The prevalence of asthma has increased since 1998, with approximately 31 million Americans being diagnosed at some point in their lifetime.1 Among adults, 106 per 1,000 are diagnosed with asthma, compared with 122 per 1,000 children aged 0-17 years. Women have more frequent asthma attacks than men. In the elderly, the prevalence of asthma ranges from 3% to 17%.2 The incidence of asthma has been reported to be 3% in individuals older than 60 and <1% in those older than 70. However, these may be underestimations caused by an overlap between asthma, chronic bronchitis, and emphysema.

A great majority of asthma deaths occur in adults, with an incidence of 1.9 per 100,000 compared with 0.3 deaths per 100,000 children.1 Mortality is higher in women, African Americans, Puerto Rican Americans, and the poor.  

Adult-onset asthma comprises a complex group of reversible airway disorders, in contrast to childhood asthma, which is largely allergic in nature. Occurring in patients older than 18 years of age, adult-onset asthma may be acquired during adulthood, or it may manifest in adults from long-standing undiagnosed or clinically silent childhood disease.3 Asthma that is diagnosed after the age of 65 years is defined as late-onset asthma and may be missed because of comorbid conditions and the normal decline in lung function associated with aging.

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Etiology and risk factors

The development of asthma includes genetic predisposition; immunologic (atopy), neurologic, infectious, and psychologic factors; and, predominantly, inflammatory changes. Cigarette smoking, exposure to secondhand smoke, and air pollution may contribute to asthma and confound the distinction between asthma and chronic obstructive pulmonary disease (COPD) in adults. Gastroesophageal reflux disease (GERD) and atypical respiratory infections can trigger asthma exacerbations. Obesity and sleep-disordered breathing are independently related to the onset of asthma and increased nocturnal symptoms.3,4 Asthma can also be triggered by drugs and chemicals, e.g., aspirin, estrogen replacement, nonsteroidal anti-inflammatory drugs, paints, isocyanates, biologic enzymes, animal secretions, dusts, metal salts, laundry detergents, flour, and cockroach allergens.


Asthma is an inflammatory disorder with both acute and chronic components. A genetic predisposition is linked to several chromosomes. Genetic polymorphism results in variability in expression of the disease.3,5-8 A similar immunologic process occurs in both nonallergic asthma and allergen-mediated (immunoglobulin E [IgE]) asthma. Acute asthma can be subdivided into early-phase and late-phase reactions. Early-phase reactions occur after antigens challenge and stimulate the production of T lymphocytes (Th2), leading to IgE-activated mast cells and eosinophils, with subsequent release of chemical mediators and cytokines. Phospholipase in the cell membrane is also activated, generating potent leukotrienes, prostaglandins, and thromboxanes. These mediators and cytokines, as well as stimulation of the autonomic nervous system, cause severe smooth-muscle contraction, edema, mucus production, and hyperresponsiveness, resulting in reversible airflow obstruction.

The late-phase response occurs several hours later and is the dominant process in ongoing inflammation.5-8 Mediators released in the early phase promote a pro-inflammatory effect. A rise in the number of Th2 lymphocytes leads to increased chemokine and cytokine production, followed by further infiltration of eosinophils, neutrophils, and macrophages, perpetuating tissue damage. Destruction of tissue and replacement by connective tissue and goblet cells results in thickened basement membrane. Tissue repair and remodeling creates subsequent scar formation. Bronchial epithelial cells also participate by releasing chemical mediators and expressing antigen, causing epithelial shedding and destruction of cilia.