Normal ageing of the lung: implications for diagnosis and monitoring of asthma in older people

Two of the most important changes involve structures in the chest wall. The first is an age-related increase in the stiffness of the chest wall due to a change in shape, calcification and articulations of the rib cage. The second is a decrease in strength of the respiratory muscles, related to multiple factors, including generalised degenerative changes in muscle, nutritional status and the impact of changes in chest wall configuration on the force generation capacity of the diaphragm. These alterations reduce the capacity for exercise and result in increased oxygen demand by the respiratory muscles at any given level of exercise. Clinical assessment of elderly patients with airway obstruction should be tempered by awareness that older subjects have smaller tidal volumes and higher frequencies of breathing1 and that there is a marked attenuation in the ventilatory responses to hypoxaemia and hypercapnia.2

With increasing age, subtle changes in the connective tissue of the lungs also occur. These include a decrease in elastic fibres and increase in type 3 collagen, together with changes in crosslinking and fibre orientation.3-5 These changes alter the elastic properties of the lung parenchyma and the airway, with loss of elastic recoil. Structural changes in the lung parenchyma, such as reduced number of alveoli and an increase in the size of alveolar ducts, reduce the alveolar surface area.6,7 This has important functional consequences for gas exchange, and contributes further to the loss of lung elastic recoil by reducing surface tension because of the increased radii of curvature of the alveolar spaces. There is no evidence of changes in the cells producing surfactant or of the composition of surfactant. The loss of lung elastic recoil, together with increased compliance of the intraparenchymal airway,8 favours airway closure. There is an age-related increase in the lung volume at which dependent airways close.9 In elderly people, this may exceed the functional residual capacity, resulting in airway closure during tidal breathing. This is an important mechanism accounting for the increased alveolar–arterial difference for oxygen with age.

As lung elastic recoil transmitted to the airway wall by alveolar attachments is a force tending to keep airways open, it constitutes a load against which airway smooth muscle must contract. Theoretically, loss of elastic recoil would thus make the ageing lung more vulnerable to bronchospastic stimuli, although increased airway responsiveness has not been found in elderly people without asthma.10 There is a decrease in β2-receptor function with age11 that has not been reported for cholinergic receptors.12 It might, therefore, be expected that anticholinergic agents in the elderly may be relatively more effective bronchodilators than β agonists. However, clinical guidelines at present do not suggest a preference for use of anticholinergic agents in elderly patients with asthma.

As most provoking stimuli in asthma are airborne and most asthma medications are administered by inhalation, it is important to consider whether there are any differences in particle deposition or aerosol distribution in elderly people. There is little information on these issues, although current evidence suggests that age-related changes in aerosol deposition are small.13 The ability of elderly patients with poor respiratory muscle strength to generate sufficient inspiratory flow to optimise lung deposition from dry powder inhalers has not been systematically studied. On the other hand, there is evidence that mucociliary clearance from the lung is impaired in elderly people, and this may allow inhaled noxious particles or allergens to remain longer in the airway.14

There is some evidence that the ageing lung may be subject to chronic low-grade inflammation in the absence of overt lung disease. Bronchoalveolar lavage has demonstrated increased levels of neutrophils, interleukin 8 and neutrophil elastase in the lungs of elderly people.15,16 These changes are similar in nature, but not in magnitude, to those seen in chronic obstructive pulmonary disease (COPD). Presumably this is related to longstanding exposure to atmospheric particles and pollutants, including sidestream (“environmental”) tobacco smoke (ie, tobacco smoke produced by burning cigarettes that is not inhaled by the smoker).

Any possible interaction between this underlying inflammation and the inflammatory processes involved in asthma or diagnostic difficulties in the overlap of asthma with COPD remain speculative.

Several other issues may affect asthma monitoring in elderly people. There is some evidence of an age-related blunting of patient perception of airway narrowing. This has been demonstrated with internal resistive loads (methacholine-induced bronchoconstriction)10 and with added external loads.17 There is also a reduction in the sensitivity of the cough reflex.18 This raises a potential problem both with early diagnosis and with symptom-based action plans. Simple objective measures of lung function can generally be performed in elderly patients, but many normal reference values are deficient for people over 80 years of age.

In summary, changes in the structure and function of the respiratory system in elderly people amplify the deleterious effects of a given degree of airway narrowing in asthma. These factors, together with altered perception of airway obstruction, may give rise to a different expression of the disease. This may affect the diagnosis and monitoring of asthma, as well as its differentiation from other obstructive diseases.