The possible role of bacterial, viral and fungal infections in the development, exacerbation and treatment of asthma are discussed. Although bacterial allergy has in the past been advocated as an important etiologic factor for asthma, the evidence is inconclusive. Hyposensitization with bacterial antigens is no longer an accepted treatment. Bacterial infection of the nasal sinuses and bronchi may exacerbate an asthmatic attack and in some cases patients benefit from antibiotic therapy. However, bacterial infections in asthma and allergic rhinitis do not always require treatment and if treated this is not sufficient alone to reverse symptoms. Opinions vary as to the importance of viral infections. There is evidence that the immunologic consequences of intrabronchial infection with Aspergillus fumigatus may cause exacerbations of asthma.

Airflow limitation in exercise-induced asthma is related to the thermal events in the intrathoracic airways. This article reviews the present knowledge about the exchange of respiratory heat and water. The evidence for the various theories proposed for the basic mechanisms involved in exercise-induced asthma are discussed. The evidence suggests that exercise-induced airways obstruction may be a vascular phenomenon dependent on the rapidity and magnitude of airway rewarming. Obstruction is induced if a thermal gradient exists at the end of exercise and the greater the gradient the greater the resultant hyperemia and edema. The basic mechanism of control of reactivity is still not known and directions for future research are outlined.

Asthma is a heterogenous disease triggered by a large number of different stimuli. This article presents a theory of the metabolic mechanisms of asthma. The theory is based on the growing understanding of the activity of lysophosphatidylcholine (LPC). Since the effect of LPC on cell membranes, membrane bound enzymes and the various types of cells involved in the pathogenesis of asthma, this may represent a unifying link between the various types of asthma.

This article review recent developments in the study of occupational asthma and implications for the overall understanding of asthma. Occupational asthma is a clinical syndrome caused by many different agents. Contribution of studies of experimental inhalation challenge using occupational agents to the knowledge of asthmatic reactions and their mechanisms is discussed. Investigations in the occupational environment into predisposing factors and persistence or recovery after exposure to an allergic agent or nonspecific irritant are reviewed. Approaches to diagnosing asthma in the occupational environment and to assessing functional impairment and disability are outlined. Directions for future research are identified.

The natural history of lung growth and senescence in individuals with variable air flow obstruction or clinical asthma has been given less attention than the natural history of chronic airflow obstruction. This article reviews the information available on lung growth during childhood in persons with asthma and on the rate of decline of lung function during adult life in individuals with asthma or bronchial hyperresponsiveness. Lung growth appears to be relatively normal in most children with asthma but is reduced throughout childhood and adolescence in those with severe and persistent symptoms. It is not known if this reflects a failure to reach full growth or reversible bronchoconstriction. During adult life, clinical asthma is associated with a slight increase in the rate of decline in FEV1. In the middle-aged and elderly smoker it is virtually impossible to separate chronic bronchitis and asthma. Bronchial hyperresponsiveness appears to be associated with an increase in the rate of decline of lung function but it is not clear if this is a result of airway disease due to smoking or a true risk factor. Further research needs are identified.

Data from various different types of cross-sectional studies are reviewed in order to examine hypotheses about the etiology of asthma and to more precisely define its relationship with nonspecific bronchial hyperreactivity (NSBH). Although cross-sectional studies have not clarified the precise etiologic links, they have established that NSBH and atopy are linked to the occurrence of asthma and to each other. In children, evidence supports the hypothesis both that atopy is a cause of asthma and that atopic diathesis is the most frequent trigger for NSHB. In adults, the associations are more complex, although in a small subset findings are similar to those in children. It is concluded that further general population-based or clinical epidemiologic cross-sectional studies based on questionnaires will contribute little more to explaining these associations. Criteria are presented for the further application of case-control studies to maximize their use in examining hypotheses of asthma etiology.

The nature of the underlying defect in asthma is still unclear. This article discusses where the primary problem might lie, starting with the assumption that it is likely to be in neurohumoral control, bronchial smooth muscle or cellular dysfunction with increased release of mediators. The weight of the evidence suggests that the latter is most likely. If true, the question of why this occurs still remains.

Mast cells are found beneath the basement membranes, near blood vessels in the submucosa, adjacent to submucous glands, scattered throughout the muscle bundles, in the interalveolar septa and in the bronchial lumen. The evidence that mast cells and mast cell-derived mediators play a role in allergic and non-allergic asthma is discussed. In allergic individuals, inhalation of specific allergens leads to mast cell degranulation and release of mediators. Many of the pathologic features of asthma may be attributed to the effects of mast cell-derived mediators. Their role is clear in allergic asthma and the presence of mast cell derived mediators in the plasma of individuals with exercise-induced and nocturnal asthma suggests involvement in other forms of asthma as well.