Inhalation of noxious particles and reactive oxygen species, particularly from cigarette smoke, is undoubtedly the most significant risk factor for chronic obstructive pulmonary disease (COPD). A number of other risk factors have also been established.
Cigarette smoke is well established as the most significant risk factor for the development and progression of COPD. However, it is now recognised that 10–20% of adults with COPD have never smoked, and that not all people with the same smoking history will develop COPD, indicating that genetic, gender, socioeconomic status and environmental factors influence the risk of COPD development.1,2 Nevertheless, around 50% of lifelong smokers will develop COPD.3
Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of lung function decline and a greater COPD mortality rate compared with non-smokers.2
In a meta-analysis of 67 population-based studies (representing >111,000 cases of COPD from 28 countries), the prevalence of COPD was significantly higher among smokers (15.4%) and ex-smokers (10.7%) than among individuals who had never smoked (4.3%).3 Among smokers, the prevalence of COPD according to Global InitiatiIn a meta-analysis of 67 population-based studies (representing >111,000 cases of COPD from 28 countries), the prevalence of COPD was significantly higher among smokers (15.4%) and ex-smokers (10.7%) than among individuals who had never smoked (4.3%).4 Similarly, in a large prospective population-based cohort study, 17.8% (1663/9169) of ever smokers – current or former – had COPD (incident and prevalent cases) compared with 6.4% of never smokers (318/4997).5 Among smokers, the prevalence of COPD according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria was 11% in those aged 46–47 years, 42% in those aged 61–62 years, and 50% in those aged 66–67 years.6 Prevalence of COPD is therefore highest in countries where cigarette smoking is common. Smoking cessation is the single most effective intervention in reducing the risk of developing COPD and disease progression.2
According to the GOLD strategy document, occupational exposure to noxious particles (including organic and inorganic dusts, chemical agents and fumes) is an under-appreciated risk factor for COPD.2 A meta-analysis of 15 epidemiological studies evaluated the correlation between exposure to biomass smoke and development of COPD worldwide, and found that the odds ratio for developing COPD was 4.30 in men, whilst in women it was 2.73,7 establishing biomass smoke as significant risk factor for development of COPD, and presenting it as a particular challenge in low- and middle-income countries.8
The role of outdoor air pollution in causing COPD is unclear, but appears to be small in comparison with that of cigarette smoking.2 Two studies in northern Europe found an increased risk of COPD in individuals living in close proximity to busy roads.9,10 In the developing world, exposure to indoor air pollution from open fires appears to be a significant risk factor for COPD,2,7,8 and inhalation of passive cigarette smoke may also be responsible for a proportion of COPD diagnoses in people who have never smoked. In the Burden of Obstructive Lung Disease Initiative (BOLD) study, never-smokers (defined as smoking <20 packs of cigarettes in a lifetime; n=4291) made up 42.9% of the study population.11 Among never-smokers, 12.7% met the criteria for COPD Stage I+; 6.8% had mild (GOLD Stage I) and 5.9% clinically significant (GOLD Stage II+) COPD. Severe childhood respiratory tract infections, exposure to passive smoking and reported asthma were associated with irreversible airways obstruction in never smokers in this study.
Reduced lung function owing to the impairment of lung development is a risk factor for COPD. Consequently, any factor that adversely affects lung growth during foetal development and childhood could increase an individual’s risk of developing COPD during adulthood.2 Low birth weight and acute respiratory infections during childhood have both been linked to reduced pulmonary function in later life.2,12
The genetic risk factor that is best documented in COPD is a severe hereditary deficiency of alpha-1 antitrypsin (AAT; an important protease inhibitor). This rare recessive trait is seen in all ethnic and racial groups globally13 and may account for 2–3% of COPD cases.14
The intervention with the highest capacity for altering the natural history of COPD is smoking cessation.2
Smoking cessation in middle-aged patients with COPD improves lung function, alleviates symptoms such as dyspnoea and cough, reduces the frequency of exacerbations and lowers risk of mortality.15 Reduction of total personal exposure to occupational dusts, fumes and gases and to indoor and outdoor air pollutants is also advised.2