There have been many attempts to explain the increases in the incidence of allergic diseases, including hay fever and allergic asthma, that have been documented worldwide in recent decades. Epidemiologic studies offer rich opportunities to uncover sometimes unexpected correlations between lifestyle, environmental exposures, temporal development of the immune system, and genetics. Examples include the differing prevalence of atopy, bronchial hyperresponsiveness, and asthma in East and West Germany around the time of reunification, which suggests that a ''western'' lifestyle presents a greater risk for the development of allergic responses than the more traditionally suspected factor of outdoor air pollutant levels. Other epidemiologic studies suggest how infections may interface with an atopic patterning: Evidence from natural measles exposure and nonwheeze-inducing lower respiratory tract infections in young children implicate early childhood viral infections as protective against the development of atopy and airway allergic sensitivity, although in later life viral airway infections exacerbate asthma symptoms. These studies and others involving the scrutiny of lymphocyte subtypes in atopic individuals, notably T H 1 and T H 2 cells, are helping to formulate a theory of interdependence between the early development of the immune system, allergen exposure, and the diverse community of airway cells whose secretory products generate the final physiologic response pattern. (J Allergy Clin Immunol 2000;105:S593-8.)