Chronic Obstructive Pulmonary Disease

August 5, 2011

Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the United States, is a chronic, progressive disease encompassing both emphysema and chronic bronchitis that lead to severe airflow obstruction. Emphysema causes irreversible lung damage by weakening and breaking the air sacs (the alveoli) within the lungs. As a result, elasticity of the lung tissue is lost, causing airways to collapse and airflow obstruction. Chronic bronchitis is an inflammatory disease that begins in the smaller airways (bronchiolitis) within the lungs and gradually advances to larger airways. It increases mucus in the airways and bacterial infections in the bronchial tubes, which, in turn, impedes airflow. Both components of COPD vary in proportion between affected individuals.

Table. Clinical development of COPD (American Thoracic Society)
Stage 1 Lung function (as measured by forced expiratory volume or FEV1 in 1 s) is greater than or equal to 50% of predicted normal lung function. There is minimal impact on health-related quality of life. Symptoms may progress during this stage, and patients may begin to experience severe breathlessness, requiring evaluation by a pulmonologist
Stage 2 FEV1 lung function is 35—49% of predicted normal lung function, and there is a significant impact on health-related quality of life
Stage 3 FEV1 lung function is less than 35% of predicted normal lung function, and there is a profound impact on health-related quality of life

The clinical development of COPD has been described by the American Thoracic Society based on lung function measured as the forced expiratory reserve volume in 1 s (FEV1) as shown in Table 1. In addition, physicians diagnose and classify COPD based on pulmonary function testing stated in the global initiative for chronic obstructive lung disease (GOLD) criteria from the World Health Organization. Individuals affected with COPD also present with certain symptoms that vary in severity, such as chronic cough, chest tightness, shortness of breath, an increased effort to breathe, increased mucus production, and frequent clearing of the throat. Among smokers, the natural history of COPD is that smoking behaviors often start during youth, lung function decline becomes apparent when smokers reach age 40-50 years, hospitalizations begin when smokers reach an age of about 69, and deaths may occur when they reach age 60-79. Research has been targeted to determine the genetic and environment interactions that are involved in the development of Chronic Obstructive Pulmonary Disease as well as gender-related differences associated with the onset of this lung disease.

Long-term cigarette smoking remains the major environmental risk factor (besides second-hand smoke or exposure to air pollution) for the development of Chronic Obstructive Pulmonary Disease, accounting for 80-90% of all cases and establishing a smoker as 10 times more likely than a nonsmoker to die of COPD; however, mounting evidence now suggests that genetic factors likely influence the variable susceptibility among individuals to develop Chronic Obstructive Pulmonary Disease.

In nonsmokers, the FEV1 (volume of air expelled on deep exhalation in 1 s) normally declines at a mean rate of about 20-30 ml per year during adult life; however, in most smokers, this mean rate of decline is increased to 30-45 ml per year, but in the subset of cigarette smokers who are susceptible to developing Chronic Obstructive Pulmonary Disease, the rate of decline is 80-100 ml per year. Therefore, even though there is evidence of a dose-response relationship between the severity of lung disease and the pack-years of cigarettes smoked (increased severity of lung disease with long-term smoking), only 15% of the variability in FEV1 is accounted for by smoking history. In addition, only a minority of cigarette smokers develop COPD, and frequent clustering of COPD has also been found in families. Such observations and recent evidence suggest a genetic predisposition to this lung disease.

There are a number of genetic associations that are currently being examined to determine how various genotype-environment interactions (interaction between the environment and the specific genetic makeup an individual has) are likely to be essential contributors to the development of COPD.

Gender-related differences are also apparent in severe, early onset COPD. Men have higher prevalence rates of COPD than women, which have been attributed to the historically higher rates of cigarette smoking in males. However, the increased rates of cigarette smoking in females have been associated with increasing rates of COPD in women. In addition, by 2000, the number of COPD deaths among women surpassed the number of men, even though the population-based mortality rates are higher among men.

Results from recent studies suggest that women may be more susceptible to the development of Chronic Obstructive Pulmonary Disease. More specifically, female first-degree relatives of early onset COPD probands (individuals with COPD) who smoke or have smoked cigarettes have increased susceptibility to severe airflow obstruction (but not of chronic bronchitis) and hence to the development of COPD. Determination of such gender-related differences in the development of COPD will enable better treatments for women and men.

SEE ALSO: Addiction, Adolescence, Lung transplantation, Nicotine, Smoking


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