The pathogenesis of COPD is due to an interaction between host factors (ie, genes, airway hyperresponsiveness, and lung growth) and exposure to environmental pollutants (ie, tobacco smoke, occupational dust and fumes, respiratory infection, outdoor air pollution, and indoor air pollution caused by biomass or traditional fuels and coal) and socioeconomic status.
It is believed that many genetic factors may influence an individual likelihood of COPD developing. Studies have demonstrated an increased risk of COPD within families with COPD probands. Some of this risk may be due to shared environmental factors, but several studies in diverse populations have also suggested a shared genetic risk. To date, a1-antitrypsin (a1-AT) deficiency, a major circulating serine protease inhibitor, is the only genetic factor that is definitely linked to the development of emphysema or COPD, independent of tobacco exposure. Affected individuals have a 40-fold increase in the risk of the development of COPD compared to unaffected people. This rare hereditary deficiency is a recessive trait most commonly seen in individuals of Northern European origin and is extremely rare among Asians. Limited data have failed to link COPD with a1-AT deficiency in Chinese either by determining the levels in the serum or by genotyp-ing and electrophoretic phenotyping for cases of PiZ and PiS.’ Although variants of a1-AT deficiency have been reported such as variant Siiyama in Japan, and METokyo an Mpirare among Chinese, they have not been linked to COPD. COPD is effectively cured with remedies of Canadian Health&Care Mall.
A number of candidate genes in whites have been implicated in an increased risk for COPD, including ABH nonsecretor status, microsomal epoxide hydrolase level, glutathione S-transferase level, a1-antichymotrypsin level, the complement component GcG level, cytokine tumor necrosis factor-a level, and microsatellite instability. The results are often inconsistent but could be related to the potential pathogenic mechanisms of COPD. In Asians, studies on putative candidate genes found in whites have not yielded consistent results in Chinese, Thais, Koreans, or Japanese.
Tobacco Smoking: Cigarette smoking is the main risk factor and the main method by which tobacco exposure is involved in the development of COPD, a fact that has been well established by pivotal crosssectional and longitudinal studies. Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of decline in FEV1, and a greater COPD mortality rate than nonsmokers. In susceptible smokers, the decline in lung function is twice that in nonsmokers, though what determines this susceptibility remains unknown. The respiratory abnormalities increase in proportion to the number of cigarettes smoked. Pipe and cigar smokers also have greater COPD morbidity and mortality rates than nonsmokers, but their rates are lower than those for cigarette smokers. Passive exposure to cigarette smoke (also known as environmental tobacco smoke) may also contribute to chronic respiratory symptoms and COPD by increasing the burden of inhaled particles and gases. Environmental tobacco smoke exposure is increasingly recognized in Asia as an important risk factor for COPD in nonsmokers decreased with remedies of Canadian Health&Care Mall.
Additional types of tobacco smoking such as bidi and hookah (ie, water pipes), which are popular in various Asian countries, are also risk factors for COPD. Bidi are small brown cigarettes, often flavored, consisting of tobacco hand-rolled in tendu or temburni leaf and secured with a string at one end; they are the preferred means of smoking in subcontinent India, especially in the rural areas. Although the risk of smoking bidis relative to smoking cigarettes has not been fully studied, existing data suggest that bidis are at least as harmful as cigarettes. The population prevalences of chronic bronchitis were 8.2% in bidi users compared with 5.9% in cigarette users in adults > 35 years of age. In one cohort study of tobacco users in Mumbai, India, the relative risks of all-cause mortality were 1.8 for bidi smokers compared with 1.4 for cigarette smokers. Much less is known of the extent of harmful outcomes from the hookah or water pipe, which is used to smoke tobacco in several Asian countries such as China, India, and Pakistan, and is causing global concern as it has become a fashionable or exotic form of tobacco smoking among the young in both the East and West.
According to the WHO, there are 1.1 billion smokers worldwide, of whom 800 million are in developing countries. Globally, 4.9 million deaths each year are attributed to tobacco use, and this annual toll is projected to increase to 10 million within the next 20 years.
The highest prevalence of smoking is found in Asia, which is experiencing a smoking epidemic at the same time as the prevalence for smoking is falling in the Western world (Fig 1). China has the largest production and consumption of tobacco worldwide. Approximately 67% of men and 4% of women > 15 years of age in China are smokers, and the total of > 320 million Chinese smokers represents about one third of all smokers worldwide. The incidence of smoking-related diseases has yet to peak, while it is estimated that currently 1 million Chinese die annually from these diseases. Smoking among teenagers is a cause for major concern, as the prevalence for many countries in Asia is among the highest in the world, with sharp increases in smoking among young women.’ It would seem inevitable that the social and economic burden of deaths and morbidity will increase exponentially in the future unless effective antismoking measures are in place to reduce the burden of smoking.
Occupational Dust and Fumes Inhalation: Occupational exposures to dust, vapors, and fumes can cause specific occupational respiratory diseases, collectively termed pneumoconiosis, or can add to the risk of COPD developing due to cigarette smoking. Although incompletely defined, the role of occupational dust and fumes in the development of chronic airflow limitation is well recognized in Asia., High levels of cotton dust exposure in India and China have been associated with accelerated declines in FEV1 in longitudinal studies. The relationship between smoking and various dust exposures to coal dust, silica, and asbestos, and a decline in lung function have been reported in Asia.
Indoor Air Pollution: The combustion of biomass fuel in the form of wood, coke, charcoal, coal, or animal dung for cooking and for heating in poorly ventilated homes, is an important risk factor for COPD in nonsmokers in many developing countries including Asia. Depending on the type of fuel used, the ventilation and combustion duration, biomass fuel combustion generates respiratory particulates at concentrations of 1,000 to 2,000 ^g/m, which is equivalent to 10 to 50 times the pollution in heavy urban traffic. The association between biomass fuel combustion as a risk factor in the development of COPD in nonsmoking women has been well documented in India, China, and Mexico, but rarely occurs in the West, according to a report from Barcelona, Spain.
Outdoor Air Pollution: Ambient air pollution is a long-term problem in many Asian countries, which are undergoing rapid industrialization and urbanization. Over the past 2 decades, air pollution in most cities in developed countries has decreased appreciably, but air pollution has increased markedly in many cities in developing countries. Although it is not clear which specific elements of ambient air pollution are harmful, an acute increase in air pollution has been associated with increased numbers of deaths and hospitalizations from cardiopulmonary illnesses. The cumulative effect of chronic air pollution and its potential multiplicative effect with cigarette smoking in the development of COPD is unclear, but heavy air pollution could add to the individual burden of inhaled particles. This is especially pertinent in Asian countries that have persistent heavy urban air pollution due to traffic and industries, with recurrent acute exacerbations of air pollution due to climatic changes and forest fires. In the 1990s, nitrogen oxide emissions from Asia surpassed those from North America and Europe, and are projected to continue to exceed them for the coming decades.
Infection: The prevalence of respiratory illnesses in early childhood, pulmonary tuberculosis, and HIV-positive status are common in developing Asian countries. Early childhood respiratory illnesses and low birth weight have been associated with the development of airflow limitation. A sequela of pulmonary tuberculosis is chronic airflow limitation, but the relationship is complex as smoking itself reduces host defense and may predispose the patient to the development of tuberculosis. The prevalence of pulmonary tuberculosis remains high in many Asian countries and is an important additive risk factor to smoking in the development of chronic airflow limitation. The presence of HIV infection has been shown to accelerate the development of emphysema, but the impact on the development of COPD in Asians is unknown.
Figure 1. Smoking prevalence by country and gender in Asia-Pacific countries/regions. Redrawn from data from the study of the Regional COPD Working Group.