis Med 1986; 64: 457460. 41 Laouissi N. La prvalence de la bronchite chronique en milieu mdical. Thse numro 17, soutenue la Facult de Mdecine et de Pharmacie de Casablanca, Maroc, 1986. 42 Department of Health and Medical Research Council. South Africa Demographic and Health Survey, 1998. Full Report. Pretoria, South Africa: Department of Health and Medical Research Council, 1998. 43 Ip M S. Chronic obstructive pulmonary disease in Hong Kong. Respirology 2001; 6 (Suppl): S3S7. 44 Tan W C. The epidemiology and clinical management of chronic obstructive pulmonary disease in Singapore. Respirology 2001; 6 (Suppl): S17S20. 45 Saenghirunvattana S, Kongngeon V, Aeimrerksiri B, et al. Chronic obstructive pulmonary diseases in Thailand: incidence, prevalence, present status and future trends. J Med Assoc Thai 2001; 84: 14071411. 46 Oussedik N, At-Khaled N (rapporteurs). Les bronchopneumopathies chroniques. Alger, Algrie: Rapport Algrien au 13e Congrs Mdical Maghrbin, 1984. 47 At-Khaled N, Hamadache M, Benhabyles K. Analysis of demand for pulmonary function testing for obstructive airway disease in an Algerian laboratory. Bull Union Int Tuberc 1990; 65: 3941. 48 Bartal M, Naciri A, Bouayad Z, El Meziane A, Benjelloul W. Prevalence du syndrome bronchite chronique chez les malades hospitaliss. Alger, Algrie: 13e Congrs Mdical Maghrbin,

1984. 49 Tidjani O, Amedome A, Grunitzy B. Aspects pidmiologiques de la bronchite chronique au Togo. Larc Medical 1985; 5: 459451. 50 Tidjani O, Grnitzky B, Kolani M, Mijiyana M, Amedome A. Aspects pidmiologiques de la bronchite chronique, propos de 108 observations au CHU de Lom. Bull Union Int Tuberc Mal Resp 1986; 61: 87. 51 Benmiled M T, Tanabene A, Maalej M, Chebbi M L, Zakhama B, El Gharbi T. Bronchopathies chroniques chez les femmes rurales en Tunisie. Alger, Algrie: Rapport au 13e Congrs Mdical Maghrbin, 1984. 52 Steen T W. Adult Lung Health in Botswana. PhD thesis. Bergen, Norway: Department of Microbiology and Immunology, Gades Institute, University of Bergen, Norway and Nordic School of Public Health, Sweden, 2001. 53 Zhu Y J. Epidemiological survey of chronic obstructive pulmonary disease and alpha-1-1deficiency in China. Respirology 2001; 6 (Suppl): S13S15. 54 Pauwels R A, Buist A S, Calverley P M A, Jenkins C R, Hurd S. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 163: 12561276. 55 Laurell C B, Eriksson S. The electrophoretic alpha-1-globulin pattern of serum in alpha-1-antitrypsin deficiency. Scand J Clin Lab Invest 1963; 15: 132140. 56 Seyama K. State of alpha1-antitrypsin deficiency in Japan. Respirology 2001; 6 (Suppl): S35S38. 57 Chen X Y, Cheng X S, Li J Z, et al. Changes of serum elastase, alpha-1-antitrypsin, procollagen III, and malonadelhyde in smokers with and without chronic obstructive pulmonary diseases. China J Intern Med 1999; 38: 178180. 58 Yin Q L, Liang Z Q. The frequency distribution of alleic gene of _1-AT in Chinese. Chin Sci (Part B) 1980; 10: 897 903. 59 Huo J M, Shi Y Z, Liu X H, et al. The phenotype and content of _1-AT in patients with COPD. J Harbin Med Univ 1990; 24: 246248. 60 Orie N G M, Sluiter H J, De Vries K, et al. The host factors in bronchitis. In: Orie N G M, Sluiter H J, eds. Bronchitis, an international symposium. Assen, Netherlands: Royal Vangorcum, 1961: pp 4351. 61 Tashkin D P, Altose M D, Connett J E, et al. Methacholine reactivity predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. The Lung Health Study Research Group. Am J Respir Crit Care Med 1996; 153: 18021811. 62 US Department of Health, Education and Welfare. Smoking and Health: a report of the Advisory Committee to the Surgeon General of the Public Health Service. PHS 113. Washington DC: US Department of Health, Education and Welfare, 1964. 63 Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ 1977; 1: 16451648. 64 Bates D V. The fate of chronic bronchitis: a report of the tenyear follow-up in the Canadian Department Veterans Affairs Coordinated study of chronic bronchitis. Am Rev Respir Dis 1973; 108: 10431065. 65 World Health Organization. Smoking Prevalence. In: Tobacco or Health: A Global Status Report. Geneva, Switzerland: World Health Organization, 1997: pp 1018. 66 Wong X Z. Comments on smoking cessation in China and
The burden and impact of COPD in Asia and Africa

13

primary health care. Br Med J (Chinese Edition) 2000; 3: 101. 67 National Tobacco Information Online System (NATIONS). http://apps.nccd.cdc.gov/nations/country-specific_indicators.asp last accessed 18 Nov 2003. 68 MacKay J, Crofton J. Tobacco and the developing world. Brit Med Bull 1996; 52: 206221.

69 Oxman A D, Muir D C, Shannon H S, et al. Occupational dust exposure and chronic obstructive lung disease. A systematic review of the evidence. Am Rev Respir Dis 1993; 148: 3848. 70 Lam T H, Ong S G, Baratawidjaja K G. A study of byssinosis in Hong Kong and Jakarta: research methods and objectives. Am J Ind Med 1987; 12: 767771. 71 Ng T P, Tsin T W, OKelly F J, Chan S L. A survey of the respiratory health of silica-exposed gemstone workers in Hong Kong. Am Rev Respir Dis 1987; 135: 12491254. 72 Smith K, Liu Y. Indoor air pollution in developing countries. In: Samet J, ed. Epidemiology of lung cancer. New York, NY: Marcel Dekker, 1993: pp 151184. 73 Smith K R. Indoor air pollution in India. Natl Med J India 1996; 9: 103104. 74 Pandey M R. Domestic smoke pollution and chronic bronchitis in a rural community of Hill Region of Nepal. Thorax 1984; 39: 337339. 75 Perez-Padilla R, Regalado J, Vedal S, et al. Exposure to biomass smoke and chronic airway disease in Mexican women. Am J Respir Crit Care Med 1996; 154: 701706. 76 Behera D, Jindal S K. Respiratory symptoms in Indian women using domestic cooking fuels. Chest 1991; 100: 385388. 77 Koning H W, Smith K R, Last J M. Biomass fuel combustion and health. Bull World Health Organ 1985; 63: 1126. 78 Chen B H, Hong C J, Pandey M R, Smith K R. Indoor air pollution in developing countries. World Health Stat Q 1990; 43: 2738. 79 Grobelaar J, Bateman E D. Hut lung: a domestically acquired pneumoconiosis of mixed aetiology in rural women. Thorax 1991; 46: 334340. 80 Rokaw S N, Detels R, Coulson A H, et al. The UCLA population studies of chronic obstructive respiratory disease. Chest 1980; 78: 252262. 81 Arden Pope C, Bates D V, Raizenne M E. Health effects of particulate air pollution: time for reassessment? Environ Health Perspect 1995; 103: 472480. 82 Kunzli N, Kaiser R, Medina S, et al. Public health impact of outdoor and traffic-related air pollution: a European assessment. Lancet 2000; 356: 795801. 83 Tan W C, Qiu D W, Liam B L, et al. The human bone marrow response to acute air pollution caused by forest fires. Am J Respir Crit Care Med 2000; 161: 12131217. 84 Samet M, Tager I B, Speizer F E. The relationship between respiratory illness in childhood and chronic airflow obstruction in adulthood. Am Rev Respir Dis 1983; 127: 508523. 85 Menezes A M B, Victoria C G, Rigatto M. Prevalence and risk factors for chronic bronchitis in Pelotas, RS, Brazil: a population based study. Thorax 1994; 49: 12171221. 86 Ehrlich R, White N, Norman R, et al. Occupation as a risk factor for obstructive lung disease in a national household survey in South Africa. La Medicina del Lavoro 2002; 93: 383. 87 Hnizdo E, Singh T, Churchyard G. Chronic pulmonary function impairment caused by initial and recurrent pulmonary tuberculosis following treatment. Thorax 2000; 55: 3238. 88 Snider G L, Doctor L, Demas T A, Shaw A R. Obstructive airway disease in patients with treated pulmonary tuberculosis. Am Rev Respir Dis 1971; 103: 625640. 89 Birath G, Caro J, Malmberg R, Simonsson B G. Airway obstruction in pulmonary tuberculosis. Scand J Respir Dis 1966; 47: 2736. 90 Bromberg P A, Robin E D. Abnormalities of lung function in tuberculosis. Adv Tuberc Res 1963; 12: 15. 91 Nur A. Frequency of bronchial hyperreactivity in ex-TB patients. Thesis, Department of Pulmonary Disease Persahabatan Hospital, Jakarta, Indonesia, 1996. 92 Diaz P T, King M A, Pacht E R, et al. Increased susceptibility to pulmonary emphysema among HIV-seropositive smokers. Ann Intern Med 2000; 132: 369372.

93 Hnizdo E, Sullivan P A, Bang K M, Wagner G. Association between chronic obstructive pulmonary disease and employment by industry and occupation in the US population: a study of data from the third National Health and Nutrition Examination Survey. Am J Epidemiol 2002; 156: 738746. 94 Mannino D M, Gagnoon R C, Petty T L, Lydick E. Obstructive lung disease and low lung function in adults in the United States. Data from the National Health and Nutrition Examination Survey, 19881994. Arch Intern Med 2000; 160: 1683 1689.

RSUM

La bronchopneumopathie chronique obstructive (BPCO) est une cause majeure de morbidit et de mortalit au niveau mondial. LOrganisation Mondiale de la Sant (OMS) a estim que la BPCO est actuellement la septime cause de mort et dinvalidit au niveau mondial, mais quelle atteindra la cinquime position en 2020. La prvalence estime de la BPCO au niveau mondial en 2001 est de 1.013/100.000 ; elle est la plus leve dans la rgion du Pacifique Occidental et la plus faible en Afrique. La mme distribution sobserve en ce qui concerne la mortalit par BPCO. La prvalence du tabagisme est en dcroissance lente dans le monde dvelopp, et augmente par contre dans les pays en dveloppement, particulirement en Asie et en Afrique. La consommation de cigarettes par adulte a galement dcru dans les Amriques, est reste stable en Europe, mais a augment dans toutes les autres rgions, et particulirement dans le Pacifique Occidental. Dans les pays en dveloppement, la pollution interne de lair provenant de la combustion des combustibles de la biomasse ou des combustibles traditionnels et du charbon, une infection tuberculeuse antrieure, la pollution de lair externe et les infections respiratoires de lenfance sont dautres facteurs de risque importants pour la BPCO. Laugmentation de morbidit et de mortalit par BPCO sera la plus dramatique dans les pays dAsie et dAfrique au cours des deux dcennies venir, principalement en rapport avec laugmentation progressive de prvalence du tabagisme. Puisque les pays en dveloppement peuvent difficilement affronter le fardeau conomique supplmentaire de la BPCO et dautres maladies lies au tabagisme, des mesures multidimensionnelles sont urgentes pour rduire le facteur de risque principal que constitue le tabagisme.

14

The International Journal of Tuberculosis and Lung Disease

RESUMEN

La enfermedad pulmonar obstructiva crnica (EPOC) es una causa importante de morbilidad y mortalidad en todo el mundo. La Organizacin Mundial de la Salud (OMS) ha estimado que la EPOC es actualmente la 7 causa de muerte e invalidez en el mundo, pero que ocupar la 5 posicin de aqu al ao 2020. En 2001, la prevalencia estimada de la EPOC en el mundo era de 1.013/100.000 ; la ms alta en la Regin del Pacfico Occidental y la ms baja en frica. La mortalidad por EPOC segua el mismo modelo. La prevalencia del tabaquismo est disminuyendo lentamente en el mundo desarrollado y aumentando en los pases en desarrollo, especialmente en Asia y frica. El consumo de cigarrillos por adulto tambin ha disminuido en las Amricas, ha

permanecido el mismo en Europa, pero ha aumentado en todas las otras regiones, especialmente en el Pacfico Occidental. Otros importantes factores de riesgo para la EPOC en los pases en desarrollo son la polucin del aire interior proveniente de la combustin de la biomasa, de combustibles tradicionales y del carbn, la infeccin tuberculosa previa, la polucin del aire exterior y las infecciones respiratorias infantiles. El aumento de morbilidad y mortalidad por EPOC ser ms dramtico en los pases de Asia y de frica en las dos prximas dcadas, debido sobre todo al aumento progresivo de la prevalencia del tabaquismo. Como los pases en desarrollo pueden abordar difcilmente la carga econmica suplementaria constituida por las EPOC y otras enfermedades relacionadas con el tabaquismo, es urgente emprender acciones multidimensionales para reducir el riesgo principal que es el tabaquismo.

Vous aimerez peut-être aussi