The risk factors for COPD are shown in table 1, and they are separated into host factors and exposures.

Table 1. - Risk factors for COPD

Host Factors

Little is known at present about the many genetic factors that probably increase (or decrease) a person’s risk of developing COPD.

The genetic risk factor that is best documented is a severe hereditary deficiency of α₁-antitrypsin, a major circulating inhibitor of serum proteases. Although α₁-antitrypsin deficiency is relevant to only a small part of the world’s population, it illustrates the importance of gene-environment interactions in the pathogenesis of COPD [9, 10]. All patients with airflow limitation and family history of respiratory illnesses, and patients presenting with airflow limitation at relatively early age (4th or 5th decade) should be evaluated for α₁-antitrypsin deficiency.

Exploratory studies have revealed a number of candidate genes that influence a person’s risk of COPD. 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 [9].

Airway hyperresponsiveness has also been demonstrated to be a risk factor for COPD [11]. The mechanism for this, however, is not clear. Some asthma patients also develop fixed airflow limitation and thus fulfil the requirements for COPD diagnosis [12].

Worldwide, COPD is more prevalent in males than in females. However, this is a consequence of the marked difference in smoking (and other) exposures between males and females. Recent data from several large studies suggest that females may in fact be more susceptible to the effects of tobacco than males. More data are needed to verify this. The importance of these new data, however, is that male sex is now clearly not a risk factor for COPD [13].

Exposures

Tobacco smoke is by far the most important risk factor for COPD worldwide [1, 10, 14].

It is helpful, conceptually, to think of a person’s exposures in terms of the total burden of inhaled particles. Each type of particle, depending on its size and composition, may contribute a different weight to the risk and the total risk will depend on the integral of the inhaled exposures. For example, tobacco smoke (active and passive tobacco smoke), outdoor and indoor air pollution, and occupational exposures probably act additively to increase a person’s risk of developing COPD.

Recent data from the US NHANES III survey indicate that occupation can be an important risk factor for COPD. The fraction of COPD attributable to work was estimated as 19.2% overall and 31.1% in never-smokers [2].

A subject’s socioeconomic background plays an important role that is not only the result of exposure to tobacco and occupational hazards [5]. Whether the effect is due to impaired growth of lungs and airways or an increased rate of infection is not clear.

In developing countries, indoor air pollution, due to the use of biomass fuels for heating and cooking, may pose a significant particulate burden and contribute to COPD, especially in females [1].