The rising incidence of allergic disorders in developed countries is unexplained. Exposure to traffic related
air pollutants may be an important cause of
wheezing and
asthma in childhood. Experimental evidence from human studies suggests that
diesel exhaust particles, constituents of fine
particulate matter less than 2.5 microns (PM(2.5)), may act to enhance
IgE mediated aeroallergen sensitization and Th2 directed
cytokine responses. To date, epidemiologic investigations indicate that children living in close proximity to heavily travelled roads are more likely to be atopic and wheeze. The Cincinnati Childhood
Allergy and Air Pollution Study (CCAAPS) birth cohort study was initiated to test the hypothesis that early high exposure to traffic related
air pollutants is associated with early aeroallergen sensitization and allergic respiratory phenotypes. Using an exposure cohort design, more than 700 infants born to atopic parents were recruited at age 1 living either less than 400 meters (high traffic
pollutant exposure) or greater than 1,500 meters (low exposure) from a major road. Children were medically evaluated and underwent skin prick testing with aeroallergen at screening, and re-evaluated sequentially at ages 1, 2, 3, 4, and 7. In this study, both proximity and land use regression (LUR) models of traffic
air pollutant exposure have been assessed. Proximity to stop and go traffic with large concentrations of bus and truck traffic predicted persistent
wheezing during infancy. The LUR model estimated elemental
carbon attributable to traffic (ECAT) as a proxy for
diesel exhaust particulate exposure. High ECAT was significantly associated with
wheezing at age 1 as well as persistent
wheezing at age 3. High mold exposure predicted a well defined
asthma phenotype at age 7.