Asthma affects a large proportion of children in the United States, accounting for more than 14 million missed school days per year¹ and costing billions of dollars in health care use.² Furthermore, asthma morbidity disproportionately affects minorities and low-income groups in inner-city neighborhoods.³ Previous studies have identified unique allergen exposures in inner-city homes as important risk factors for asthma morbidity⁴ and demonstrated that interventions to reduce home exposure to these allergens improve asthma outcomes.⁵ There are some published data on the presence of allergens in schools^6-12; however, to our knowledge, there are no comprehensive studies evaluating asthma outcomes resulting from allergen exposures in schools, where children spend most of their day.¹³ The primary purpose of the School Inner-City Asthma Study was to comprehensively evaluate the role of school-specific indoor allergen exposures on asthma morbidity, adjusting for home allergen exposures.

Objectives. The forced expiratory volume in 1 second (FEV₁) felt to be an objective measure of airway obstruction is often normal in asthmatic children. The forced expiratory flow between 25% and 75% of vital capacity (FEF_25–75) reflects small airway patency and has been found to be reduced in children with asthma. The aim of this study was to determine whether FEF_25–75 is associated with increased childhood asthma severity and morbidity in the setting of a normal FEV₁, and to determine whether bronchodilator responsiveness (BDR) as defined by FEF_25–75 identifies more childhood asthmatics than does BDR defined by FEV₁. Methods. The Boston Children’s Hospital Pulmonary Function Test database was queried and the most recent spirometry result was retrieved for 744 children diagnosed with asthma between 10 and 18 years of age between October 2000 and October 2010. Electronic medical records in the 1 year prior and the 1 year following the date of spirometry were examined for asthma severity (mild, moderate, or severe) and morbidity outcomes for the three age, race, and gender-matched subgroups: Group A (n = 35) had a normal FEV₁, FEV₁/forced vital capacity (FVC), and FEF_25–75; Group B (n = 36) had solely a diminished FEV₁/FVC; and Group C (n = 37) had a normal FEV₁, low FEV₁/FVC, and low FEF_25–75. Morbidity outcomes analyzed included the presence of hospitalization, emergency department visit, intensive care unit admission, asthma exacerbation, and systemic steroid use. Results. Subjects with a low FEF_25–75 (Group C) had nearly 3 times the odds ratio (OR) (OR = 2.8, p < .01) of systemic corticosteroid use and 6 times the OR of asthma exacerbations (OR = 6.3, p > .01) compared with those who had normal spirometry (Group A). Using FEF_25–75 to define BDR identified 53% more subjects with asthma than did using a definition based on FEV₁. Conclusions. A low FEF_25–75 in the setting of a normal FEV₁ is associated with increased asthma severity, systemic steroid use, and asthma exacerbations in children. In addition, using the percent change in FEF_25–75 from baseline may be helpful in identifying BDR in asthmatic children with a normal FEV₁.

Purpose of review Asthma prevalence has markedly increased over the past 30 years. Although atopy and exposure to environmental allergens are known to exacerbate asthma, recent literature supports a causal role of indoor allergens in disease development. Recent findings High-risk birth cohorts continue to point to atopy as the main risk factor for developing asthma. Exposure to perennial allergens has also been linked to the development of asthma, though with less consistency. Intervention at the level of allergen exposure and allergic immune response is promising. Summary The current model of atopic asthma, the predominant phenotype, incorporates genetic and environmental factors in the development of disease. Although genetic factors are less malleable, the environmental component lends itself to analysis and modification. For many, the development of asthma starts with allergen exposure leading to atopic sensitization and subsequent disease. Several studies support the progression from exposure to sensitization with the potential of extremely high levels of exposure leading to tolerance. Likewise, the progression from atopy to asthma is well documented, especially in genetically predisposed children. Recent intervention trials confirm these findings and begin to show promise for the prevention of asthma by interrupting the allergen exposure → allergen sensitization → atopic asthma pathway.