- Email: [email protected]
Diabetes and the global burden of non-communicable disease
CORRESPONDENCE
1 2
3
Dalakas M, Hohlfeld H. Polymyositis and dermatomyositis. Lancet 2003; 362: 971–82. Bohan A, Peter JB. Polymyositis and dermatomyositis. N Engl J Med 1975; 292: 344–47. Targoff IN, Miller FW, Medsger, TA, Oddis CV. Classification criteria for the idiopathic inflammatory myopathies, Curr Opin Rheumatol 1997; 9: 527–36.
Authors’ reply Sir—Frederick Miller and colleagues contend that our muscle-biopsy-based diagnostic criteria for polymyositis are “untested and impractical”, whereas the old Bohan and Peter criteria are “accepted, sensitive, and specific”. We strongly disagree for the following reasons. The MHC/CD8 lesion is central to the definition of polymyositis.1,2 Contrary to what Miller and colleagues suggest, this lesion has been extensively validated by screening other myopathies with inflammation, such as dystrophies and toxic and metabolic myopathies.3,4 The observation has been a breakthrough in our understanding of polymyositis during the past 20 years, and has been greatly appreciated by neuromuscular disease diagnosticians who have recognised the pitfalls associated with the diagnosis of polymyositis. Immunohistochemistry is routinely done by modern laboratories to diagnose tumours, lymphomas, skin lesions, etc; the assertion that it is impractical or subjective is untenable. Although inflammation could be patchy, immunocytochemistry is very sensitive in the identification of CD8 cells that cannot be identified by routine histology. Furthermore, MHC-I expression is not patchy but widely upregulated even in areas without inflammation. If it is polymyositis, you will always find the MHC/CD8 lesion. The 30-year-old Bohan and Peter criteria endorsed by Miller and colleagues have been a source of constant error because they result in the diagnosis of polymyositis in patients with muscle weakness, myopathic electromyograms, and increased concentrations of creatine kinase without a diagnostic muscle biopsy, or without a biopsy at all.2 As a result, cases of inclusion-body myositis or dystrophies, especially without a positive family history, are diagnosed as polymyositis and treated unsuccessfully and unnecessarily for many years, thereby exposing patients to the long-term side-effects of prednisone and immunosuppressants. Referrals of patients with “polymyositis unresponsive to therapies”, represent the most commonly misdiagnosed disorder in large neuromuscular centres.
Miller and colleagues seem to lump polymyositis, dermatomyositis, and inclusion-body myositis into one category. Although in dermatomyositis and inclusion-body myositis creatine kinase concentrations can be normal, such concentrations are never normal in patients with active polymyositis. Also, the presence of the MHC/CD8 complex does not apply to dermatomyositis, only to polymyositis and inclusion-body myositis. If the typical skin changes are present, histological diagnosis of dermatomyositis might not be necessary. Contrary to Miller and colleagues’ contentions, the Bohan and Peter criteria have never been tested for their specificity. They have been tested against other connective tissue diseases, but not against other myopathies. Despite being insensitive and untested, they have been “accepted” by the community. However, as pointed out more than 10 years ago, they cannot distinguish several common myopathies, such as dystrophies or inclusion-body myositis, from true polymyositis. It is unfortunate that Miller and colleagues do not recognise the evolution of muscle immunopathology, which has given us the tools to avoid the mistakes of the past. The IMACS consensus is a highly commendable effort. We do hope that Miller and colleagues will incorporate the modern histological criteria or consult with internationally recognised experts on muscle histopathology to avoid misdiagnosis. Otherwise, the misinterpretation of polymyositis will be perpetuated. Marinos C Dalakas, Reinhard Hohlfeld Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, Building 10, Room 4N248, Bethesda, MD 20892, USA (MCD); Max Planck Institute of Neurobiology and Institute for Clinical Neuroimmunology, Klinikum Grosshadern, Ludwig Maximilians University, Munich, Germany (RH) (e-mail: [email protected]) 1
2
3
4
Engel AG, Arahata K. Monoclonal antibody analysis of mononuclear cells in myopathies, II: phenotypes of autoinvasive cells in polymyositis and inclusion body myositis. Ann Neurol 1984; 16: 209–15. Dalakas MC. Polymyositis, dermatomyositis and inclusion-body myositis. N Engl J Med 1991; 325: 1487–98. Karpati G, Pouliot Y, Carpenter S. Expression of immunoreactive major histocompatibility complex products in human skeletal muscles. Ann Neurol 1988; 23: 64–72. Emslie-Smith AM, Arahata K, Engel AG. Major histocompatibility complex class I antigen expression, immunolocalization of interferon subtypes and T-cell-mediated cytotoxicity in myopathies. Hum Pathol 1989; 20: 224–31.
THE LANCET • Vol 362 • November 22, 2003 • www.thelancet.com
Diabetes and the global burden of noncommunicable disease Sir—In their overview of globalisation and the prevention and control of noncommunicable disease (Sept 13, p 903),1 R Beaglehole and D Yach correctly draw attention to the importance of ischaemic heart disease and cerebrovascular disease. Their tabulations place these as ranking first and second, respectively, in both developed and developing countries. By contrast, diabetes—generally regarded as one of the most serious pandemics affecting all societies today2—ranks ninth as cause of death in developed countries, and does not appear at all in the top ten causes of death in the year 2000 in developing countries. The reason is unfortunately clear from previous publications on reporting bias in death certification. Events tend to be recorded preferentially, whereas underlying causes of such events can often be neglected. Even if underlying causes are recorded, these are sometimes ignored in statistical analysis in favour of event codes. Thus with coding according to the International Classification of Diseases revision 9, myocardial infarction (410) is more likely to be recorded as the underlying cause of death than diabetes mellitus (250), even though the antecedent cause for accelerated atherosclerosis will have been the diabetes. Fuller3 described this deficiency of reportage as early as 1983. The UK Prospective Diabetes Study recorded 981 deaths in a prospective study of median duration 10 years. Of these deaths in the UK, only 42% of the certificates mentioned diabetes overall, and even in the case of cardiovascular death (for which there is a prima facie case for regarding diabetes as antecedent) the mention was made in only 46% of cases. Nor is this bias confined to the UK: estimates from Denmark suggest that only half the diabetes-associated mortality is registered in the national statistics. Does the under-reporting matter? We think it does, because diabetes is treatable and intensive treatment reduces risk.4 If governments and health-care providers believe that diabetes does not even rank in the top ten causes of early death, then resources will not be appropriately allocated and the 150 million people with diabetes (rising to 300 million in 2025)5 will find themselves struggling
1763
For personal use. Only reproduce with permission from The Lancet publishing Group.
CORRESPONDENCE
with a burden of morbidity and mortality that could have been avoided. *David R Matthews, Stig Pramming *Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK (DRM); Novo Nordisk A/S, Bagsvaerd, Denmark (SP) (e-mail: [email protected]) 1
2
3
4
5
Beaglehole R, Yach D. Globalisation and the prevention and control of noncommunicable disease: the neglected chronic diseases of adults. Lancet 2003; 362: 903–08. King H, Aubert RE, Herman WH. Global burden of diabetes 1995–2025: prevalence, numerical estimates and projections. Diabetes Care 1998; 21: 1414–31. Fuller JH, Elford J, Goldblatt P, Adelstein AM. Diabetes mortality: new light on an underestimated public health problem. Diabetologia1983; 24: 336–41. UKPDS Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998; 352: 837–53. Zimmet P, Alberti KG, Shaw J. Global and social implications of the diabetes epidemic. Nature 2001; 414: 782–87.
Argument for partial nicotine deregulation Sir—Tobacco products enjoy growing worldwide popularity, despite the staggering health toll attributed to them. As Nigel Gray and Peter Boyle discuss in their Commentary (Sept 13, p 845),1 the most effective response to this pandemic may be a policy of harm reduction. They encourage “clean addictive recreational nicotine delivery”, and cite a decade-old call for an accommodating policy.2 Regarding the potential harms of clean addictive nicotine, they conclude: “Any risks linked with such a product are dwarfed by the magnitude of the tobacco problem.” A quantitative analysis of the probable health effect of a nicotine inhaler By reinforces this expectation.3 extending the methods of the SAMMEC (Smoking Attributable Morbidity, Mortality and Economic Costs) computer programs,4 the analysis predicted how the USA’s smokingrelated mortality in 1990 would have changed if clean nicotine inhalers had completely displaced cigarettes. In plausible scenarios, an addictive nicotine inhaler should benefit public health, even if everyone used it. Reductions in current smokers’ disease burden should improve public health even more than reducing smoking prevalence to 12%. Public health could improve with a policy that also reduces public investments in tobacco control and related research, smoking-related fires,
1764
smoking breaks, withdrawal symptoms at work, and environmental tobacco smoke. In addition, deregulation preserves any benefits of nicotine use and offers an alternative tax base as tobacco sales decline. The argument for deregulating nicotine demands serious consideration. Gray and Boyle quote that “There is no compelling objection to the recreational and even addictive use of nicotine provided it is not shown to be physically, psychologically, or socially harmful to the user or to others”. Snus (Swedish oral moist snuff) and nicotine replacement products meet these criteria. These forms of nicotine are so safe that one criterion for nicotine dependence according to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders— continued use in spite of harm5—seems irrelevant. However, cigarettes briefly deliver higher concentrations of nicotine to the arterial circulation than any other currently available tobacco product. The consequences in human beings of long-term inhalation of nicotine without smoke are unknown. Unexpected consequences, perhaps involving new disease processes or increased abuse of other substances, could temper the public-health gains that many of us expect. Trials of clean, addictive nicotine as an alternative to smoking cessation would reveal such problems. Gray and Boyle remind us that manufacturers investing in these studies need reassurance from regulators that recreational nicotine is tolerable. Other unintended consequences could include increased smoking initiation, delayed smoking cessation, increased teenage addiction to nicotine, and increased nicotine use in pregnancy. Prospective smokers might reason that they can switch to nicotine inhalers when cigarettes start to injure them. Teenagers might develop expensive addictions before they understand the financial burden. Furthermore, manufacturers should bear much responsibility for devising safe delivery systems. These concerns are reasons to regulate the manufacturing, advertising, and youth sales of addictive nicotine products, much as we regulate cigarettes, for the immediate future. Clean, addictive, nonprescription, recreational nicotine deserves enthusiastic study by and encouragement from the tobacco control community, but for now, only partial deregulation. Walton Sumner General Medical Sciences, Washington University School of Medicine, Campus Box 8005, 660 South Euclid Avenue, St Louis, MO 63110, USA (e-mail: [email protected])
1 2 3
4
5
Gray N, Boyle P. The future of the nicotineaddiction market. Lancet 2003; 362: 845–46. Anon. Nicotine use after the year 2000. Lancet 1991; 337: 1191–92. Sumner W 2nd. Estimating the health consequences of replacing cigarettes with nicotine inhalers. Tob Control 2003; 12: 124–32. Nelson DE, Kirkendall RS, Lawton RL, et al. Surveillance for smoking-attributable mortality and years of potential life lost, by state—United States, 1990. Morb Mortal Wkly Rep CDC Surveill Summ 1994; 43: 1–8. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Washington DC: American Psychiatric Association, 1994.
Global burden of COPD in Japan and Asia Sir—P M A Calverley and Paul Walker (Sept 27, p 1053)1 have comprehensively summarised that chronic obstructive pulmonary disease (COPD) is a major cause of death and disability worldwide, and that the burden of disease will continue to increase over the next 20 years. However, they do not point out that the weight of this burden is very different between Asian countries and those of Europe and the USA. Because tobacco consumption is the main contributing factor in COPD, the prevalence of the disease will increase over the next 20 years in the USA and Europe, but will reach a plateau after that. However, the disease prevalence is likely to keep increasing for more than 40 years in Japan and Asia. China, the country with the largest production and consumption of tobacco worldwide, has seen a striking increase in consumption over the past 2 decades. A survey found that the average daily consumption of tobacco per person in China rose from one cigarette in 1952 to ten cigarettes in 1990—a rate similar to that of the USA 40 years earlier.2 The survey also estimated that the prevalence of COPD was 3% of the total population, but could increase to 10%. In Japan, a national survey revealed that 220 000 people had COPD in 1997, but the NIPPON COPD epidemiology study revealed that more than 5·3 million people—8·5% of the population aged 40 years and older— should be diagnosed as having COPD.3 Tobacco consumption was still increasing, particularly among women. Past occupational exposures to dust, airborne chemicals, and chemical products have also been suggested to significantly increase the likelihood of COPD, independent of the effects of smoking.4 On this point, the USA, Europe, and Asia differ greatly.
THE LANCET • Vol 362 • November 22, 2003 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet publishing Group.
1 2
3
Dalakas M, Hohlfeld H. Polymyositis and dermatomyositis. Lancet 2003; 362: 971–82. Bohan A, Peter JB. Polymyositis and dermatomyositis. N Engl J Med 1975; 292: 344–47. Targoff IN, Miller FW, Medsger, TA, Oddis CV. Classification criteria for the idiopathic inflammatory myopathies, Curr Opin Rheumatol 1997; 9: 527–36.
Authors’ reply Sir—Frederick Miller and colleagues contend that our muscle-biopsy-based diagnostic criteria for polymyositis are “untested and impractical”, whereas the old Bohan and Peter criteria are “accepted, sensitive, and specific”. We strongly disagree for the following reasons. The MHC/CD8 lesion is central to the definition of polymyositis.1,2 Contrary to what Miller and colleagues suggest, this lesion has been extensively validated by screening other myopathies with inflammation, such as dystrophies and toxic and metabolic myopathies.3,4 The observation has been a breakthrough in our understanding of polymyositis during the past 20 years, and has been greatly appreciated by neuromuscular disease diagnosticians who have recognised the pitfalls associated with the diagnosis of polymyositis. Immunohistochemistry is routinely done by modern laboratories to diagnose tumours, lymphomas, skin lesions, etc; the assertion that it is impractical or subjective is untenable. Although inflammation could be patchy, immunocytochemistry is very sensitive in the identification of CD8 cells that cannot be identified by routine histology. Furthermore, MHC-I expression is not patchy but widely upregulated even in areas without inflammation. If it is polymyositis, you will always find the MHC/CD8 lesion. The 30-year-old Bohan and Peter criteria endorsed by Miller and colleagues have been a source of constant error because they result in the diagnosis of polymyositis in patients with muscle weakness, myopathic electromyograms, and increased concentrations of creatine kinase without a diagnostic muscle biopsy, or without a biopsy at all.2 As a result, cases of inclusion-body myositis or dystrophies, especially without a positive family history, are diagnosed as polymyositis and treated unsuccessfully and unnecessarily for many years, thereby exposing patients to the long-term side-effects of prednisone and immunosuppressants. Referrals of patients with “polymyositis unresponsive to therapies”, represent the most commonly misdiagnosed disorder in large neuromuscular centres.
Miller and colleagues seem to lump polymyositis, dermatomyositis, and inclusion-body myositis into one category. Although in dermatomyositis and inclusion-body myositis creatine kinase concentrations can be normal, such concentrations are never normal in patients with active polymyositis. Also, the presence of the MHC/CD8 complex does not apply to dermatomyositis, only to polymyositis and inclusion-body myositis. If the typical skin changes are present, histological diagnosis of dermatomyositis might not be necessary. Contrary to Miller and colleagues’ contentions, the Bohan and Peter criteria have never been tested for their specificity. They have been tested against other connective tissue diseases, but not against other myopathies. Despite being insensitive and untested, they have been “accepted” by the community. However, as pointed out more than 10 years ago, they cannot distinguish several common myopathies, such as dystrophies or inclusion-body myositis, from true polymyositis. It is unfortunate that Miller and colleagues do not recognise the evolution of muscle immunopathology, which has given us the tools to avoid the mistakes of the past. The IMACS consensus is a highly commendable effort. We do hope that Miller and colleagues will incorporate the modern histological criteria or consult with internationally recognised experts on muscle histopathology to avoid misdiagnosis. Otherwise, the misinterpretation of polymyositis will be perpetuated. Marinos C Dalakas, Reinhard Hohlfeld Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, Building 10, Room 4N248, Bethesda, MD 20892, USA (MCD); Max Planck Institute of Neurobiology and Institute for Clinical Neuroimmunology, Klinikum Grosshadern, Ludwig Maximilians University, Munich, Germany (RH) (e-mail: [email protected]) 1
2
3
4
Engel AG, Arahata K. Monoclonal antibody analysis of mononuclear cells in myopathies, II: phenotypes of autoinvasive cells in polymyositis and inclusion body myositis. Ann Neurol 1984; 16: 209–15. Dalakas MC. Polymyositis, dermatomyositis and inclusion-body myositis. N Engl J Med 1991; 325: 1487–98. Karpati G, Pouliot Y, Carpenter S. Expression of immunoreactive major histocompatibility complex products in human skeletal muscles. Ann Neurol 1988; 23: 64–72. Emslie-Smith AM, Arahata K, Engel AG. Major histocompatibility complex class I antigen expression, immunolocalization of interferon subtypes and T-cell-mediated cytotoxicity in myopathies. Hum Pathol 1989; 20: 224–31.
THE LANCET • Vol 362 • November 22, 2003 • www.thelancet.com
Diabetes and the global burden of noncommunicable disease Sir—In their overview of globalisation and the prevention and control of noncommunicable disease (Sept 13, p 903),1 R Beaglehole and D Yach correctly draw attention to the importance of ischaemic heart disease and cerebrovascular disease. Their tabulations place these as ranking first and second, respectively, in both developed and developing countries. By contrast, diabetes—generally regarded as one of the most serious pandemics affecting all societies today2—ranks ninth as cause of death in developed countries, and does not appear at all in the top ten causes of death in the year 2000 in developing countries. The reason is unfortunately clear from previous publications on reporting bias in death certification. Events tend to be recorded preferentially, whereas underlying causes of such events can often be neglected. Even if underlying causes are recorded, these are sometimes ignored in statistical analysis in favour of event codes. Thus with coding according to the International Classification of Diseases revision 9, myocardial infarction (410) is more likely to be recorded as the underlying cause of death than diabetes mellitus (250), even though the antecedent cause for accelerated atherosclerosis will have been the diabetes. Fuller3 described this deficiency of reportage as early as 1983. The UK Prospective Diabetes Study recorded 981 deaths in a prospective study of median duration 10 years. Of these deaths in the UK, only 42% of the certificates mentioned diabetes overall, and even in the case of cardiovascular death (for which there is a prima facie case for regarding diabetes as antecedent) the mention was made in only 46% of cases. Nor is this bias confined to the UK: estimates from Denmark suggest that only half the diabetes-associated mortality is registered in the national statistics. Does the under-reporting matter? We think it does, because diabetes is treatable and intensive treatment reduces risk.4 If governments and health-care providers believe that diabetes does not even rank in the top ten causes of early death, then resources will not be appropriately allocated and the 150 million people with diabetes (rising to 300 million in 2025)5 will find themselves struggling
1763
For personal use. Only reproduce with permission from The Lancet publishing Group.
CORRESPONDENCE
with a burden of morbidity and mortality that could have been avoided. *David R Matthews, Stig Pramming *Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK (DRM); Novo Nordisk A/S, Bagsvaerd, Denmark (SP) (e-mail: [email protected]) 1
2
3
4
5
Beaglehole R, Yach D. Globalisation and the prevention and control of noncommunicable disease: the neglected chronic diseases of adults. Lancet 2003; 362: 903–08. King H, Aubert RE, Herman WH. Global burden of diabetes 1995–2025: prevalence, numerical estimates and projections. Diabetes Care 1998; 21: 1414–31. Fuller JH, Elford J, Goldblatt P, Adelstein AM. Diabetes mortality: new light on an underestimated public health problem. Diabetologia1983; 24: 336–41. UKPDS Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998; 352: 837–53. Zimmet P, Alberti KG, Shaw J. Global and social implications of the diabetes epidemic. Nature 2001; 414: 782–87.
Argument for partial nicotine deregulation Sir—Tobacco products enjoy growing worldwide popularity, despite the staggering health toll attributed to them. As Nigel Gray and Peter Boyle discuss in their Commentary (Sept 13, p 845),1 the most effective response to this pandemic may be a policy of harm reduction. They encourage “clean addictive recreational nicotine delivery”, and cite a decade-old call for an accommodating policy.2 Regarding the potential harms of clean addictive nicotine, they conclude: “Any risks linked with such a product are dwarfed by the magnitude of the tobacco problem.” A quantitative analysis of the probable health effect of a nicotine inhaler By reinforces this expectation.3 extending the methods of the SAMMEC (Smoking Attributable Morbidity, Mortality and Economic Costs) computer programs,4 the analysis predicted how the USA’s smokingrelated mortality in 1990 would have changed if clean nicotine inhalers had completely displaced cigarettes. In plausible scenarios, an addictive nicotine inhaler should benefit public health, even if everyone used it. Reductions in current smokers’ disease burden should improve public health even more than reducing smoking prevalence to 12%. Public health could improve with a policy that also reduces public investments in tobacco control and related research, smoking-related fires,
1764
smoking breaks, withdrawal symptoms at work, and environmental tobacco smoke. In addition, deregulation preserves any benefits of nicotine use and offers an alternative tax base as tobacco sales decline. The argument for deregulating nicotine demands serious consideration. Gray and Boyle quote that “There is no compelling objection to the recreational and even addictive use of nicotine provided it is not shown to be physically, psychologically, or socially harmful to the user or to others”. Snus (Swedish oral moist snuff) and nicotine replacement products meet these criteria. These forms of nicotine are so safe that one criterion for nicotine dependence according to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders— continued use in spite of harm5—seems irrelevant. However, cigarettes briefly deliver higher concentrations of nicotine to the arterial circulation than any other currently available tobacco product. The consequences in human beings of long-term inhalation of nicotine without smoke are unknown. Unexpected consequences, perhaps involving new disease processes or increased abuse of other substances, could temper the public-health gains that many of us expect. Trials of clean, addictive nicotine as an alternative to smoking cessation would reveal such problems. Gray and Boyle remind us that manufacturers investing in these studies need reassurance from regulators that recreational nicotine is tolerable. Other unintended consequences could include increased smoking initiation, delayed smoking cessation, increased teenage addiction to nicotine, and increased nicotine use in pregnancy. Prospective smokers might reason that they can switch to nicotine inhalers when cigarettes start to injure them. Teenagers might develop expensive addictions before they understand the financial burden. Furthermore, manufacturers should bear much responsibility for devising safe delivery systems. These concerns are reasons to regulate the manufacturing, advertising, and youth sales of addictive nicotine products, much as we regulate cigarettes, for the immediate future. Clean, addictive, nonprescription, recreational nicotine deserves enthusiastic study by and encouragement from the tobacco control community, but for now, only partial deregulation. Walton Sumner General Medical Sciences, Washington University School of Medicine, Campus Box 8005, 660 South Euclid Avenue, St Louis, MO 63110, USA (e-mail: [email protected])
1 2 3
4
5
Gray N, Boyle P. The future of the nicotineaddiction market. Lancet 2003; 362: 845–46. Anon. Nicotine use after the year 2000. Lancet 1991; 337: 1191–92. Sumner W 2nd. Estimating the health consequences of replacing cigarettes with nicotine inhalers. Tob Control 2003; 12: 124–32. Nelson DE, Kirkendall RS, Lawton RL, et al. Surveillance for smoking-attributable mortality and years of potential life lost, by state—United States, 1990. Morb Mortal Wkly Rep CDC Surveill Summ 1994; 43: 1–8. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Washington DC: American Psychiatric Association, 1994.
Global burden of COPD in Japan and Asia Sir—P M A Calverley and Paul Walker (Sept 27, p 1053)1 have comprehensively summarised that chronic obstructive pulmonary disease (COPD) is a major cause of death and disability worldwide, and that the burden of disease will continue to increase over the next 20 years. However, they do not point out that the weight of this burden is very different between Asian countries and those of Europe and the USA. Because tobacco consumption is the main contributing factor in COPD, the prevalence of the disease will increase over the next 20 years in the USA and Europe, but will reach a plateau after that. However, the disease prevalence is likely to keep increasing for more than 40 years in Japan and Asia. China, the country with the largest production and consumption of tobacco worldwide, has seen a striking increase in consumption over the past 2 decades. A survey found that the average daily consumption of tobacco per person in China rose from one cigarette in 1952 to ten cigarettes in 1990—a rate similar to that of the USA 40 years earlier.2 The survey also estimated that the prevalence of COPD was 3% of the total population, but could increase to 10%. In Japan, a national survey revealed that 220 000 people had COPD in 1997, but the NIPPON COPD epidemiology study revealed that more than 5·3 million people—8·5% of the population aged 40 years and older— should be diagnosed as having COPD.3 Tobacco consumption was still increasing, particularly among women. Past occupational exposures to dust, airborne chemicals, and chemical products have also been suggested to significantly increase the likelihood of COPD, independent of the effects of smoking.4 On this point, the USA, Europe, and Asia differ greatly.
THE LANCET • Vol 362 • November 22, 2003 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet publishing Group.