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 op
portunities to uncover sometimes unexpected correlations between lifestyle,
environmental exposures, temporal development of the immune system, and ge
netics, Examples include the differing prevalence of atopy, bronchial hyper
responsiveness, and asthma in East and West Germany around the time of reun
ification, which suggests that a "western" lifestyle presents a greater ris
k for the development of allergic responses than the more traditionally sus
pected factor of outdoor air pollutant levels. Other epidemiologic studies
suggest how infections may interface with an atopic patterning: Evidence fr
om 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-H1 and T-H2 cells, are helping to formulate
a theory of interdependence between the early development of the immune sys
tem, allergen exposure, and the diverse community of airway cells whose sec
retory products generate the final physiologic response pattern.