among racial and ethnic groups in the distribution of genetic risk factors or to the differences in exposure to environmental factors (Atkinson and Eisenbarth, 2001). In any case, the worldwide incidence of type 1 diabetes appears to be increasing 3% a year, and the rate of increase is greatest where incidence has been low (Onkamo et al., 1999). Data from Europe also indicate that incidence is increasing more rapidly among the youngest children (ages 0–4 years) (EURODIAB, 2000).


Allergy is responsible for a variety of acute and chronic health problems, including anaphylaxis and allergic rhinitis, asthma, and eczema. These conditions reflect an overreaction of the immune system to allergens—normally harmless environmental agents such as pollens, dust mites, insect venom, and certain foods—that can be encountered through inhalation, ingestion, injection, or skin contact. Under certain circumstances, exposure to an allergen primes the immune system for hypersensitivity reactions involving allergen-specific IgE antibodies and Th2 cells.

The committee focused its attention on allergic asthma for this report. Characteristic symptoms of asthma are episodes of shortness of breath, coughing, wheezing, and chest tightness. These symptoms reflect an acute bronchial hyperresponsiveness to specific allergens and other environmental factors, and a chronic inflammation of the airways (Busse and Lemanske, 2001; IOM, 2000; Kay, 2001; Parham, 2000). The acute response involves activation of mast cells in the lower airways and their release of histamine, cytokines, and other molecules. These mast-cell mediators induce accumulation of fluid, secretion of mucus, and contraction of the smooth muscle around the airways. A “late phase” response includes persistent or recurrent bronchial constriction and infiltration of airway tissue by inflammatory cells. The inflammation can produce temporary or permanent tissue damage.

Exposures to allergens and other environmental factors are known to induce new episodes of asthma when the disease is established, but the underlying factors that account for the development of this type of hyperresponsiveness are not fully understood. Several genetic factors may combine in various ways to establish susceptibility, but they remain poorly defined (Barnes, 2000; Kay, 2001). Environmental exposures may also influence the development of asthma, but current evidence is mixed for exposure such as cockroach allergens or cat dander (e.g., IOM, 2000; Lau et al., 2000; Litonjua et al., 2001; Peat et al., 1993). The presence of older siblings or attendance at day-care (factors that may be markers for the nature or timing of certain exposures) has shown protective effects (Ball et al., 2000). Early exposure to certain viral infections also has shown protective effects (Illi et al., 2001; Openshaw and Hewitt, 2000), but some

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