The independent and combined effects of lifetime smoke exposures and asthma as they relate to COPD

Abstract

Chronic obstructive pulmonary disease (COPD) is part of a worldwide tobacco-related disease epidemic, and is associated with progressive airflow obstruction and varying degrees of emphysema and/or hyperinflation. Greater focus has been placed recently on the potential for early life factors to influence the development of COPD, based on the premise that delayed lung growth during childhood and adolescence might predispose to lung disease in later life. For most people, the adverse effects on lung function of adult and early childhood factors are additive, which provides no additional incentive for current smokers to quit. However, if there is a (synergistic) interaction between active smoking and asthma, smoking cessation is likely to have a greater lung function benefit for the smoker who is also asthmatic, especially if quitting occurs at an early age. This article critically evaluates the evidence for the independent associations of lifetime asthma, smoking and smoke exposures with airflow obstruction, plus their interaction when multiple factors are present.

Keywords::

• active smoking
• asthma
• COPD
• Interaction
• lung function
• second-hand smoke
• tobacco

Financial & competing interests disclosure

MJ Abramson has received an investigator initiated grant for unrelated research from Pfizer. MJ Abramson has received conference support from Boehringer-Ingelheim and has also received consultancy payment from AstraZeneca. CF McDonald serves on advisory boards for Novartis, Pfizer and GlaxoSmithKline. CF McDonald has received honoraria for lecturing from Boehringer-Ingelheim and Novartis and has developed educational presentations from AstraZeneca. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• COPD is a major global health problem that is considered to be largely preventable and predominantly due to active smoking in Westernized countries.

• While the variation in lung function for a given smoking history might be explained by an individual's susceptibility, interactions with environmental risk factors other than active smoking may well play a role.

• Many studies in adults that have examined asthma–smoking interactions have used pre-bronchodilator spirometry, which is not appropriate for the diagnosis of COPD.

• Asthma has been found to augment the adverse effect of active smoking on post-bronchodilator airflow obstruction when both factors are present, particularly for those with atopic sensitization and current asthma symptoms, and this might have important implications for the development of COPD at community and individual levels.

• For interactions that involve active smoking, the additional deficit in lung function beyond the sum of individual associations provides another compelling reason for current smokers to quit, especially at an earlier age.

• Further research is needed to address whether maternal smoking might be a predisposing factor in the development of COPD for adult offspring.

• Given increasing recognition of the importance of the overlap between asthma-related irreversible airflow limitation and smoking-related COPD, further revisions of the nomenclature and change in policies around therapeutic trials may well be indicated.

Notes