Risk Factors For COPD

(Based on the 2005 update of the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease – sponsored by NHLBI, and WHO.)

• Host Factors
• Exposures
• Classification of Severity

Risk factors for COPD include both host factors and envi­ronmental exposures, and the disease usually arises from an interaction between these two types of factors. The major environmental factors are tobacco smoke; heavy exposure to occupational dusts and chemicals (vapors, irritants, fumes); and indoor/outdoor air pollution.

The role of gender as a risk factor for COPD remains unclear. In the past, most studies showed that COPD prevalence and mortality were greater among men than women^36-39. More recent studies^1,4O  from developed coun­tries show that the prevalence of the disease is almost equal in men and women, which probably reflects chang­ing patterns of tobacco smoking. Some studies have in fact suggested that women are more susceptible to the effects of tobacco smoke than men^38,41. This is an impor­tant question given the increasing rate of smoking among women in both developed and developing countries.

Host Factors

Genes: It is believed that many genetic factors increase (or decrease) a person's risk of developing COPD. The genetic risk factor that is best documented is a rare hereditary deficiency of alpha-1 antitrypsin^42,44. Premature and accelerated development of pan lobular emphysema and decline in lung function occurs in many smokers and nonsmokers with the severe deficiency, although smoking increases the risk appreciably.

Exploratory studies have revealed a number of candidate genes that may influence a person’s risk of COPD, including ABO secretor status, microsomal epoxide hydrolase, glutathione S-transferase, alpha-1 antichymotrypsin, the complement component GcG, cytokine TNF-alpha, and microsatellite instability.  However, when several studies of a given trait are available, the results are often inconsistent.  Several of these genes are thought to be involved in inflammation, and therefore are related to potential pathogenic mechanisms of COPD.

Airway Hyperresponsiveness: Asthma and airway hyper­responsiveness, identified as risk factors that contribute to the development of COPD₄₅, are complex disorders related to a number of genetic and environmental factors. How they influence the development of COPD is unknown. Airway hyperresponsiveness may also devel­op after exposure to tobacco smoke or other environmen­tal insults and thus may be a result of smoking-related airway disease.

Lung Growth: Lung growth is related to processes occurring during gestation, birth weight, and exposures during childhood^46-50.  Reduced maximal attained lung function (as measured by spirometry) may identify individuals who are at increased risk for the development of COPD51.

Exposures

Tobacco Smoke: Cigarette smoking is by far the most important risk factor for COPD and the most important way that tobacco contributes to the risk of COPD. Cigarette smokers have a higher prevalence of lung-function abnormalities and respiratory symptoms, a greater annual rate of decline in FEV 1, and higher death rates for COPD than nonsmokers. Pipe and cigar smokers have higher COPD morbidity and mortality rates than nonsmokers, although their rates are lower than those for cigarette smokers⁵². Not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual's risk. Passive exposure to cigarette smoke may also contribute to respiratory symptoms and COPD by increasing the lungs' total burden of inhaled particulates and gases^36,53,54. Smoking during pregnancy may also pose a risk for the fetus, by affecting lung growth and development in utero and possibly the priming of the immune system⁵⁰.

Occupational Dusts and Chemicals: When the expo­sures are sufficiently intense or prolonged, occupational dusts and chemicals (vapors, irritants, fumes) can cause COPD independently of cigarette smoking and increase the risk of the disease in the presence of concurrent ciga­rette smoking⁵⁶. Exposure to particulate matter, irritants, organic dusts, and sensitizing agents can cause an increase in airway hyperresponsiveness⁵⁷, especially in airways already damaged by other occupational exposures, cigarette smoke, or asthma.

Outdoor and Indoor Air Pollution: High levels of urban air pollution are harmful to persons with existing heart or lung disease. The role of outdoor air pollution in causing COPD is unclear, but appears to be small when com­pared with cigarette smoking. Indoor air pollution from biomass fuel, burned for cooking and heating in poorly vented dwellings, has been implicated as a risk factor for the development of COPD^58-67.

Infections: A history of severe childhood respiratory infection has been associated with reduced lung function and increased respiratory symptoms in adulthood⁵¹. However, viral infections may be related to another factor, e.g., low birth weight, that itself is related to COPD.

Socioeconomic Status: There is evidence that the risk of developing COPD is inversely related to socioeconomic status⁶⁸, It is not clear, however, whether this pattern reflects exposures to indoor and outdoor air pollutants, crowding, poor nutrition, or other factors that are related to socioeconomic status^67,69.

Classification of Severity

For educational reasons, a simple classification of disease severity into five stages is recommended (Table 1). The management of COPD is largely symptom driven, and there is only an imperfect relationship between the degree of airflow limitation and the presence of symptoms. The staging, therefore, is a pragmatic approach aimed at practi­cal implementation and should only be regarded as an educational tool, and a very general indication of the approach to management.

The staging is based on airflow limitation as measured by spirometry, which is essential for diagnosis and provides a useful description of the severity of pathological changes in COPD.

References

This information has been approved by Scott Glenn Van Da Walker, C-FNP, MSN, RN (March 2006)