Air Pollution and Occupational Exposure

The role of outdoor air pollution in the evolution of COPD is still controversial. Respiratory deaths in the UK reached a peak during the great smogs of the 1950's. Following the passing of the Clean Air Acts of 1956 and 1968 which established "smokeless zones" in populated areas and allowing only the use of smokeless fuels, the quality of British air has improved. The people that died during the smogs were people at the greatest risk, i.e. the elderly and infirmed, and those with chronic respiratory and cardiac problems. The question of whether atmospheric pollution itself can cause or contribute to the development of COPD is still uncertain.

Outdoor air pollution is very heterogeneous and is different in different areas. It is mainly comprised of particulates and gases with some background radioactivity. The particulates mainly originate from the incomplete combustion of solid fuels and diesel, ash and fine dusts. The main gaseous components are the various oxides of sulphur, nitrogen and carbon, again from the combustion of fossil fuels; hydrocarbons and ozone. Studies from the UK have shown a relationship between levels of atmospheric pollution and respiratory problems (particularly cough and sputum production) in both adults and children, and similar studies from the USA have confirmed these findings. Some studies have reported lower levels of lung function in adults living in highly polluted areas and this seems to related to pollution by acidic gases and particulates. As with the problem of smoking, there will be individuals who are more susceptible to the effects of atmospheric pollution than others.

Once the diagnosis has been established, the aims of treatment are to alleviate symptoms, prevent progression of disease and preserve optimum lung function to improve performance of activities of daily living and enhance quality of life. The European guidelines comment that the pharmacological and rehabilitation therapies that are currently being used in the management of COPD are not truly evidence based and thus a proportion of current practice is empirical.

The cause of expiratory airflow limitation in COPD is narrowing of the small airways caused by chronic inflammation, hypertrophy of the airway smooth muscle and enlargement of the bronchial mucus glands.. The bronchoconstriction that results differs from asthma in that it is mainly located in the small airways rather than medium sized ones, it is not due to increased bronchial wall smooth muscle activity, and it is largely irreversible, although there may be a degree of reversibility to bronchodilators in a proportion of patients. The bronchoconstriction that accompanies inflammation may also produce a reversible element. This is the rationale behind the use of bronchodilator agents in the treatment of COPD, and they are used to maximise airway calibre. However, not all patients will show a measurable spirometric response to bronchodilating agents, but most will report symptomatic and functional benefit despite the lack of objective evidence of improvement.