Chronic Obstructive Pulmonary Disease Disease Background

Introduction 

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with an overall severity contributed by exacerbations and comorbidities. It should be suspected in any patient who has a chronic cough, sputum production, or dyspnea with or without a history of risk factors for the disease.

It is considered a group of lung conditions which is characterized by chronic respiratory symptoms of dyspnea, cough, and sputum production, as a consequence of abnormalities of the airways (eg bronchitis, bronchiolitis) and/or alveoli (eg emphysema) which cause persistent and often progressive airflow obstruction.

The persistent airflow limitation is usually progressive and is associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Chronic airflow limitation is caused by a mixture of small airway disease and parenchymal destruction.

Epidemiology 

The estimated global prevalence of COPD is 10.3% based on the Burden of Obstructive Lung Disease (BOLD) study. Its prevalence is higher in smokers and ex-smokers, individuals ≥40 years of age, and men. It is considered the third leading cause of mortality worldwide. Based on the Epidemiology and Impact of COPD (EPIC) Asia population-based survey, there is a high prevalence of the disease in the Asia-Pacific Region.

In 2010, it was considered the second leading cause of death in South Asia according to a report by the World Bank. According to the Indian Study of Asthma, Respiratory Symptoms and Chronic Bronchitis’ (INSEARCH) study, the prevalence of chronic bronchitis was 3.5% among adults aged >35 years old. Several systematic reviews in India concluded that the prevalence of COPD in the country ranged from 5.5-7.4%.

The prevalence of COPD in China was estimated to be 4.4-16.7%. According to the most recent Chinese national survey, it encompasses almost 25% of the cases worldwide.

In Hong Kong, the Centre for Health Protection reported that in 2014-2015, the prevalence of the disease was 0.5% affecting a total of 29,900 individuals aged ≥15 years old. It also resulted in 30,000 hospital admissions and accounted for 2.7% of mortality in 2017, mostly among those ≥65 years old.

In Korea, the Korean Academy of Tuberculosis and Respiratory Diseases reported that the prevalence of the disease was at 13% in 2008, which was almost similar to the report by the Korea National Health and Nutrition Examination Survey (KNHANES) at 13.1-14.6% in 2010-2015.

In Southeast Asia, the prevalence of the disease is <5% in Malaysia, 7.1% among males and 1.9% among females in Vietnam, 3.5-20.8% in the Philippines, and 3.7-6.8% in Thailand. Singapore shows a similar prevalence of the disease as compared globally, highest among smokers and older people, but without gender predilection.

Pathophysiology 

COPD is a consequence of complex, cumulative, and dynamic gene-environment interactions occurring over the individual's lifetime resulting in lung damage and/or alteration of normal lung development or the aging process.

Inflammatory and structural changes lead to increased severity of airway obstruction. An increased number of inflammatory cells (eg macrophages in peripheral airways, lung parenchyma, and pulmonary vessels, activated neutrophils, and lymphocytes) together with epithelial cells and other structural cells release multiple inflammatory mediators attracting inflammatory cells from the circulation leading to the amplification of the inflammatory process and causing structural changes. Chronic inflammation leads to structural changes, small airway narrowing, luminal exudates in small airways, and lung parenchyma destruction causing loss of alveolar attachments to the small airways and decreasing the elastic recoil of the lung, which in turn reduces the ability of the airways to remain open during expiration. COPD may also be secondary to oxidative stress.

Additionally, structural changes may be due to an imbalance between proteases from inflammatory and epithelial cells responsible for breaking down connective tissue components and antiproteases. This includes peribronchial fibrosis and interstitial opacities.

These structural abnormalities in the airways, alveoli, and pulmonary circulation lead to abnormal pulmonary gas exchange. Inflammatory and structural changes can also lead to gas trapping and hyperinflation.

Airflow obstruction is due to small airway disease, increasing airway resistance and parenchymal destruction. It may also be caused by the loss of small airways. Parenchymal destruction secondary to emphysema can cause decreased lung diffusing capacity. 

Risk Factors 

Host Factors

Individuals may have reduced maximal attained lung function due to processes during gestation and childhood affecting lung growth and development.

Reduced lung function can be associated with a history of severe childhood respiratory infections. Previous tuberculosis is also a known risk factor for COPD.

Genetic factors (eg deficiency of alpha-1 antitrypsin) and other genetic conditions are also risk factors for the development of COPD.

Airway hyper-responsiveness can exist without a clinical diagnosis of asthma. In population studies, airway hyper-responsiveness has been shown to be an independent predictor of COPD and respiratory mortality. Airway hyper-responsiveness can be an indicator of the risk of excess decline in lung function in patients with mild COPD.

Patients with chronic bronchitis are likewise at risk of developing COPD.

Exposures

Tobacco smoke is the most commonly encountered risk factor for COPD, and this includes a history of tobacco use or prolonged exposure to second-hand smoke. Smoking during pregnancy can put the fetus at risk.

Other risk factors include exposure to occupational dust and chemicals, air pollution, smoke from home cooking and heating fuels, and low socioeconomic status.